Редактирование: Публикации о генах и старении (titles)

__NOTOC__

==ABCG2==

{{medline-entry
|title=[[ABCG2]] rs2231142 variant in hyperuricemia is modified by SLC2A9 and SLC22A12 polymorphisms and cardiovascular risk factors in an elderly community-dwelling population.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32183743
|abstract=The [[ABCG2]] rs2231142 single nucleotide polymorphism (SNP) is one of the most significant genetic variants associated with hyperuricemia (HUA) in Asian populations. However, the risk of [[ABCG2]] rs2231142 variants for HUA could interact with other important HUA risk variants and cardiovascular factors. This study investigated the effects of the combined association among [[ABCG2]] rs2231142 and multiple HUA genetic variants or cardiovascular risk factors on HUA risk and serum uric acid (sUA) levels in an elderly Chinese population. A total of 1206 participants over 65 years old were enrolled in this study. Physical and laboratory examinations were performed for all participants. The [[ABCG2]] rs2231142, SLC2A9 rs3733591, and SLC22A12 rs893006 SNPs were assayed using a standardized protocol. Logistic regression analysis and liner regression were adjusted respectively to account for the association between [[ABCG2]] rs2231142 and other genetic variants, as well as between cardiovascular risk factors and HUA risk and sUA levels. The prevalence of HUA was 14.71% in the elderly community-dwelling population. The [[ABCG2]] rs2231142 risk T allele was associated with HUA risk (odds ratio (OR) = 1.63, 95% confidence interval (CI): 1.27-2.11; p = 1.65 × 10 ) and with increased sUA levels (Beta = 0.16, p = 6.75 × 10 ) in the whole study population. Linear regression analysis showed that the mean sUA level increased linearly with the number of risk alleles of the three candidate genetic variants (Beta = 0.18, p = 1.94 × 10 ) The joint effect of the [[ABCG2]] rs2231142 T allele and cardiovascular risk factors (obesity, hypertension and dyslipidemia) was also associated with increased HUA risk and sUA levels. Each copy of the risk T allele was significantly associated with enhanced HUA risk in patients with hypertriglyceridemia (OR = 2.52, 95% CI: 1.33-4.60; p = 0.003) compared to controls. Our findings reinforce the importance of the [[ABCG2]] rs2231143 variant as a crucial genetic locus for HUA in Chinese populations and demonstrated the combined effects of multiple genetic risk variants and cardiovascular risk exposures on HUA risk and increased sUA level.
|mesh-terms=* ATP Binding Cassette Transporter, Subfamily G, Member 2
* Aged
* Aged, 80 and over
* Aging
* Cardiovascular Diseases
* China
* Cohort Studies
* Effect Modifier, Epidemiologic
* Epistasis, Genetic
* Female
* Genes, Modifier
* Genetic Predisposition to Disease
* Genome-Wide Association Study
* Glucose Transport Proteins, Facilitative
* Humans
* Hyperuricemia
* Independent Living
* Male
* Neoplasm Proteins
* Organic Anion Transporters
* Organic Cation Transport Proteins
* Polymorphism, Single Nucleotide
* Risk Factors
* Uric Acid
|keywords=* ABCG2
* Hypertension
* Polymorphisms
* Triglyceridemia
* Uric acid
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7077001
}}
==ABL1==

{{medline-entry
|title=European LeukemiaNet 2020 recommendations for treating chronic myeloid leukemia.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32127639
|abstract=The therapeutic landscape of chronic myeloid leukemia (CML) has profoundly changed over the past 7 years. Most patients with chronic phase (CP) now have a normal life expectancy. Another goal is achieving a stable deep molecular response (DMR) and discontinuing medication for treatment-free remission (TFR). The European LeukemiaNet convened an expert panel to critically evaluate and update the evidence to achieve these goals since its previous recommendations. First-line treatment is a tyrosine kinase inhibitor (TKI; imatinib brand or generic, dasatinib, nilotinib, and bosutinib are available first-line). Generic imatinib is the cost-effective initial treatment in CP. Various contraindications and side-effects of all TKIs should be considered. Patient risk status at diagnosis should be assessed with the new EUTOS long-term survival (ELTS)-score. Monitoring of response should be done by quantitative polymerase chain reaction whenever possible. A change of treatment is recommended when intolerance cannot be ameliorated or when molecular milestones are not reached. Greater than 10% BCR-[[ABL1]] at 3 months indicates treatment failure when confirmed. Allogeneic transplantation continues to be a therapeutic option particularly for advanced phase CML. TKI treatment should be withheld during pregnancy. Treatment discontinuation may be considered in patients with durable DMR with the goal of achieving TFR.
|mesh-terms=* Aniline Compounds
* Antineoplastic Agents
* Clinical Decision-Making
* Consensus Development Conferences as Topic
* Dasatinib
* Disease Management
* Fusion Proteins, bcr-abl
* Gene Expression
* Humans
* Imatinib Mesylate
* Leukemia, Myelogenous, Chronic, BCR-ABL Positive
* Life Expectancy
* Monitoring, Physiologic
* Nitriles
* Protein Kinase Inhibitors
* Pyrimidines
* Quality of Life
* Quinolines
* Survival Analysis
|keywords=#f
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7214240
}}
==ACE==

{{medline-entry
|title=Angiotensin-Converting Enzyme ([[ACE]]) genetic variation and longevity in Peruvian older people: a cross-sectional study.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32281429
|abstract= Some studies have suggested that the insertion(I)/deletion(D) polymorphism of the Angiotensin-Converting Enzyme ([[ACE]]) gene may be associated with human longevity, especially in centenarians. However, this association is still controversial. Besides, there have been no studies in Peruvians.  To describe the age distribution of the [[ACE]] polymorphism in a convenience sample of Peruvian older people.  This was a cross-sectional study in 104 Geriatric Day Hospital patients in Lima, Perú. The [[ACE]] polymorphism was determined in all patients. For the purpose of association with age, the sample was divided into four categories: young (< 65), youngest-old (65-74), middle-old (75-84) and oldest-old (85 or more).  The distribution of genotype frequencies was consistent with a population in Hardy-Weinberg equilibrium ([i]p[/i] = 0.62). The number (%) of D/D, I/D and I/I genotypes in the young was 2 (14.3%), 3 (21.4%) and 9 (64.3%), respectively; in youngest-old: 4 (11.4%), 15 (42.9%) and 16 (45.7%); in middle-old: 6 (12.2%), 20 (40.8%) and 23 (46.9%); and in oldest-old: 0 (0.0%), 4 (66.7%) and 2 (33.3%). A chi-square analysis showed no significant differences in genotype distribution between age groups ([i]p[/i] = 0.647).  No significant age differences were found in the distribution of the [[ACE]] polymorphism in this sample. Further studies with greater statistical power are recommended.
|mesh-terms=* Aged
* Aged, 80 and over
* Cross-Sectional Studies
* Female
* Genetic Variation
* Humans
* Longevity
* Male
* Middle Aged
* Peptidyl-Dipeptidase A
* Peru
* Polymorphism, Genetic
|keywords=* ACE gene
* Longevity
* Perú
* ageing
|full-text-url=https://sci-hub.do/10.1080/03014460.2020.1748227
}}
{{medline-entry
|title=COVID-19 and chronological aging: senolytics and other anti-aging drugs for the treatment or prevention of corona virus infection?
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32229706
|abstract=COVID-19, also known as SARS-CoV-2, is a new emerging zoonotic corona virus of the SARS (Severe Acute Respiratory Syndrome) and the MERS (Middle East Respiratory Syndrome) family. COVID-19 originated in China and spread world-wide, resulting in the pandemic of 2020. For some reason, COVID-19 shows a considerably higher mortality rate in patients with advanced chronological age. This begs the question as to whether there is a functional association between COVID-19 infection and the process of chronological aging. Two host receptors have been proposed for COVID-19. One is CD26 and the other is [[ACE]]-2 (angiotensin-converting enzyme 2). Interestingly, both CD26 and the angiotensin system show associations with senescence. Similarly, two proposed therapeutics for the treatment of COVID-19 infection are Azithromycin and Quercetin, both drugs with significant senolytic activity. Also, Chloroquine-related compounds inhibit the induction of the well-known senescence marker, Beta-galactosidase. Other anti-aging drugs should also be considered, such as Rapamycin and Doxycycline, as they behave as inhibitors of protein synthesis, blocking both SASP and viral replication. Therefore, we wish to speculate that the fight against COVID-19 disease should involve testing the hypothesis that senolytics and other anti-aging drugs may have a prominent role in preventing the transmission of the virus, as well as aid in its treatment. Thus, we propose that new clinical trials may be warranted, as several senolytic and anti-aging therapeutics are existing FDA-approved drugs, with excellent safety profiles, and would be readily available for drug repurposing efforts. As Azithromycin and Doxycycline are both commonly used antibiotics that inhibit viral replication and IL-6 production, we may want to consider this general class of antibiotics that functionally inhibits cellular protein synthesis as a side-effect, for the treatment and prevention of COVID-19 disease.
|mesh-terms=* Age Factors
* Aged
* Aged, 80 and over
* Aging
* Angiotensin-Converting Enzyme 2
* Antiviral Agents
* Azithromycin
* Betacoronavirus
* COVID-19
* Coronavirus Infections
* Dipeptidyl Peptidase 4
* Humans
* Hydroxychloroquine
* Pandemics
* Peptidyl-Dipeptidase A
* Pneumonia, Viral
* Quercetin
* Receptors, Virus
* SARS-CoV-2
|keywords=* Azithromycin
* COVID-19
* Doxycycline
* Hydroxy-chloroquine
* Quercetin
* Rapamycin
* aging
* antibiotic
* corona virus
* drug repurposing
* prevention
* senescence
* senolytic drug therapy
* viral replication
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7202514
}}
==ACR==

{{medline-entry
|title=Progenitor cell niche senescence reflects pathology of the parotid salivary gland in primary Sjögren's syndrome.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32159757
|abstract=Salivary gland (SG) progenitor cells (SGPCs) maintain SG homeostasis. We have previously shown that in primary Sjögren's syndrome (pSS), SGPCs are likely to be senescent, and may underpin SG dysfunction. This study assessed the extent of senescence of cells in a SGPC niche in pSS patients' SGs, and its correlation with functional and clinical parameters. The expression of p16 and p21 as markers of senescence in both total SG epithelium and a SGPC niche (basal striated duct cells, BSD) was examined in SGs of pSS (n = 35), incomplete pSS (n = 13) (patients with some signs of pSS, but not fulfilling all classification criteria) and non-SS sicca control (n = 21) patients. This was correlated with functional and clinical parameters. pSS patient SGs contained significantly more p16+ cells both in the epithelium in general (P <0.01) and in the BSD layer (P <0.001), than non-SS SGs. Significant correlations were found in pSS patients between p16+ BSD cells and secretion of unstimulated whole saliva, stimulated whole saliva, stimulated parotid saliva, CD45+ infiltrate, ultrasound total score and [[ACR]]-EULAR classification score, but not with EULAR Sjögren's syndrome disease activity index (ESSDAI) and EULAR Sjögren's Syndrome Patient Reported Index (ESSPRI) scores. Correlations with total epithelium p16+ cells were weaker. Incomplete pSS patients also had increased numbers of p16+ epithelial and BSD cells. Based on protein and mRNA expression, p21+ appears not to play a significant role in the SG in pSS. These findings suggest SGPC senescence may be an early feature of primary Sjögren's syndrome and may contribute to defective SG function in pSS but not to systemic disease activity.

|keywords=* p16
* primary Sjögren’s syndrome
* salivary gland
* salivary gland progenitor cells
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7516109
}}
==ADAM10==

{{medline-entry
|title=NKG2D Ligand Shedding in Response to Stress: Role of [[ADAM10]].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32269567
|abstract=NKG2D is an activating receptor expressed by NK cells and some subsets of T cells and represents a major recognition receptor for detection and elimination of cancer cells. The ligands of NKG2D are stress-induced self-proteins that can be secreted as soluble molecules by protease-mediated cleavage. The release of NKG2D ligands in the extracellular milieu is considered a mode of finely controlling their surface expression levels and represents a relevant immune evasion mechanism employed by cancer cells to elude NKG2D-mediated immune surveillance. A disintegrin and metalloproteinase 10 ([[ADAM10]]), a catalytically active member of the ADAM family of proteases, is involved in the cleavage of some NKG2D ligands in various types of cancer cells either in steady state conditions and in response to an ample variety of stress stimuli. Appealing immunotherapeutic strategies devoted to promoting NK cell-mediated recognition and elimination of cancer cells are based on the upregulation of NK cell activating ligands. In particular, activation of DNA damage response (DDR) and the induction of cellular senescence by chemotherapeutic agents are associated with increased expression of NKG2D ligands on cancer cell surface. Herein, we will review advances on the protease-mediated cleavage of NKG2D ligands in response to chemotherapy-induced stress focusing on: (i) the role played by [[ADAM10]] in this process and (ii) the implications of NKG2D ligand shedding in the course of cancer therapy and in senescent cells.

|keywords=* ADAM10
* NKG2D
* NKG2D ligands
* cancer
* chemotherapy
* senescence
* shedding
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7109295
}}
==AFM==

{{medline-entry
|title=The Effect of Waste Engine Oil and Waste Polyethylene on UV Aging Resistance of Asphalt.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32155867
|abstract=Waste engine oil (WEO) and waste polyethylene (WPE) are two common wastes, which are easy to pollute the environment. As the primary material in road construction, natural asphalt is a non-renewable energy source and asphalt is vulnerable to ultraviolet (UV) radiation during the service life. It results in degradation of asphalt pavement performance. In this paper, 22 wt % to 82 wt % of WEO and WPE were used to modify asphalts and the UV aging simulation experiment was carried out. The physical parameters of asphalts before the UV aging experiment show that the asphalt containing 42 wt % WPE and 62 wt % WEO mixture (42 wt % WPE + 62 wt % WEO) has similar physical properties with that of the matrix asphalt. Besides, gel permeation chromatography (GPC) verifies that the molecular weight distribution of the asphalt containing 42 wt % WPE + 62 wt % WEO is close to that of the matrix asphalt. The storage stability test shows that 42 wt % WPE + 62 wt % WEO has good compatibility with the matrix asphalt. The functional groups and micro-morphology of asphalts before and after the UV aging experiment were investigated by Fourier transform infrared spectroscopy (FTIR) and atomic force microscopy ([[AFM]]). FTIR results display that 42 wt % WPE + 62 wt % WEO can effectively reduce the formation of carbonyl and sulfoxide functional groups. [[AFM]] shows that 42 wt % WPE + 62 wt % WEO can also retard the formation of a "bee-like" structure in asphalt after the UV aging experiment. Based on the above results, it can be concluded that WEO and WPE mixture can replace part of asphalt and improve the UV aging resistance of asphalt.

|keywords=* Fourier transform infrared spectroscopy
* atomic force microscopy
* gel permeation chromatography
* ultraviolet aging
* waste engine oil
* waste polyethylene
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7182932
}}
{{medline-entry
|title=Mechanical properties measured by atomic force microscopy define health biomarkers in ageing C. elegans.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32098962
|abstract=Genetic and environmental factors are key drivers regulating organismal lifespan but how these impact healthspan is less well understood. Techniques capturing biomechanical properties of tissues on a nano-scale level are providing new insights into disease mechanisms. Here, we apply Atomic Force Microscopy ([[AFM]]) to quantitatively measure the change in biomechanical properties associated with ageing Caenorhabditis elegans in addition to capturing high-resolution topographical images of cuticle senescence. We show that distinct dietary restriction regimes and genetic pathways that increase lifespan lead to radically different healthspan outcomes. Hence, our data support the view that prolonged lifespan does not always coincide with extended healthspan. Importantly, we identify the insulin signalling pathway in C. elegans and interventions altering bacterial physiology as increasing both lifespan and healthspan. Overall, [[AFM]] provides a highly sensitive technique to measure organismal biomechanical fitness and delivers an approach to screen for health-improving conditions, an essential step towards healthy ageing.
|mesh-terms=* Aging
* Animal Feed
* Animals
* Bacillus subtilis
* Biomarkers
* Caenorhabditis elegans
* Caenorhabditis elegans Proteins
* Comamonas
* Escherichia coli
* Forkhead Transcription Factors
* Hot Temperature
* Insulin
* Microbiota
* Microscopy, Atomic Force
* Mutation
* Receptor, Insulin
* Signal Transduction
* Ultraviolet Rays
|keywords=#f
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7042263
}}
==ALOX12==

{{medline-entry
|title=Arachidonate 12-lipoxygenase and 12-hydroxyeicosatetraenoic acid contribute to stromal aging-induced progression of pancreatic cancer.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32265301
|abstract=The incidence of pancreatic cancer increases with age, suggesting that chronological aging is a significant risk factor for this disease. Fibroblasts are the major nonmalignant cell type in the stroma of human pancreatic ductal adenocarcinoma (PDAC). In this study, we investigated whether the chronological aging of normal human fibroblasts (NHFs), a previously underappreciated area in pancreatic cancer research, influences the progression and therapeutic outcomes of PDAC. Results from experiments with murine xenografts and 2D and 3D co-cultures of NHFs and PDAC cells revealed that older NHFs stimulate proliferation of and confer resistance to radiation therapy of PDAC. MS-based metabolite analysis indicated that older NHFs have significantly increased arachidonic acid 12-lipoxygenase ([[ALOX12]]) expression and elevated levels of its mitogenic metabolite, 12-([i]S[/i])-hydroxy-5,8,10,14-eicosatetraenoic acid (12-([i]S[/i])-HETE) compared with their younger counterparts. In co-cultures with older rather than with younger NHFs, PDAC cells exhibited increases in mitogen-activated protein kinase signaling and cellular metabolism, as well as a lower oxidation state that correlated with their enhanced proliferation and resistance to radiation therapy. Expression of [[ALOX12]] was found to be significantly lower in PDAC cell lines and tumor biopsies, suggesting that PDAC cells rely on a stromal supply of mitogens for their proliferative needs. Pharmacological (hydroxytyrosol) and molecular (siRNA) interventions of [[ALOX12]] in older NHFs suppressed their ability to stimulate proliferation of PDAC cells. We conclude that chronological aging of NHFs contributes to PDAC progression and that [[ALOX12]] and 12-([i]S[/i])-HETE may be potential stromal targets for interventions that seek to halt progression and improve therapy outcomes.

|keywords=* aging
* arachidonic acid (AA) (ARA)
* cancer biology
* cell proliferation
* fibroblast
* pancreatic cancer
* stromal cell
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7242692
}}
==AMH==

{{medline-entry
|title=Modeling Variation in the Reproductive Lifespan of Female Adolescent and Young Adult Cancer Survivors Using [[AMH]].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32270202
|abstract=Many female survivors of adolescent and young adult cancers (AYA survivors) have shortened reproductive lifespans. However, the timing and duration of ovarian function after cancer treatment are largely unknown. To model the trajectory of ovarian function over two decades following cancer treatment and evaluate how trajectories vary by treatment gonadotoxicity and age. In a prospective cohort, AYA survivors aged 18-39 at variable times since cancer treatment completion provided dried blood spots (DBS) every 6 months for up to 18 months. Anti-Müllerian hormone ([[AMH]]) levels were measured using the Ansh DBS [[AMH]] enzyme-linked immunosorbent assay. The mean [[AMH]] trajectory was modeled for the entire cohort and separately by treatment gonadotoxicity and age using functional principal components analysis. 763 participants, mean (standard deviation) enrollment age 33.3 (4.7) and age at cancer diagnosis 25.9 (5.7) years, contributed 1905 DBS samples. The most common cancers were breast (26.9%), lymphoma (24.8%), and thyroid (18.0%). [[AMH]] trajectories differed among survivors by treatment gonadotoxicity (low, moderate, or high) (P < 0.001). Following low or moderately gonadotoxic treatments, [[AMH]] levels increased over 2-3 years and plateaued over 10-15 years before declining. In contrast, following highly gonadotoxic treatment, [[AMH]] levels were lower overall and declined shortly after peak at 2-3 years. Younger age at treatment was associated with higher trajectories, but a protective effect of younger age was not observed in survivors exposed to highly gonadotoxic treatments (Pinteraction < 0.001). In this large AYA survivor cohort, timing and duration of ovarian function strongly depended on treatment gonadotoxicity and age at treatment. The findings provide novel, more precise information to guide reproductive decision-making.

|keywords=* AMH
* adolescent and young adult cancer
* functional principal components analysis
* ovarian reserve
* reproductive lifespan
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7329316
}}
{{medline-entry
|title=Improving Prediction of Age at Menopause Using Multiple Anti-Müllerian Hormone Measurements: the Tehran Lipid-Glucose Study.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109280
|abstract=Several statistical models were introduced for the prediction of age at menopause using a single measurement of anti-müllerian hormone ([[AMH]]); however, individual prediction is challenging and needs to be improved. The objective of this study was to determine whether multiple [[AMH]] measurements can improve the prediction of age at menopause. All eligible reproductive-age women (n = 959) were selected from the Tehran Lipid and Glucose Study. The serum concentration of [[AMH]] was measured at the time of recruitment and twice after that at an average of 6-year intervals. An accelerated failure-time model with Weibull distribution was used to predict age at menopause, using a single [[AMH]] value vs a model that included the annual [[AMH]] decline rate. The adequacy of these models was assessed using C statistics. The median follow-up period was 14 years, and 529 women reached menopause. Adding the annual decline rate to the model that included single [[AMH]] improved the model's discrimination adequacy from 70% (95% CI: 67% to 71%) to 78% (95% CI: 75% to 80%) in terms of C statistics. The median of differences between actual and predicted age at menopause for the first model was -0.48 years and decreased to -0.21 in the model that included the decline rate. The predicted age at menopause for women with the same amount of age-specific [[AMH]] but an annual [[AMH]] decline rate of 95 percentiles was about one decade lower than in those with a decline rate of 5 percentiles. Prediction of age at menopause could be improved by multiple [[AMH]] measurements; it will be useful in identifying women at risk of early menopause.

|keywords=* Tehran Lipid and Glucose Study (TLGS)
* anti-müllerian hormone (AMH)
* menopause
* reproductive aging
|full-text-url=https://sci-hub.do/10.1210/clinem/dgaa083
}}
==AMT==

{{medline-entry
|title=A multi-method comparison of autobiographical memory impairments amongst younger and older adults.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32162531
|abstract= Research indicates that, compared to younger adults, older adults have difficulty recalling memories of specific past events (those lasting less than 24 h) and this difficulty is associated with depression. These studies are largely confined to a single measure of specific memory recall and there are conflicting findings when alternative measures are used. This investigation provides the first comparison of memory specificity between younger and older adults using several different measures.  Older ([i]n[/i] = 105) and younger ([i]n[/i] = 88) adults completed the Autobiographical Memory Test ([[AMT]]), Autobiographical Memory Interview (AMI) and Sentence Completion for Events from the Past Test (SCEPT) and the number of specific memories was quantified for each measure. Participants also completed the Beck Depression Inventory Version II (BDI-II).  Compared to younger adults, older adults recalled fewer specific memories in the [[AMT]] and more specific memories in the AMI. This latter effect was particularly pronounced for memories related to childhood. There was no group difference in responses in the SCEPT. There was no evidence of an association between memory specificity and depression for any of the measures.  Older adults have difficulty retrieving specific memories after cuing by nouns and adjectives, as in the [[AMT]], but they have enhanced recall of specific memories after cuing by life periods, as in the AMI, and this is particularly true of memories related to childhood. Individual differences in memory specificity are not related to depression symptoms in healthy samples.

|keywords=* Depression
* aging
* episodic memory
* overgeneral
* specificity
|full-text-url=https://sci-hub.do/10.1080/13607863.2020.1729338
}}
==APOE==

{{medline-entry
|title=Alzheimer's Risk Factors Age, [[APOE]] Genotype, and Sex Drive Distinct Molecular Pathways.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32199103
|abstract=Evidence suggests interplay among the three major risk factors for Alzheimer's disease (AD): age, [[APOE]] genotype, and sex. Here, we present comprehensive datasets and analyses of brain transcriptomes and blood metabolomes from human apoE2-, apoE3-, and apoE4-targeted replacement mice across young, middle, and old ages with both sexes. We found that age had the greatest impact on brain transcriptomes highlighted by an immune module led by Trem2 and Tyrobp, whereas [[APOE]]4 was associated with upregulation of multiple Serpina3 genes. Importantly, these networks and gene expression changes were mostly conserved in human brains. Finally, we observed a significant interaction between age, [[APOE]] genotype, and sex on unfolded protein response pathway. In the periphery, [[APOE]]2 drove distinct blood metabolome profile highlighted by the upregulation of lipid metabolites. Our work identifies unique and interactive molecular pathways underlying AD risk factors providing valuable resources for discovery and validation research in model systems and humans.
|mesh-terms=* Adaptor Proteins, Signal Transducing
* Age Factors
* Aging
* Alzheimer Disease
* Animals
* Apolipoprotein E2
* Apolipoprotein E3
* Apolipoprotein E4
* Apolipoproteins E
* Brain
* Female
* Gene Expression
* Gene Expression Profiling
* Gene Regulatory Networks
* Genotype
* Humans
* Male
* Membrane Glycoproteins
* Membrane Proteins
* Metabolome
* Mice
* Mice, Transgenic
* Protective Factors
* Receptors, Immunologic
* Risk Factors
* Serpins
* Sex Factors
* Unfolded Protein Response
|keywords=* APOE
* Alzheimer’s disease
* Serpina3
* age
* extracellular vesicles
* inflammation
* lipid metabolism
* metabolomics
* sex
* transcriptomics
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388065
}}
{{medline-entry
|title=Less agreeable, better preserved? A PET amyloid and MRI study in a community-based cohort.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32169357
|abstract=The relationship between personality profiles and brain integrity in old age is still a matter of debate. We examined the association between Big Five factor and facet scores and MRI brain volume changes on a 54-month follow-up in 65 elderly controls with 3 neurocognitive assessments (baseline, 18 months, and 54 months), structural brain MRI (baseline and 54 months), brain amyloid PET during follow-up, and [[APOE]] genotyping. Personality was assessed with the Neuroticism Extraversion Openness Personality Inventory-Revised. Regression models were used to identify predictors of volume loss including time, age, sex, personality, amyloid load, presence of [[APOE]] ε4 allele, and cognitive evolution. Lower agreeableness factor scores (and 4 of its facets) were associated with lower volume loss in the hippocampus, entorhinal cortex, amygdala, mesial temporal lobe, and precuneus bilaterally. Higher openness factor scores (and 2 of its facets) were also associated with lower volume loss in the left hippocampus. Our findings persisted when adjusting for confounders in multivariable models. These data suggest that the combination of low agreeableness and high openness is an independent predictor of better preservation of brain volume in areas vulnerable to neurodegeneration.
|mesh-terms=* Aged
* Aged, 80 and over
* Amyloidogenic Proteins
* Apolipoproteins E
* Brain
* Cognition
* Cohort Studies
* Female
* Follow-Up Studies
* Humans
* Magnetic Resonance Imaging
* Male
* Neuroimaging
* Organ Size
* Personality
* Positron-Emission Tomography
|keywords=* Amyloid load
* Cognitive aging
* Cohort studies
* Personality
* Structural MRI
|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.02.004
}}
{{medline-entry
|title=Physical Activity as Moderator of the Association Between [[APOE]] and Cognitive Decline in Older Adults: Results from Three Longitudinal Cohort Studies.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32110803
|abstract=Previous studies have suggested that the association between [[APOE]] ɛ 4 and dementia is moderated by physical activity (PA), but the results remain inconclusive and longitudinal data on cognitive decline are missing. In this study, we examine whether there is a gene-environment interaction between [[APOE]] and PA on cognitive decline in older adults using 9-year follow-up data of three cohort studies. We followed 7,176 participants from three longitudinal cohort studies: Longitudinal Aging Study Amsterdam (LASA), InCHIANTI, and Rotterdam Study for 9 years. PA was assessed with self-reported questionnaires and was categorized in low, moderate, and high PA. Cognitive function was assessed with the Mini-Mental State Examination (MMSE) and cognitive decline was defined as a decrease of three points or more on the MMSE during 3 years follow-up. We fitted logistic regression models using generalized estimating equations adjusting for age, sex, education, depressive symptoms, and number of chronic disease. Interaction between [[APOE]] and PA was tested on multiplicative and additive scale. Cohorts were similar in most aspects but InCHIANTI participants were on average older and had lower education. [[APOE]] ɛ 4 carriers had higher odds of cognitive decline (odds ratio [OR] = 1.46, 95% confidence interval [CI]: 1.29-1.64) while PA was not significantly associated with cognitive decline overall (moderate PA: OR = 0.87, 0.67-1.13; high PA: OR = 0.71, 0.36-1.40). There was no evidence for an interaction effect between PA and [[APOE]] ɛ 4 in cognitive decline in older adults ([[APOE]] × moderate PA: p = .83; [[APOE]] × high PA: p = .90). Previous claims of a gene-environment interaction between [[APOE]] ɛ 4 and PA in cognitive decline are not supported by our results.

|keywords=* Gene–environment interaction
* InCHIANTI
* Longitudinal Aging Study Amsterdam
* Rotterdam Study
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7518558
}}
{{medline-entry
|title=Longitudinal Maintenance of Cognitive Health in Centenarians in the 100-plus Study.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32101309
|abstract=Some individuals who reach ages beyond 100 years in good cognitive health may be resilient against risk factors associated with cognitive decline. Exploring the processes underlying resilience may contribute to the development of therapeutic strategies that help to maintain cognitive health while aging. To identify individuals who escape cognitive decline until extreme ages and to investigate the prevalence of associated risk factors. The 100-plus Study is a prospective observational cohort study of community-based Dutch centenarians enrolled between 2013 and 2019 who were visited annually until death or until participation was no longer possible. The centenarians self-reported their cognitive health, as confirmed by a proxy. Of the 1023 centenarians approached for study inclusion, 340 fulfilled the study criteria and were included in analyses. Data analysis was performed from April 2019 to December 2019. Cognition was assessed using the Mini-Mental State Examination (MMSE). To identify centenarians who escape cognitive decline, this study investigated the association of baseline cognition with survivorship and cognitive trajectories for at least 2 years of follow-up using linear mixed models, adjusted for sex, age, and education. This study investigated the prevalence of apolipoprotein E ([[APOE]]) genotypes and cardiovascular disease as risk factors associated with cognitive decline. At baseline, the median age of 340 centenarians was 100.5 years (range, 100.0-108.2 years); 245 participants (72.1%) were female. The maximum survival estimate plateaued at 82% per year (95% CI, 77% to 87%) across centenarians who scored 26 to 30 points on the baseline MMSE (hazard ratio, 0.56; 95% CI, 0.42 to 0.75; P < .001), suggesting that an MMSE score of 26 or higher is representative of both cognitive and physical health. Among the 79 centenarians who were followed up for 2 years or longer, those with baseline MMSE score less than 26 experienced a decline in MMSE score of 1.68 points per year (95% CI, -2.45 to -0.92 points per year; P = .02), whereas centenarians with MMSE scores of 26 or higher at baseline experienced a decline of 0.71 point per year (95% CI, -1.08 to -0.35 points per year). For 73% of the centenarians with baseline MMSE scores of 26 or higher, no cognitive changes were observed, which often extended to ensuing years or until death. It is estimated that this group is representative of less than 10% of Dutch centenarians. In this group, 18.6% carried at least 1 [[APOE]]-ε4 allele, compared with 5.6% of the centenarians with lower and/or declining cognitive performance. Most centenarians who scored 26 or higher on the MMSE at baseline maintained high levels of cognitive performance for at least 2 years, in some cases despite the presence of risk factors associated with cognitive decline. Investigation of this group might reveal the processes underlying resilience against risk factors associated with cognitive decline.
|mesh-terms=* Aged, 80 and over
* Aging
* Apolipoprotein E4
* Cognition
* Female
* Humans
* Longitudinal Studies
* Male
* Mental Status and Dementia Tests
* Prospective Studies
|keywords=#f
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7137688
}}
==APP==

{{medline-entry
|title=Transcriptomic profiling of microglia and astrocytes throughout aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32238175
|abstract=Activation of microglia and astrocytes, a prominent hallmark of both aging and Alzheimer's disease (AD), has been suggested to contribute to aging and AD progression, but the underlying cellular and molecular mechanisms are largely unknown. We performed RNA-seq analyses on microglia and astrocytes freshly isolated from wild-type and [[APP]]-PS1 (AD) mouse brains at five time points to elucidate their age-related gene-expression profiles. Our results showed that from 4 months onward, a set of age-related genes in microglia and astrocytes exhibited consistent upregulation or downregulation (termed "age-up"/"age-down" genes) relative to their expression at the young-adult stage (2 months). And most age-up genes were more highly expressed in AD mice at the same time points. Bioinformatic analyses revealed that the age-up genes in microglia were associated with the inflammatory response, whereas these genes in astrocytes included widely recognized AD risk genes, genes associated with synaptic transmission or elimination, and peptidase-inhibitor genes. Overall, our RNA-seq data provide a valuable resource for future investigations into the roles of microglia and astrocytes in aging- and amyloid-β-induced AD pathologies.

|keywords=* Aging
* Alzheimer’s disease (AD)
* Astrocyte
* Microglia
* RNA-seq
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7115095
}}
{{medline-entry
|title=Platelets in Amyloidogenic Mice Are Activated and Invade the Brain.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32194368
|abstract=Alzheimer's disease (AD) is a neurodegenerative disease with a complex and not fully understood pathogenesis. Besides brain-intrinsic hallmarks such as abnormal deposition of harmful proteins, i.e., amyloid beta in plaques and hyperphosphorylated Tau in neurofibrillary tangles, blood-derived elements, in particular, platelets have been discussed to be involved in AD pathogenesis. The underlying mechanisms, however, are rather unexplored. Here, we investigate a potential role of platelets in an AD transgenic animal model with severe amyloid plaque formation, the [[APP]]-PS1 transgenic mice, and analyzed the presence, spatial location and activation status of platelets within the brain. In [[APP]]-PS1 mice, a higher number of platelets were located within the brain parenchyma, i.e., outside the cerebral blood vessels compared to WT controls. Such platelets were activated according to the expression of the platelet activation marker CD62P and to morphological hallmarks such as membrane protrusions. In the brain, platelets were in close contact exclusively with astrocytes suggesting an interaction between these two cell types. In the bloodstream, although the percentage of activated platelets did not differ between transgenic and age-matched control animals, [[APP]]-PS1 blood-derived platelets showed remarkable ultrastructural peculiarities in platelet-specific organelles such as the open canalicular system (OCS). This work urges for further investigations on platelets and their yet unknown functional roles in the brain, which might go beyond AD pathogenesis and be relevant for various age-related neurodegenerative diseases.

|keywords=* Alzheimer’s disease
* aging
* astrocytes
* platelets
* vascular pathology
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7063083
}}
==ATF6==

{{medline-entry
|title=ER stress activates immunosuppressive network: implications for aging and Alzheimer's disease.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32279085
|abstract=The endoplasmic reticulum (ER) contains stress sensors which recognize the accumulation of unfolded proteins within the lumen of ER, and subsequently these transducers stimulate the unfolded protein response (UPR). The ER sensors include the IRE1, PERK, and [[ATF6]] transducers which activate the UPR in an attempt to restore the quality of protein folding and thus maintain cellular homeostasis. If there is excessive stress, UPR signaling generates alarmins, e.g., chemokines and cytokines, which activate not only tissue-resident immune cells but also recruit myeloid and lymphoid cells into the affected tissues. ER stress is a crucial inducer of inflammation in many pathological conditions. A chronic low-grade inflammation and cellular senescence have been associated with the aging process and many age-related diseases, such as Alzheimer's disease. Currently, it is known that immune cells can exhibit great plasticity, i.e., they are able to display both pro-inflammatory and anti-inflammatory phenotypes in a context-dependent manner. The microenvironment encountered in chronic inflammatory conditions triggers a compensatory immunosuppression which defends tissues from excessive inflammation. Recent studies have revealed that chronic ER stress augments the suppressive phenotypes of immune cells, e.g., in tumors and other inflammatory disorders. The activation of immunosuppressive network, including myeloid-derived suppressor cells (MDSC) and regulatory T cells (Treg), has been involved in the aging process and Alzheimer's disease. We will examine in detail whether the ER stress-related changes found in aging tissues and Alzheimer's disease are associated with the activation of immunosuppressive network, as has been observed in tumors and many chronic inflammatory diseases.

|keywords=* Ageing
* Immunometabolism
* Immunosenescence
* Immunosuppression
* Inflammaging
* Neurodegeneration
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7220864
}}
==ATG3==

{{medline-entry
|title=Estrogen Signaling Induces Mitochondrial Dysfunction-Associated Autophagy and Senescence in Breast Cancer Cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32244623
|abstract=Previous work has shown that although estrogen (E2) disrupts cellular iron metabolism and induces oxidative stress in breast and ovarian cancer cells, it fails to induce apoptosis. However, E2 treatment was reported to enhance the apoptotic effects of doxorubicin in cancer cells. This suggests that E2 can precipitate anti-growth effects that render cancer cells more susceptible to chemotherapy. To investigate such anti-growth non-apoptotic, effects of E2 in cancer cells, MDA-MB-231 and MCF-7 cells were evaluated for the expression of key autophagy and senescence markers and for mitochondrial damage following E2 treatment. Treated cells experienced mitochondrial membrane depolarization along with increased expression of LC3-I/II, Pink1 and LAMP2, increased LC3-II accumulation and increased lysosomal and mitochondrial accumulation and flattening. E2-treated MCF-7 cells also showed reduced P53 and pRb780 expression and increased Rb and P21 expression. Increased expression of the autophagy markers [[ATG3]] and Beclin1 along with increased levels of β-galactosidase activity and IL-6 production were evident in E2-treated MCF-7 cells. These findings suggest that E2 precipitates a form of mitochondrial damage that leads to cell senescence and autophagy in breast cancer cells.

|keywords=* Estrogen
* MCF-7
* MDA-MB-231
* autophagy
* mitochondria
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7235898
}}
==ATM==

{{medline-entry
|title=[[ATM]] is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32201398
|abstract=NF-κB is a transcription factor activated in response to inflammatory, genotoxic and oxidative stress and important for driving senescence and aging. Ataxia-telangiectasia mutated ([[ATM]]) kinase, a core component of DNA damage response signaling, activates NF-κB in response to genotoxic and oxidative stress via post-translational modifications. Here we demonstrate that [[ATM]] is activated in senescent cells in culture and murine tissues from [i]Ercc1[/i]-deficient mouse models of accelerated aging, as well as naturally aged mice. Genetic and pharmacologic inhibition of [[ATM]] reduced activation of NF-κB and markers of senescence and the senescence-associated secretory phenotype (SASP) in senescent [i]Ercc1 [/i] MEFs. [i]Ercc1 [/i] mice heterozygous for [i]Atm[/i] have reduced NF-κB activity and cellular senescence, improved function of muscle-derived stem/progenetor cells (MDSPCs) and extended healthspan with reduced age-related pathology especially age-related bone and intervertebral disc pathologies. In addition, treatment of [i]Ercc1[/i]  mice with the [[ATM]] inhibitor KU-55933 suppressed markers of senescence and SASP. Taken together, these results demonstrate that the [[ATM]] kinase is a major mediator of DNA damage-induced, NF-κB-mediated cellular senescence, stem cell dysfunction and aging and thus represents a therapeutic target to slow the progression of aging.

|keywords=* ATM
* DNA damage response
* NF-κB
* aging
* cellular senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7138542
}}
{{medline-entry
|title=[[ATM]] suppresses leaf senescence triggered by DNA double-strand break through epigenetic control of senescence-associated genes in Arabidopsis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32163596
|abstract=All living organisms are unavoidably exposed to various endogenous and environmental stresses that trigger potentially fatal DNA damage, including double-strand breaks (DSBs). Although a growing body of evidence indicates that DNA damage is one of the prime drivers of aging in animals, little is known regarding the importance of DNA damage and its repair on lifespan control in plants. We found that the level of DSBs increases but DNA repair efficiency decreases as Arabidopsis leaves age. Generation of DSBs by inducible expression of I-PpoI leads to premature senescence phenotypes. We examined the senescence phenotypes in the loss-of-function mutants for 13 key components of the DNA repair pathway and found that deficiency in ATAXIA TELANGIECTASIA MUTATED ([[ATM]]), the chief transducer of the DSB signal, results in premature senescence in Arabidopsis. [[ATM]] represses DSB-induced expression of senescence-associated genes, including the genes encoding the WRKY and NAC transcription factors, central components of the leaf senescence process, via modulation of histone lysine methylation. Our work highlights the significance of [[ATM]] in the control of leaf senescence and has significant implications for the conservation of aging mechanisms in animals and plants.

|keywords=* 
Arabidopsis thaliana

* ATM
* DNA repair
* double-strand breaks
* histone methylation
* leaf senescence
|full-text-url=https://sci-hub.do/10.1111/nph.16535
}}
{{medline-entry
|title=Glioblastoma Cells Do Not Affect Axitinib-Dependent Senescence of HUVECs in a Transwell Coculture Model.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32098270
|abstract=Axitinib is an orally available inhibitor of tyrosine kinases, with high specificity for vascular endothelial growth factor receptors (VEGFRs) 1, 2, and 3. It is approved for the treatment of advanced renal cell carcinoma and is in phase II clinical trials for recurrent glioblastoma (GBM). GBM is a brain tumor peculiar in its ability to induce neoangiogenesis. Since both GBM tumor cells and endothelial cells of tumor vasculature express VEGFRs, Axitinib exerts its inhibitory action on both tumor and endothelial cells. We and others previously demonstrated that Axitinib triggers cellular senescence. In particular, Axitinib-dependent senescence of HUVECs (human umbilical vein endothelial cells) is accompanied by intracellular reactive oxygen species(ROS) increase and early ataxia telangiectasia mutated([[ATM]]) activation. Here we wondered if the presence of glioblastoma tumor cells could affect the HUVEC senescence upon Axitinib exposure. To address this issue, we cocultured HUVECs together with GBM tumor cells in transwell plates. HUVEC senescence did not result in being affected by GBM cells, neither in terms of β galactosidase activity nor of proliferation index or [[ATM]] phosphorylation. Conversely, Axitinib modulation of HUVEC gene expression was altered by cocultured GBM cells. These data demonstrate that the GBM secretome modifies HUVECs' transcriptomic profile upon Axitinib exposure, but does not prevent drug-induced senescence.
|mesh-terms=* Ataxia Telangiectasia Mutated Proteins
* Axitinib
* Cell Line, Tumor
* Cellular Senescence
* Coculture Techniques
* Gene Expression Profiling
* Glioblastoma
* Human Umbilical Vein Endothelial Cells
* Humans
* Phosphorylation
|keywords=* Axitinib
* endothelial cells
* glioblastoma
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7073100
}}
==ATR==

{{medline-entry
|title=Supraphysiological protection from replication stress does not extend mammalian lifespan.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32253367
|abstract=Replication Stress (RS) is a type of DNA damage generated at the replication fork, characterized by single-stranded DNA (ssDNA) accumulation, and which can be caused by a variety of factors. Previous studies have reported elevated RS levels in aged cells. In addition, mouse models with a deficient RS response show accelerated aging. However, the relevance of endogenous or physiological RS, compared to other sources of genomic instability, for the normal onset of aging is unknown. We have performed long term survival studies of transgenic mice with extra copies of the [i]Chk1[/i] and/or [i]Rrm2[/i] genes, which we previously showed extend the lifespan of a progeroid [[ATR]]-hypomorphic model suffering from high levels of RS. In contrast to their effect in the context of progeria, the lifespan of [i]Chk1, Rrm2[/i] and [i]Chk1/Rrm2[/i] transgenic mice was similar to WT littermates in physiological settings. Most mice studied died due to tumors -mainly lymphomas- irrespective of their genetic background. Interestingly, a higher but not statistically significant percentage of transgenic mice developed tumors compared to WT mice. Our results indicate that supraphysiological protection from RS does not extend lifespan, indicating that RS may not be a relevant source of genomic instability on the onset of normal aging.

|keywords=* DNA damage
* aging
* cancer
* mouse models
* replication stress
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185120
}}
{{medline-entry
|title=Assessing the Retest Reliability of Prefrontal EEG Markers of Brain Rhythm Slowing in the Eyes-Closed Resting State.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32253926
|abstract=[i]Objective[/i]. We examined whether prefrontal lobe EEG markers of slower brain rhythms, which are correlated with functional brain aging, can reliably reflect those of other brain lobes, as measured by a multichannel device. [i]Methods[/i]. EEG measurements were taken of 112 healthy individuals aged 20 to 69 years in the eyes-closed resting state. A 5-minute measurement was taken at 8 regions (Fp1, Fp2, F3, F4, T3, T4, O1, O2). Indices (median frequency [MDF], peak frequency [PF]) that quantitatively reflect the characteristics of EEG slowing, and traditional commonly used spectral indices (absolute powers as delta, theta, alpha, beta, and relative power as alpha-to-theta ratio [[[ATR]]]), were extracted from the EEG signals. For these indices, the differences between the prefrontal lobe and other areas were analyzed and the test-retest reproducibility was investigated. [i]Results[/i]. The EEG slowing indicators showed high conformity over all brain lobes and stable reproducibility. On the other hand, the typical EEG spectral indicators delta, theta, alpha, beta, and [[ATR]] differed between brain regions. [i]Conclusion[/i]. It was found that EEG slowing markers, which were used for assessing the aging or degeneration of brain functions, could be reliably extracted from a prefrontal EEG alone. [i]Significance[/i]. These findings suggest that EEG prefrontal markers may reflect markers of other brain regions when a multi-channel device is used. Thus, this method may constitute a low-cost, wearable, wireless, easily accessible, and noninvasive tool for neurological assessment that could be used in the early detection of cognitive decline and in the prevention of dementia.

|keywords=* EEG
* EEG slowing
* brain aging
* dominant frequency
* prefrontal
|full-text-url=https://sci-hub.do/10.1177/1550059420914832
}}
==BAZ2B==

{{medline-entry
|title=Two conserved epigenetic regulators prevent healthy ageing.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32103178
|abstract=It has long been assumed that lifespan and healthspan correlate strongly, yet the two can be clearly dissociated . Although there has been a global increase in human life expectancy, increasing longevity is rarely accompanied by an extended healthspan . Thus, understanding the origin of healthy behaviours in old people remains an important and challenging task. Here we report a conserved epigenetic mechanism underlying healthy ageing. Through genome-wide RNA-interference-based screening of genes that regulate behavioural deterioration in ageing Caenorhabditis elegans, we identify 59 genes as potential modulators of the rate of age-related behavioural deterioration. Among these modulators, we found that a neuronal epigenetic reader, BAZ-2, and a neuronal histone 3 lysine 9 methyltransferase, SET-6, accelerate behavioural deterioration in C. elegans by reducing mitochondrial function, repressing the expression of nuclear-encoded mitochondrial proteins. This mechanism is conserved in cultured mouse neurons and human cells. Examination of human databases  shows that expression of the human orthologues of these C. elegans regulators, [[BAZ2B]] and EHMT1, in the frontal cortex increases with age and correlates positively with the progression of Alzheimer's disease. Furthermore, ablation of Baz2b, the mouse orthologue of BAZ-2, attenuates age-dependent body-weight gain and prevents cognitive decline in ageing mice. Thus our genome-wide RNA-interference screen in C. elegans has unravelled conserved epigenetic negative regulators of ageing, suggesting possible ways to achieve healthy ageing.
|mesh-terms=* Aging
* Animals
* Caenorhabditis elegans
* Caenorhabditis elegans Proteins
* Cognition
* Cognitive Dysfunction
* Epigenesis, Genetic
* Healthy Aging
* Histone-Lysine N-Methyltransferase
* Histones
* Humans
* Longevity
* Lysine
* Male
* Memory
* Methylation
* Mice
* Mitochondria
* Neurons
* Proteins
* RNA Interference
* Spatial Learning
* Transcription Factors, General
|keywords=#f
|full-text-url=https://sci-hub.do/10.1038/s41586-020-2037-y
}}
==BDNF==

{{medline-entry
|title=Spermidine and spermine delay brain aging by inducing autophagy in SAMP8 mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32268299
|abstract=The natural polyamine spermidine and spermine have been reported to ameliorate aging and aging-induced dementia. However, the mechanism is still confused. An aging model, the senescence accelerated mouse-8 (SAMP8), was used in this study. Novel object recognition and the open field test results showed that oral administration of spermidine, spermine and rapamycin increased discrimination index, modified number, inner squares distance and times. Spermidine and spermine increased the activity of SOD, and decreased the level of MDA in the aging brain. Spermidine and spermine phosphorylate AMPK and regulate autophagy proteins (LC3, Beclin 1 and p62). Spermidine and spermine balanced mitochondrial and maintain energy for neuron, with the regulation of MFN1, MFN2, DRP1, COX IV and ATP. In addition, western blot results (Bcl-2, Bax and Caspase-3, NLRP3, IL-18, IL-1β) showed that spermidine and spermine prevented apoptosis and inflammation, and elevate the expression of neurotrophic factors, including NGF, PSD95and PSD93 and [[BDNF]] in neurons of SAMP8 mice. These results indicated that the effect of spermidine and spermine on anti-aging is related with improving autophagy and mitochondrial function.

|keywords=* aging
* autophagy
* mitochondrial dysfunction
* polyamine
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185103
}}
{{medline-entry
|title=Microglia senescence occurs in both substantia nigra and ventral tegmental area.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32275335
|abstract=During aging humans lose midbrain dopamine neurons, but not all dopamine regions exhibit vulnerability to neurodegeneration. Microglia maintain tissue homeostasis and neuronal support, but microglia become senescent and likely lose some of their functional abilities. Since aging is the greatest risk factor for Parkinson's disease, we hypothesized that aging-related changes in microglia and neurons occur in the vulnerable substantia nigra pars compacta (SNc) but not the ventral tegmental area (VTA). We conducted stereological analyses to enumerate microglia and dopaminergic neurons in the SNc and VTA of 1-, 6-, 9-, 18-, and 24-month-old C57BL/J6 mice using sections double-stained with tyrosine hydroxylase (TH) and Iba1. Both brain regions show an increase in microglia with aging, whereas numbers of TH+ cells show no significant change after 9 months of age in SNc and 6 months in VTA. Morphometric analyses reveal reduced microglial complexity and projection area while cell body size increases with aging. Contact sites between microglia and dopaminergic neurons in both regions increase with aging, suggesting increased microglial support/surveillance of dopamine neurons. To assess neurotrophin expression in dopaminergic neurons, [[BDNF]] and TH mRNA were quantified. Results show that the ratio of [[BDNF]] to TH decreases in the SNc, but not the VTA. Gait analysis indicates subtle, aging-dependent changes in gait indices. In conclusion, increases in microglial cell number, ratio of microglia to dopamine neurons, and contact sites suggest that innate biological mechanisms compensate for the aging-dependent decline in microglia morphological complexity (senescence) to ensure continued neuronal support in the SNc and VTA.

|keywords=* Parkinson's disease
* aging-dependent neurodegeneration
* dopamine neurons
* microglia complexity
* stereological analyses
* tyrosine hydroxylase; microglia senescence
|full-text-url=https://sci-hub.do/10.1002/glia.23834
}}
{{medline-entry
|title=Towards an understanding of the physical activity-[[BDNF]]-cognition triumvirate: A review of associations and dosage.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32171785
|abstract=Physical activity has received substantial research attention due to its beneficial impact on cognition in ageing, particularly via the action of brain-derived neurotrophic factor ([[BDNF]]). It is well established that physical activity can elevate circulating levels of [[BDNF]], and that [[BDNF]] has neurotrophic, neuroprotective and cognitively beneficial properties. Yet, practical implementation of this knowledge is limited by a lack of clarity on context and dose-effect. Against a shifting backdrop of gradually diminishing physical and cognitive capacity in normal ageing, the type, intensity, and duration of physical activity required to elicit elevations in [[BDNF]], and more importantly, the magnitude of [[BDNF]] elevation required for detectable neuroprotection remains poorly characterised. The purpose of this review is to provide an overview of the association between physical activity, [[BDNF]], and cognition, with a focus on clarifying the magnitude of these effects in the context of normative ageing. We discuss the implications of the available evidence for the design of physical activity interventions intended to promote healthy cognitive ageing.
|mesh-terms=* Aging
* Brain-Derived Neurotrophic Factor
* Cognition
* Exercise
* Healthy Aging
* Humans
|keywords=* Ageing
* BDNF
* Brain
* Physical activity
|full-text-url=https://sci-hub.do/10.1016/j.arr.2020.101044
}}
==BMP2==

{{medline-entry
|title=Interleukin-1β-Induced Senescence Promotes Osteoblastic Transition of Vascular Smooth Muscle Cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32126555
|abstract=Interleukin (IL)-1β, as a key biomarker and mediator of vascular calcification in patients with end-stage renal disease (ESRD), may be involved in the process of premature senescence of vascular smooth muscle cells (VSMCs). This work sought to investigate whether IL-1β-induced premature senescence contributes to the process of osteoblastic transition and vascular calcification in VSMCs. Eighty-eight patients with ESRD (aged 25-81 years), 11 healthy individuals, and 15 cases of lesion-free distal radial arteries from dialysis ESRD patients with angiostomy were collected in this study. Immunohistochemical analysis was performed to detect expression of IL-1β, p21, and bone morphogenetic protein-2 ([[BMP2]]) in the distal radial arteries. Primary human VSMCs from healthy neonatal umbilical cords were incubated with test agents for 1-3 days. Intracellular levels of reactive oxygen species (ROS) and senescence-associated-β-galactosidase (SA-β-gal) staining were used to detect senescent cells. Alizarin red staining and the calcium content of the cell layer were used to detect mineral deposition in VSMCs. Coincident with positive staining of IL-1β, p21, and [[BMP2]] in the lesion-free distal radial arteries, 66.67% patients showed mineral deposition. Serum IL-1β was 0.24 ± 0.57, 1.20 ± 2.95, and 9.41 ± 40.52 pg/mL in 11 healthy individuals, 20 patients without calcification, and 53 patients with calcification, respectively. Analysis of the cross-table chi-square test showed cardiovascular calcification is not correlated with levels of serum IL-1β in patients with ESRD (p = 0.533). In response to IL-1β, VSMCs showed a senescence-like phenotype, such as flat and enlarged morphology, increased expression of p21, an increased activity of SA-β-gal, and increased levels of ROS. IL-1β-induced senescence of VSMCs was required for the activation of IL-1β/NF-κB/p53/p21 signaling pathway. IL-1β-induced senescent VSMCs underwent calcification due to osteoblastic transition mainly depending upon the upregulation of [[BMP2]]. Resveratrol, an activator of sirtuin-1, postponed the IL-1β-induced senescence through blocking the NF-κB/p53/p21 pathway and attenuated the osteoblastic transition and calcification in VSMCs. High levels of IL-1β in medial smooth muscles of arteries may play roles in inducing senescence-associated calcification. IL-1β-induced senescence depending on the activation of the NF-κB/p53/p21 signaling pathway and contributing to osteoblastic transition of VSMCs.
|mesh-terms=* Adult
* Aged
* Aged, 80 and over
* Female
* Humans
* Interleukin-1beta
* Male
* Middle Aged
* Muscle, Smooth, Vascular
* Osteoblasts
|keywords=* Interleukin-1β
* Osteoblastic transition
* Senescence
* Vascular calcification
|full-text-url=https://sci-hub.do/10.1159/000504298
}}
==BOC==

{{medline-entry
|title=Protein Requirements of Elderly Chinese Adults Are Higher than Current Recommendations.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32140711
|abstract=Due to a lack of research data on the protein requirements of the elderly in China, the estimated average requirement (EAR) and the recommended nutrient intake (RNI) of protein in the elderly remain the same as those in young and middle-aged people at 0.98 g/(kg·d). The objective of this study was to determine the protein requirements of healthy Chinese adults >65y old through use of the indicator amino acid oxidation (IAAO) method. Seven healthy adult men and 7 healthy adult women participated in the study, with protein intakes ranging from 0.3 to 1.8 g/(kg·d). The diets were isocaloric and provided energy at a 1.5 resting energy expenditure. Protein was given based on the lactalbumin. Phenylalanine and tyrosine were added to protein doses of 0.3-1.5 g/kg according to the highest dose of protein content [1.8 g/(kg·d)]. Phenylalanine and tyrosine concentrations were kept constant at each protein dose. The mean protein requirement was determined by applying a nonlinear mixed-effects model analysis to the F13CO2, which identified a breakpoint in F13CO2 in response to graded amounts of protein. This trial was registered with the Chinese clinical trial registry as ChiCTR-[[BOC]]-17010930. Protein EAR and RNI for healthy elderly Chinese adults were determined to be 0.91 and 1.17 g/(kg·d), respectively, based on the indicator amino acid oxidation technique. The estimates of protein requirements for Chinese adults >65 y in the present study are 3.4% and 19.4% higher than the current estimated requirements, 0.88 g/(kg·d) for EAR and 0.98 g/(kg·d) for RNI.
|mesh-terms=* Aged
* Aging
* Amino Acids
* Body Weight
* China
* Dietary Proteins
* Energy Intake
* Energy Metabolism
* Female
* Humans
* Male
* Nutritional Requirements
* Oxidation-Reduction
* Phenylalanine
* Recommended Dietary Allowances
* Tyrosine
|keywords=* indicator amino acid oxidation
* older adults
* phenylalanine oxidation
* protein requirement
* stable isotope
|full-text-url=https://sci-hub.do/10.1093/jn/nxaa031
}}
==C3==

{{medline-entry
|title=Reduced sialylation triggers homeostatic synapse and neuronal loss in middle-aged mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32087947
|abstract=Sialic acid-binding Ig-like lectin (Siglec) receptors are linked to neurodegenerative processes, but the role of sialic acids in physiological aging is still not fully understood. We investigated the impact of reduced sialylation in the brain of mice heterozygous for the enzyme glucosamine-2-epimerase/N-acetylmannosamine kinase (GNE+/-) that is essential for sialic acid biosynthesis. We demonstrate that GNE+/- mice have hyposialylation in different brain regions, less synapses in the hippocampus and reduced microglial arborization already at 6 months followed by increased loss of neurons at 12 months. A transcriptomic analysis revealed no pro-inflammatory changes indicating an innate homeostatic immune process leading to the removal of synapses and neurons in GNE+/- mice during aging. Crossbreeding with complement [[C3]]-deficient mice rescued the earlier onset of neuronal and synaptic loss as well as the changes in microglial arborization. Thus, sialic acids of the glycocalyx contribute to brain homeostasis and act as a recognition system for the innate immune system in the brain.
|mesh-terms=* Aging
* Animals
* Brain
* Homeostasis
* Immunity, Innate
* Mice, Transgenic
* Neurons
* Racemases and Epimerases
* Sialic Acid Binding Immunoglobulin-like Lectins
* Sialic Acids
* Synapses
|keywords=* Aging
* GNE
* Glycocalyx
* Microglia
* Neurodegeneration
* Neuroinflammation
* Sialic acid
|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.01.008
}}
==CA1==

{{medline-entry
|title=Functional Connectivity of Hippocampal CA3 Predicts Neurocognitive Aging via [[CA1]]-Frontal Circuit.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32239141
|abstract=The CA3 and [[CA1]] principal cell fields of the hippocampus are vulnerable to aging, and age-related dysfunction in CA3 may be an early seed event closely linked to individual differences in memory decline. However, whether the differential vulnerability of CA3 and [[CA1]] is associated with broader disruption in network-level functional interactions in relation to age-related memory impairment, and more specifically, whether CA3 dysconnectivity contributes to the effects of aging via [[CA1]] network connectivity, has been difficult to test. Here, using resting-state fMRI in a group of aged rats uncontaminated by neurodegenerative disease, aged rats displayed widespread reductions in functional connectivity of CA3 and [[CA1]] fields. Age-related memory deficits were predicted by connectivity between left CA3 and hippocampal circuitry along with connectivity between left [[CA1]] and infralimbic prefrontal cortex. Notably, the effects of CA3 connectivity on memory performance were mediated by [[CA1]] connectivity with prefrontal cortex. We additionally found that spatial learning and memory were associated with functional connectivity changes lateralized to the left CA3 and [[CA1]] divisions. These results provide novel evidence that network-level dysfunction involving interactions of CA3 with [[CA1]] is an early marker of poor cognitive outcome in aging.

|keywords=* aging
* functional connectivity
* hippocampus
* spatial memory
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7325802
}}
{{medline-entry
|title=Integration of qRT-PCR and Immunohistochemical Techniques for mRNA Expression and Localization of m1AChR in the Brain of Aging Rat.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32219760
|abstract=The neurotransmitter acetylcholine (ACh) is involved in memory and cognitive functions, which normally decline with age. In this chapter, we describe qRT-PCR and immunohistochemical protocols for measurement of muscarinic ACh receptor M1 (m1AChR) levels in the brains of middle-aged rats, with and without administration of grape seed proanthocyanidin extract (GSPE) and exercise training. The analyses revealed that the interventions led to an increase in m1AChR mRNA and protein levels in the [[CA1]] subfield of hippocampus. This would be expected to enhance Ach levels at synapses and thereby boost cognitive ability. The protocols can be applied to m1AChR measurements in neurodegenerative diseases and dementia.

|keywords=* Acetylcholine
* Aging
* Brain
* Immunohistochemistry
* m1AChR
* qRT-PCR
|full-text-url=https://sci-hub.do/10.1007/978-1-0716-0471-7_23
}}
{{medline-entry
|title=Role of Eclipta prostrata extract in improving spatial learning and memory deficits in D-galactose-induced aging in rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32186114
|abstract=To investigate the role of Eclipta prostrata (E. prostrata) extract in improving spatial learning and memory deficits in D-galactose-induced aging in rats. Rats were divided into five groups, with 10 animals in each group. Aging rats were produced by treatment with 100 mg·kg-1·d-1 of D-galactose for 6 weeks. Rats in the E. prostrata treatment groups received an aqueous extract of E. prostrata orally at a concentration of 50, 100, or 200 mg·kg-1·d-1 for 3 weeks. Animals in both the normal and model groups were treated with similar volumes of saline. Spatial memory performance was measured using the Morris water maze. The mRNA levels and enzyme activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) were analyzed using real-time quantitative PCR and spectrophotometry, respectively. The levels of induced nitric oxide synthase (iNOS), nitric oxide (NO), dopamine (DA), norepinephrine (NE), and serotonin (5-HT) were determined using enzyme-linked immunosorbent assay and spectrophotometry. Compared with the normal group, rats in the D-galactose-treated model group exhibited significant memory loss. There was severe damage to the hippocampal [[CA1]] area, and expression levels of SOD, CAT, GPx, and GR were significantly decreased in the model group compared with the normal group. In the model group, levels of iNOS and NO were significantly increased compared with the normal group. However, treatment with E. prostrata extract reversed the conditions caused by D-galactose-induced aging, especially in the groups with higher treatment concentrations. Compared with the normal group, the levels of DA, NE, and 5-HT were significantly lower in the D-galactose-treated model group. In the E. prostrata extract-treated groups, however, there was a dose-dependent upregulation of DA, NE, and 5-HT expression. Our results suggest that administration of E. prostrata extract can result in an improvement in the learning and memory impairments that are induced by D-galactose treatment in rats. This improvement may be the result of enhanced antioxidative ability, decreased iNOS and NO levels, and the induction of DA, NE, and 5-HT expression in the brain.
|mesh-terms=* Aging
* Animals
* Behavior, Animal
* CA1 Region, Hippocampal
* Catalase
* Dopamine
* Eclipta
* Galactose
* Gene Expression Regulation, Enzymologic
* Glutathione Peroxidase
* Glutathione Reductase
* Male
* Memory Disorders
* Nitric Oxide
* Nitric Oxide Synthase Type II
* Norepinephrine
* Plant Extracts
* RNA, Messenger
* Rats
* Rats, Sprague-Dawley
* Serotonin
* Spatial Learning
* Superoxide Dismutase
|keywords=* Antioxidants
* Eclipta
* Galactose
* Memory disorders
* Spatial learning

}}
{{medline-entry
|title=Differential annualized rates of hippocampal subfields atrophy in aging and future Alzheimer's clinical syndrome.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32107063
|abstract=Several studies have investigated the differential vulnerability of hippocampal subfields during aging and Alzheimer's disease (AD). Results were often contradictory, mainly because these works were based on concatenations of cross-sectional measures in cohorts with different ages or stages of AD, in the absence of a longitudinal design. Here, we investigated 327 participants from a population-based cohort of nondemented older adults with a 14-year clinical follow-up. MRI at baseline and 4 years later were assessed to measure the annualized rates of hippocampal subfields atrophy in each participant using an automatic segmentation pipeline with subsequent quality control. On the one hand, CA4 dentate gyrus was significantly more affected than the other subfields in the whole population ([[CA1]]-3: -0.68%/year; subiculum: -0.99%/year; and CA4-DG: -1.39%/year; p < 0.0001). On the other hand, the annualized rate of [[CA1]]-3 atrophy was associated with an increased risk of developing Alzheimer's clinical syndrome over time, independently of age, gender, educational level, and ApoE4 genotype (HR = 2.0; CI 95% 1.4-3.0). These results illustrate the natural history of hippocampal subfields atrophy during aging and AD by showing that the dentate gyrus is the most vulnerable subfield to the effects of aging while the cornu-ammonis is the primary target of AD pathophysiological processes, years before symptom onset.
|mesh-terms=* Aged
* Aging
* Alzheimer Disease
* Atrophy
* Cohort Studies
* Cross-Sectional Studies
* Dentate Gyrus
* Female
* Hippocampus
* Humans
* Magnetic Resonance Imaging
* Male
* Neuropsychological Tests
* Risk
|keywords=* Aging
* Alzheimer's disease
* Hippocampal subfields
* MRI
|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.01.011
}}
==CCK==

{{medline-entry
|title=Effects of Age on Acute Appetite-Related Responses to Whey-Protein Drinks, Including Energy Intake, Gastric Emptying, Blood Glucose, and Plasma Gut Hormone Concentrations-A Randomized Controlled Trial.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32268554
|abstract=Protein-rich supplements are used commonly to increase energy intake in undernourished older people. This study aimed to establish age effects on energy intake, appetite, gastric emptying, blood glucose, and gut hormones in response to protein-rich drinks. In a randomized double-blind, order, 13 older men (age: 75 ± 2 yrs, body mass index (BMI): 26 ± 1 kg/m ) and 13 younger (23 ± 1 yrs, 24 ± 1 kg/m ) men consumed (i) a control drink (~2 kcal) or drinks (450 mL) containing protein/fat/carbohydrate: (ii) 70 g/0 g/0 g (280 kcal/'P ), (iii) 14 g/12.4 g/28 g (280 kcal/'M ), (iv) 70 g/12.4 g/28 g (504 kcal/'M ), on four separate days. Appetite (visual analog scales), gastric emptying (3D ultrasonography), blood glucose, plasma insulin, ghrelin, cholecystokinin ([[CCK]]), glucagon-like peptide-1 (GLP-1) concentrations (0-180 min), and ad-libitum energy intake (180-210 min) were determined. Older men, compared to younger men, had higher fasting glucose and [[CCK]] concentrations and lower fasting GLP-1 concentrations (all [i]p[/i] < 0.05). Energy intake by P  compared to control was less suppressed in older men (increase: 49 ± 42 kcal) than it was in younger men (suppression: 100 ± 54 kcal, [i]p[/i] = 0.038). After the caloric drinks, the suppression of hunger and the desire to eat, and the stimulation of fullness was less ([i]p[/i] < 0.05), and the stimulation of plasma GLP-1 was higher ([i]p[/i] < 0.05) in older men compared to younger men. Gastric emptying, glucose, insulin, ghrelin, and [[CCK]] responses were similar between age groups. In conclusion, ageing reduces the responses of caloric drinks on hunger, the desire to eat, fullness, and energy intake, and protein-rich nutrition supplements may be an effective strategy to increase energy intake in undernourished older people.

|keywords=* aging
* appetite
* energy intake
* gastric emptying
* glucose
* gut hormones
* whey protein
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7231005
}}
==CCL20==

{{medline-entry
|title=p53 and p53-related mediators PAI-1 and IGFBP-3 are downregulated in peripheral blood mononuclear cells of HIV-patients exposed to non-nucleoside reverse transcriptase inhibitors.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32272174
|abstract=The improved effectiveness and safety of the combined antiretroviral therapy (cART) has largely diminished mortality and AIDS-defining morbidity of HIV-patients. Nevertheless, chronic age-related diseases in these individuals are more common and their underlying pathogenic mechanisms of these actions seem to involve accelerated aging and enhanced inflammation. The present study explores markers of these processes in a heterogenous Spanish HIV cohort using peripheral blood samples of HIV-patients and matched uninfected controls. We isolated periheral blood mononuclear cells (PBMCs) and i) compared the expression of a panel of 14 genes related to inflammation and senescence in PBMCs of HIV-patients vs matched uninfected controls, ii) analyzed the expression in HIV-patients in association with a number of demographic, biochemical and immunological parameters and iii) in relation with the current cART they received. PBMCs of HIV-patients displayed significantly increased expression of general inflammatory genes (IL6, IL18 and CXCL10) and this occurs irrespectively of the antiviral therapy they have been receiving. Conversely, levels of senescence-associated genes TP53, SERPINE1andIGFBP3 were slightly but significantly reduced in patients compared to uninfected matched individuals and this effect is related to NNRTI-containing treatments. The expression of the inflammatory markers IL6, IL18, IL1B, TNFA, RELA, CCL2, [[CCL20]] and CXCL10 displayed correlation with certain demographic, morbidity- and HIV infection-related parameters. The levels of TP53 mRNA were positively associated only with plasma LDL. Correlation analysis between the expressions of pairs of genes revealed a different pattern between HIV-patients and controls. The diminished expression of TP53 and SERPINE1 in HIV-patients was also observed at a protein level, and the correlation between the two proteins (p53 and PAI1) in patients and controls showed the opposite trend. In conclusion, HIV-patients show dysregulation of p53 and p53-related mediators, a phenomenon which may be of pathophysiological relevance and could be related to the shorter health- and/or life-span observed in these individuals.

|keywords=* Aging
* Antiretroviral drugs
* HIV
* Inflammation
* NNRTI
* Senescence
* p53
|full-text-url=https://sci-hub.do/10.1016/j.antiviral.2020.104784
}}
==CCL28==

{{medline-entry
|title=Age-related chemokine alterations affect IgA secretion and gut immunity in female mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32277312
|abstract=The chemokines CCL25 and [[CCL28]], which promote immune cell migration, are primarily expressed in the small and large intestines and play critical roles in sustaining gut immunity. In particular, these chemokines are closely related to intestinal IgA secretion. However, there is no research regarding the effects of aging on CCL25 and [[CCL28]] expression and function. Therefore, in the present study, we investigated the effects of aging on production of CCL25 and [[CCL28]], and on gut immunity, especially IgA secretion, using young and aged female mice. By aging, the levels of small intestinal mRNA and protein of CCL25 lowered, while these levels of [[CCL28]] in colon became higher. Moreover, the number of IgA-antibody secreting cells (IgA-ASCs) and total IgA concentration decreased in the small intestine due to the age-associated reduction of CCL25. In contrast, colonic IgA production was increased due to up-regulation of [[CCL28]], while the number of colonic IgA-ASCs was unchanged with aging. These results clearly demonstrate that aging-associated decrease in small intestinal CCL25 production and increase in colonic [[CCL28]] production c be involved in aging-associated deterioration of gut immunity.

|keywords=* Aging
* CCL25
* CCL28
* Gut immunity
* IgA
|full-text-url=https://sci-hub.do/10.1007/s10522-020-09877-9
}}
==CCR2==

{{medline-entry
|title=Tet2-mediated clonal hematopoiesis in nonconditioned mice accelerates age-associated cardiac dysfunction.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32154790
|abstract=Clonal hematopoiesis of indeterminate potential is prevalent in elderly individuals and associated with increased risks of all-cause mortality and cardiovascular disease. However, mouse models to study the dynamics of clonal hematopoiesis and its consequences on the cardiovascular system under homeostatic conditions are lacking. We developed a model of clonal hematopoiesis using adoptive transfer of unfractionated ten-eleven translocation 2-mutant (Tet2-mutant) bone marrow cells into nonirradiated mice. Consistent with age-related clonal hematopoiesis observed in humans, these mice displayed a progressive expansion of Tet2-deficient cells in multiple hematopoietic stem and progenitor cell fractions and blood cell lineages. The expansion of the Tet2-mutant fraction was also observed in bone marrow-derived [[CCR2]]+ myeloid cell populations within the heart, but there was a negligible impact on the yolk sac-derived [[CCR2]]- cardiac-resident macrophage population. Transcriptome profiling revealed an enhanced inflammatory signature in the donor-derived macrophages isolated from the heart. Mice receiving Tet2-deficient bone marrow cells spontaneously developed age-related cardiac dysfunction characterized by greater hypertrophy and fibrosis. Altogether, we show that Tet2-mediated hematopoiesis contributes to cardiac dysfunction in a nonconditioned setting that faithfully models human clonal hematopoiesis in unperturbed bone marrow. Our data support clinical findings that clonal hematopoiesis per se may contribute to diminished health span.

|keywords=* Aging
* Bone marrow transplantation
* Cardiology
* Hematopoietic stem cells
* Macrophages
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7213793
}}
==CD27==

{{medline-entry
|title=The Interplay between [[CD27]]  and [[CD27]]  B Cells Ensures the Flexibility, Stability, and Resilience of Human B Cell Memory.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32130900
|abstract=Memory B cells (MBCs) epitomize the adaptation of the immune system to the environment. We identify two MBC subsets in peripheral blood, [[CD27]]  and [[CD27]]  MBCs, whose frequency changes with age. Heavy chain variable region (VH) usage, somatic mutation frequency replacement-to-silent ratio, and CDR3 property changes, reflecting consecutive selection of highly antigen-specific, low cross-reactive antibody variants, all demonstrate that [[CD27]]  and [[CD27]]  MBCs represent sequential MBC developmental stages, and stringent antigen-driven pressure selects [[CD27]]  into the [[CD27]]  MBC pool. Dynamics of human MBCs are exploited in pregnancy, when 50% of maternal MBCs are lost and [[CD27]]  MBCs transit to the more differentiated [[CD27]]  stage. In the postpartum period, the maternal MBC pool is replenished by the expansion of persistent [[CD27]]  clones. Thus, the stability and flexibility of human B cell memory is ensured by [[CD27]]  MBCs that expand and differentiate in response to change.

|keywords=* CD27
* VH repertoire
* aging
* germinal center
* immunodeficiency
* immunological memory
* memory B cells
* pregnancy
* spleen
* vaccine
|full-text-url=https://sci-hub.do/10.1016/j.celrep.2020.02.022
}}
==CD28==

{{medline-entry
|title=Immunosenescent characteristics of T cells in young patients following haploidentical haematopoietic stem cell transplantation from parental donors.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32280463
|abstract=Paediatric and adolescent patients in need of allogeneic haematopoietic stem cell transplantation (HSCT) generally receive stem cells from older, unrelated or parental donors when a sibling donor is not available. Despite encouraging clinical outcomes, it has been suggested that immune reconstitution accompanied by increased replicative stress and a large difference between donor and recipient age may worsen immunosenescence in paediatric recipients. In this study, paired samples were collected at the same time from donors and recipients of haploidentical haematopoietic stem cell transplantation (HaploSCT). We then conducted flow cytometry-based phenotypic and functional analyses and telomere length (TL) measurements of 21 paired T-cell sets from parental donors and children who received T-cell-replete HaploSCT with post-transplant cyclophosphamide (PTCy). Senescent T cells, [[CD28]]  or CD57  cells, were significantly expanded in patients. Further, not only CD4 [[CD28]]  T cells, but also CD4 [[CD28]]  T cells showed reduced cytokine production capacity and impaired polyfunctionality compared with parental donors, whereas their TCR-mediated proliferation capacity was comparable. Of note, the TL in patient T cells was preserved, or even slightly longer, in senescent T cells compared with donor cells. Regression analysis showed that senescent features of CD4  and CD8  T cells in patients were influenced by donor age and the frequency of [[CD28]]  cells, respectively. Our data suggest that in paediatric HaploSCT, premature immunosenescent changes occur in T cells from parental donors, and therefore, long-term immune monitoring should be conducted.

|keywords=* CD28− T cells
* HaploSCT
* immune monitoring
* immunosenescence
* telomere length
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7142179
}}
{{medline-entry
|title=Diagnosis-independent loss of T-cell costimulatory molecules in individuals with cytomegalovirus infection.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32209361
|abstract=Major depressive disorder (MDD) is associated with physiological changes commonly observed with increasing age, such as inflammation and impaired immune function. Age-related impaired adaptive immunity is characterized by the loss of naive T-cells and the reciprocal accumulation of memory T-cells together with the loss of T-cell co-stimulatory molecules. Additionally, the presence and activity of cytomegalovirus (CMV) alters the architecture of the T-cell compartment in a manner consistent with premature aging. Because CMV is also thought to reactivate with psychological stress, this study tested whether MDD influences age-related phenotypes of T-cell populations in the context of CMV infection in young and middle-aged adults. Morning blood samples from volunteers with a DSM-IV diagnosis of MDD (n = 98, mean age(SD) = 36(10) years, 74.5% female, 57.1% CMV ) and comparison controls (n = 98, mean age(SD) = 34(10) years, 68.4% female, 51.0% CMV ) were evaluated for CMV IgG antibody status and the distribution of late differentiated (CD27 [[CD28]] ) cells within CD4  and CD8  T-cell subsets, i.e. naive (CCR7 CD45RA ), effector memory (EM, CCR7 CD45RA ), central memory (CM, CCR7 CD45RA ) and effector memory cells re-expressing CD45RA (EMRA, CCR7 CD45RA ). Mixed linear regression models controlling for age, sex, ethnicity and flow cytometry batch showed that CMV seropositivity was associated with a reduction in naive T-cells, expansion of EMRA T-cells, and a greater percent distribution of CD27 [[CD28]]  cells within CD4  and CD8  memory T-cell subsets (p's < 0.004), but there was no significant effect of MDD, nor any significant interaction between CMV and diagnosis. Unexpectedly, depressed men were less likely to be CMV  and depressed women were more likely to be CMV  than sex-matched controls suggesting a possible interaction between sex and MDD on CMV susceptibility, but this three-way interaction did not significantly affect the T-cell subtypes. Our findings suggest that depression in young and middle-aged adults does not prematurely advance aging of the T-cell compartment independently of CMV, but there may be significant sex-specific effects on adaptive immunity that warrant further investigation.

|keywords=* Biological aging
* Cytomegalovirus
* Depression
* Immunosenescence
* Major depressive disorder
* Sex differences
* T-cells
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7594105
}}
{{medline-entry
|title=Accelerated immunosenescence in rheumatoid arthritis: impact on clinical progression.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32190092
|abstract=Patients with rheumatoid arthritis (RA) develop features of accelerated ageing, including immunosenescence. These changes include decreased thymic functionality, expansion of late-differentiated effector T cells, increased telomeric attrition, and excessive production of cytokines (senescence-associated secretory phenotype). The progression of RA has been associated with the early development of age-related co-morbidities, including osteoporosis, cardiovascular complications, and cognitive impairment. Here I review data supporting the hypothesis that immune-senescence contributes to the aggravation of both articular and extra-articular manifestations. Of note, poor cognitive functions in RA were associated with senescent [[CD28]]- T cells, inflammaging, and autoantibodies against brain antigens. The pathways of immune-to-brain communication are discussed and provide the rationale for the cognitive impairment reported in RA.

|keywords=* Ageing
* Cell senescence
* Cognitive impairment
* Immune ageing
* Rheumatoid arthritis
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7068869
}}
{{medline-entry
|title=Accelerated immune aging was correlated with lupus-associated brain fog in reproductive-age systemic lupus erythematosus patients.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32107852
|abstract=Cognitive impairment is common in systemic lupus erythematosus (SLE) patients with substantial adverse effects on function and quality of life. One hypothesis to understand the mechanisms of cognitive impairment in SLE is accelerated immunosenescence. The aim of this study is to observe the correlation between immunosenescence with cognitive impairment in patients with SLE. Sixty-one female SLE patient were measured for CD4 and CD8 T cell-associated senescence markers, including percentage of end-stage differentiated T cells (CD4 and CD8 T cells expressing CD57  or loss of [[CD28]] expression), of naïve T cells (CD4  CD45RA  and CD8  CD45RA  ), memory T cells (CD4  CD45RO  and CD8  CD45RO  ), and antigen-experienced T cells (CD4  KLRG1  and CD8  KLRG1  ) which were measured using flow cytometry. One hallmark of immunosenescence called immune risk profile (IRP) was defined by an inverted ratio of CD4 and CD8. Cognitive functions were measured by Mini-Mental State Examination (MMSE) and Montréal Cognitive Assessment (MOCA) questionnaire. Thirty-six (59.1%) SLE patients who had IRP develop significantly lower attention and recall from both MMSE (P = .005 and P = .000) and MOCA (P = .017 and P = .000) examinations. Decreased visuospatial ability was also found in patients with IRP measured by MOCA (P = .046). There was a negative correlation between memory CD4  CD45RO  T cells with recall and visuospatial domain (R = -0.204, P = .039 and R = -0.250, P = .033; respectively), and negative correlation between CD8  [[CD28]]  T cells with recall and attention domain (R = -0.249, P = .027 and R = -0.145, P = .048, respectively). Systemic lupus erythematosus patients develop an accelerated immunosenescence which contributes to cognitive dysfunction, especially in attention, recall, and visuospatial domains.

|keywords=* immunosenescence
* lupus-associated brain fog
* systemic lupus erythematosus
|full-text-url=https://sci-hub.do/10.1111/1756-185X.13816
}}
{{medline-entry
|title=T cells, aging and senescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32092501
|abstract=The T cell compartment undergoes characteristic changes with age, which contribute to increased incidence and severity of infections and reduced immunogenicity and efficacy of many vaccines in the older population. Production of naïve T cells is severely impaired due to a decreased output of lymphoid cells from the bone marrow and the involution of the thymus. At the same time, antigen-experienced, highly differentiated T cells accumulate resulting in a diminished T cell receptor repertoire. These cells show some similarities with senescent cells, such as shorter telomers, accumulated DNA damage and metabolic changes. Latent infection with Cytomegalovirus also impacts the T cell compartment and aggravates several of its age-associated changes. Loss of [[CD28]] expression is one hallmark of T cells after repeated antigenic stimulation, but [[CD28]]  T cells cannot be considered truly senescent as e.g. they are still able to proliferate upon adequate stimulation. Several additional markers have been suggested in order to define a potential fully senescent T cell population, but no consensus definition has been reached so far. It has been postulated that highly differentiated senescent-like T cells are unable to eliminate other senescent cell types. Removal of senescent non-immune cells has been shown to be beneficial for the organism and a reliable definition of senescent T cells is essential for an extension of this concept to T cells.

|keywords=* Aging
* Senescence
* T cells
|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110887
}}
==CD38==

{{medline-entry
|title=[[CD38]] in Neurodegeneration and Neuroinflammation.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32085567
|abstract=Neurodegenerative diseases are characterized by neuronal degeneration as well as neuroinflammation. While [[CD38]] is strongly expressed in brain cells including neurons, astrocytes as well as microglial cells, the role played by [[CD38]] in neurodegeneration and neuroinflammation remains elusive. Yet, [[CD38]] expression increases as a consequence of aging which is otherwise the primary risk associated with neurodegenerative diseases, and several experimental data demonstrated that [[CD38]] knockout mice are protected from neurodegenerative and neuroinflammatory insults. Moreover, nicotinamide adenine dinucleotide, whose levels are tightly controlled by [[CD38]], is a recognized and potent neuroprotective agent, and NAD supplementation was found to be beneficial against neurodegenerative diseases. The aims of this review are to summarize the physiological role played by [[CD38]] in the brain, present the arguments indicating the involvement of [[CD38]] in neurodegeneration and neuroinflammation, and to discuss these observations in light of [[CD38]] complex biology.

|keywords=* ALS.
* Alzheimer’s disease
* CD38
* NAD
* Parkinson’s disease
* aging
* neurodegeneration
* neuroinflammation
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072759
}}
==CD4==

{{medline-entry
|title=The effects of advanced maternal age on T-cell subsets at the maternal-fetal interface prior to term labor and in the offspring: a mouse study.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32279324
|abstract=Women who conceive at 35 years of age or older, commonly known as advanced maternal age, have a higher risk of facing parturition complications and their children have an increased risk of developing diseases later in life. However, the immunological mechanisms underlying these pathological processes have yet to be established. To fill this gap in knowledge, using a murine model and immunophenotyping, we determined the effect of advanced maternal age on the main cellular branch of adaptive immunity, T cells, at the maternal-fetal interface and in the offspring. We report that advanced maternal age impaired the process of labor at term, inducing dystocia and delaying the timing of delivery. Advanced maternal age diminished the number of specific proinflammatory T-cell subsets [T helper type 1 (Th1): [[CD4]]  IFN-γ  , CD8  IFN-γ  and Th9: [[CD4]]  IL-9  ], as well as [[CD4]]  regulatory T cells ([[CD4]]  CD25  FoxP3  T cells), at the maternal-fetal interface prior to term labor. Advanced maternal age also altered fetal growth and survival of the offspring in early life. In addition, infants born to advanced-age mothers had alterations in the T-cell repertoire but not in CD71  erythroid cells (CD3  CD71  TER119  cells). This study provides insight into the immune alterations observed at the maternal-fetal interface of advanced-age mothers and their offspring.
|mesh-terms=* Adult
* Aging
* Animals
* Female
* Humans
* Live Birth
* Mice
* Mice, Transgenic
* Placenta
* Pregnancy
* T-Lymphocyte Subsets
|keywords=* birth weight
* neonate
* offspring
* pregnancy
* preterm labor
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7290081
}}
{{medline-entry
|title=Structural and Functional Changes in the Mesenteric Lymph Nodes in Humans during Aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32248450
|abstract=Morphometric analysis of structural and functional changes in the human mesenteric lymph nodes during aging revealed the development of fibrous connective tissue, fragmentation of the lymphoid parenchyma, the absence of follicles with germinal centers, and a decrease in the level of lymphocyte proliferation, which was confirmed by the absence of Ki-67  cells. The paracortical zone lacked [[CD4]]  T helpers that regulate both cellular and humoral immunity. High content of plasma cells and eosinophilic granulocytes in the medullary cords and sinuses reflects the development of autoimmune processes associated with a decrease in the number of regulatory T lymphocytes. The development of fibrous connective tissue in the sinus system complicates lymph flow through the lymph node and impairs lymph filtration.

|keywords=* age-related involution
* aging
* immune system
* immunomorphology
* mesenteric lymph nodes
|full-text-url=https://sci-hub.do/10.1007/s10517-020-04782-0
}}
{{medline-entry
|title=Neurocognitive Functioning is Associated with Self-Reported and Performance-Based Treatment Management Abilities in People Living with HIV with Low Health Literacy.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32090235
|abstract=People living with HIV (PLWH) are at higher risk for poorer neurocognitive functioning and health literacy than uninfected persons, which are associated with worse medical outcomes. Aging research suggests that the effect of neurocognitive functioning on health outcomes may be more pronounced in those with low health literacy. We aimed to determine whether low health literacy might amplify the adverse effects of neurocognitive functioning on treatment management outcomes in 171 PLWH aged 40+. In this cross-sectional, observational study, participants completed a well-validated battery of neurocognitive, health literacy, and treatment management measures. A binary health literacy variable (low vs. adequate) was determined via established cut points on the well-validated health literacy tests. Treatment management outcomes included biomarkers of HIV (i.e., [[CD4]] counts and viral load), self-management of HIV disease (i.e., self-reported medication adherence and self-efficacy for HIV disease management), and performance-based health-related decision-making. Forty-seven percent of the sample met the criteria for low health literacy. Multivariable regressions adjusting for clinicodemographic (e.g., race, socioeconomic status) covariates revealed significant interactions for self-efficacy for HIV disease management and health-related decision-making, such that neurocognitive functioning was associated with these outcomes among those with low, but not adequate health literacy. Findings suggest that low health literacy may increase the vulnerability of PLWH to the adverse effects of neurocognitive impairment on health outcomes, or conversely that adequate health literacy may provide a buffer against the health risks associated neurocognitive impairment. Interventions targeting health literacy in PLWH may mitigate the effects of neurocognitive impairment on health outcomes.
|mesh-terms=* Adult
* Cognition
* Cross-Sectional Studies
* HIV Infections
* Health Literacy
* Humans
* Neuropsychological Tests
* Self Report
|keywords=* Adherence
* Aging
* Cognitive impairment
* HIV/AIDS
* Health illiteracy
* Observational study
|full-text-url=https://sci-hub.do/10.1093/arclin/acaa005
}}
{{medline-entry
|title=Blockade of Stat3 oncogene addiction induces cellular senescence and reveals a cell-nonautonomous activity suitable for cancer immunotherapy.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32064174
|abstract=Stat3 is constitutively activated in several tumor types and plays an essential role in maintaining their malignant phenotype and immunosupression. To take advantage of the promising antitumor activity of Stat3 targeting, it is vital to understand the mechanism by which Stat3 regulates both cell autonomous and non-autonomous processes. Here, we demonstrated that turning off Stat3 constitutive activation in different cancer cell types induces senescence, thus revealing their Stat3 addiction. Taking advantage of the senescence-associated secretory phenotype (SASP) induced by Stat3 silencing (SASP-siStat3), we designed an immunotherapy. The administration of SASP-siStat3 immunotherapy induced a strong inhibition of triple-negative breast cancer and melanoma growth associated with activation of [[CD4]] + T and NK cells. Combining this immunotherapy with anti-PD-1 antibody resulted in survival improvement in mice bearing melanoma. The characterization of the SASP components revealed that type I IFN-related mediators, triggered by the activation of the cyclic GMP-AMP synthase DNA sensing pathway, are important for its immunosurveillance activity. Overall, our findings provided evidence that administration of SASP-siStat3 or low dose of Stat3-blocking agents would benefit patients with Stat3-addicted tumors to unleash an antitumor immune response and to improve the effectiveness of immune checkpoint inhibitors.

|keywords=* Stat3
* immune checkpoint blockade
* immunotherapy
* oncogene addiction
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996562
}}
{{medline-entry
|title=Age-related changes in T lymphocytes of patients with head and neck squamous cell carcinoma.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32082401
|abstract=The number of aging cancer patients has increased continuously and will do so further in the future. The immune system of elderly people experiences critical changes over the time. Therefore, tumor-induced changes in the immune system are believed to differ in young and elderly cancer patients as well. The effect of aging on the immune system was measured in peripheral blood lymphocytes (PBL) of healthy volunteers ([i]n[/i] = 48, 21-84 yrs.) divided into three different age groups. Seventy years was set as a cut-off for defining subjects as elderly. Results were compared to two groups of adult cancer patients, which donated PBL and tumor infiltrating lymphocytes (TIL): young cancer patients (40-69 yrs.; blood: [i]n[/i] = 13; TIL: [i]n[/i] = 17) and elderly cancer patients (70-90 yrs.; blood: [i]n[/i] = 20; TIL: [i]n[/i] = 15) with head and neck squamous cell carcinoma (HNSCC). Frequencies and phenotypes of [[CD4]]  and CD8  T cells as well as regulatory T cells (T ) were assessed by flow cytometry. We observed lower frequencies of CD8  cytotoxic T cells during aging in both groups. Frequencies of tumor infiltrating regulatory T cells were significantly higher than in the peripheral blood but showed a significant decline in older tumor patients. With increasing age, expression of immunosuppressive CD73 and CCR7 was lower and expression of PD1 elevated on peripheral T cells in healthy volunteers and tumor patients. Immunosenescence takes place in healthy donors and cancer patients. Our results suggest that in elderly tumor patients, the immune system is impaired and the tumor-induced immune escape is less pronounced. The increased expression of PD1 implies the potential for effective immunotherapies in elderly, as treatment with checkpoint inhibitors could be more beneficial for elderly HNSCC patients.

|keywords=* Aging
* Head and neck cancer
* Immune escape
* Immunosenescence
* T cells
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7017629
}}
==CD68==

{{medline-entry
|title=Cellular senescence in recurrent tonsillitis and tonsillar hypertrophy in children.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32200310
|abstract=To observe the difference in cellular senescence patterns between recurrent tonsillitis and tonsillar hypertrophy. Forty-three patients diagnosed with recurrent tonsillitis or tonsillar hypertrophy, based on medical history and symptoms, underwent tonsillectomy. The specimens were collected and examined using senescence β-galactosidase staining for cellular senescence. Macrophages were detected by immunochemistry. Cellular senescence was found in both recurrent tonsillitis and tonsillar hypertrophy groups. The comparison of cellular senescence in microcompartments of tonsil tissue (germinal centre, mantle zone, subepithelial and intraepithelial) revealed a significant increase of senescent cells in germinal centres in tonsillar hypertrophy compared with that in tonsillar hypertrophy. The majority of senescent cells in both groups were [[CD68]]-positive. Different cellular senescence patterns were found between the two studied paediatric tonsillar diseases. Macrophage senescence may play a role in the pathogenesis of these diseases.
|mesh-terms=* Antigens, CD
* Antigens, Differentiation, Myelomonocytic
* Cellular Senescence
* Child
* Germinal Center
* Humans
* Hypertrophy
* Macrophages
* Palatine Tonsil
* Recurrence
* Tonsillectomy
* Tonsillitis
|keywords=* Cellular senescence
* Recurrent tonsillitis
* Tonsillar hypertrophy
|full-text-url=https://sci-hub.do/10.1016/j.ijporl.2020.110004
}}
==CD80==

{{medline-entry
|title=The aging common marmoset's immune system: From junior to senior.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32246726
|abstract=The social, health, and economic challenges of a steadily increasing aging population demand the use of appropriate translational animal models to address questions like healthy aging, vaccination strategies, or potential interventions during the aging process. Due to their genetic proximity to humans, especially nonhuman primates (NHPs) with a relatively short generation period compared to humans, qualify as excellent animal models for these purposes. The use of common marmosets (Callithrix jacchus) in gerontology research steadily increased over the last decades, yet important information about their aging parameters are still missing. We therefore aimed to characterize their aging immune system by comprehensive flow cytometric phenotyping of blood immune cells from juvenile, adult, aging, and geriatric animals. Aged and geriatric animals displayed clear signs of immunosenescence. A decline in CD4/CD8 ratio, increased expression of HLA-DR and PD-1, higher frequencies of CD95  memory cells, alterations in cytokine secretion, and a decline in the proliferative capacity proved T cell senescence in aging marmosets. Also, the B cell compartment was affected by age-related changes: while overall B cell numbers remained stable with advancing age, expression of the activation marker [[CD80]] increased and immunoglobulin M expression decreased. Interestingly, marmoset B cell memory subset distribution rather mirrored the human situation than that of other NHP. CD21  CD27  naïve B cell frequencies decreased while those of CD21  CD27  tissue memory B cells increased with age. Furthermore, frequencies and numbers of NK cells as part of the innate immune system declined with advancing age. Thus, the observed immunological changes in common marmosets over their life span revealed several similarities to age-related changes in humans and encourages further studies to strengthen the common marmoset as a potential aging model.
|mesh-terms=* Aging
* Animals
* CD4-CD8 Ratio
* Callithrix
* Female
* Flow Cytometry
* Immune System
* Longevity
* Male
* Models, Animal
* Sex Factors
|keywords=* aging
* common marmoset
* immune system
* immunosenescence
* innate and adaptive immunity
* sex
|full-text-url=https://sci-hub.do/10.1002/ajp.23128
}}
==CD81==

{{medline-entry
|title=Increased production of functional small extracellular vesicles in senescent endothelial cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32101370
|abstract=Small extracellular vesicles (EVs) are novel players in vascular biology. However, a thorough understanding of their production and function remains elusive. Endothelial senescence is a key feature of vascular ageing and thus, is an attractive therapeutic target for the treatment of vascular disease. In this study, we sought to characterize the EV production of senescent endothelial cells. To achieve this, Human Umbilical Vascular Endothelial Cells (HUVECs) were replicated until they reached senescence, as determined by measurement of Senescence-Associated β-Galactosidase activity via microscopy and flow cytometry. Expression of the endosomal marker Rab7 and the EV marker CD63 was determined by immunofluorescence. Small EVs were isolated by ultracentrifugation and characterized using electron microscopy, nanoparticle tracking analysis and immunoassays to assess morphology, size, concentration and expression of exosome markers CD9 and [[CD81]]. Migration of HUVECs in response to EVs was studied using a transwell assay. The results showed that senescent endothelial cells express higher levels of Rab7 and CD63. Moreover, senescent endothelial cells produced higher levels of CD9- and [[CD81]]-positive EVs. Additionally, small EVs from both young and senescent endothelial cells promoted HUVEC migration. Overall, senescent endothelial cells produce an increased number of functional small EVs, which may have a role in vascular physiology and disease.

|keywords=* endothelium
* exosomes
* extracellular vesicles
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7176858
}}
==CDK2==

{{medline-entry
|title=p57  is a master regulator of human adipose derived stem cell quiescence and senescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32224418
|abstract=Although human adipose derived stem cells (hADSCs) hold great promises for regenerative medicine, their key biological properties remain poorly understood. In particular, proliferation defects resulted from deep quiescence (dormancy) and senescence represent a major hurdle in hADSC production and clinical application. We have developed a model system for mechanistic dissection of hADSC quiescence and senescence. p57 , a major CDK inhibitor, was highly expressed in quiescent and senescent hADSCs but its level quickly declined upon stem cell activation. p57  overexpression induced quiescence in spite of proliferative signals and its knockdown promoted cell cycle reentry even with induction of quiescence presumably through modulating the [[CDK2]]-CyclinE1 complex. Given its key role in quiescence and senescence, p57  may be exploited for innovative strategies to amplify hADSCs of high quality for clinics.

|keywords=* Human adipose derived stem cells
* Quiescence
* Senescence
* p57(Kip2)
|full-text-url=https://sci-hub.do/10.1016/j.scr.2020.101759
}}
==CDKN1A==

{{medline-entry
|title=Involvement of [[CDKN1A]] (p21) in cellular senescence in response to heat and irradiation stress during preimplantation development.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32253738
|abstract=This study examined the role of cyclin-dependent kinase inhibitor 1a (CDK1A, p21) in response to exogenous stressors during mouse preimplantation embryo development. [[CDKN1A]] knockdown (KD) one-cell zygotes were exposed to 39 °C heat stress (HS) for 4 days or irradiated by 1 (1-Gy) or 3 (3-Gy) Gy X-rays, and their developmental competence and gene expression were compared with control embryos. [[CDKN1A]] KD and HS did not influence early cleavage or subsequent embryonic development; however, HS delayed cavitation and induced elevated Cdkn1a expression in control embryos. Exposure to 1- or 3-Gy had no effect on development to the morula stage; however, a significant number of morulae failed to develop to the blastocyst stage. Interestingly, under the 1-Gy condition, the blastocyst rate of [[CDKN1A]] KD embryos (77.7%) was significantly higher than that of the controls (44.4%). In summary, exposure to cellular stressors resulted in the upregulation of Cdkn1a in embryos exposed to HS or X-ray irradiation, particularly in response to heat stress or low-dose X-ray irradiation, and depleting Cdkn1a mRNA alleviated cell cycle arrest. These findings suggest that [[CDKN1A]] plays a vital role in cellular senescence during preimplantation embryo development.

|keywords=* Cdkn1a
* Heat stress
* Irradiation
* Preimplantation
* Senescence
* p21
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7193008
}}
==CFI==

{{medline-entry
|title=The decision about retirement: A scale to describe representations and practices of medical doctors and nurses.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32258559
|abstract=New reliable and valid instrument to describe health professionals representations about retirement.A valid instrument that can be used to compare different health professionals.Job satisfaction is the major factor associated with positions about general policies about retirement. To test the psychometric properties of a newly designed instrument to describe the REpresentations and Practices About REtirement (the PREPARE instrument). Participants were nurses and doctors working in the two public hospitals of Porto, aged 55-65 years, in 2011. Among the 367 eligible participants, 231 (65.9%) participated in the study. The PREPARE instrument consists of four sections: 9, 5 and 12, respectively. A principal component analysis was performed to evaluate the scale's dimensionality, followed by a confirmatory factor analysis to test the fit using different indexes (TLI - Tucker-Lewis Index and [[CFI]] - Confirmatory fit index). Principal confirmatory analysis and confirmatory factor analysis identified 3, 1 and 2 factors for section 1, 2 and 3. All confirmatory factor analysis models had a value of [[CFI]] and TLI higher than 0.9. Section 1 showed a first factor related with items about the importance of personal competences, a second factor related with items about the importance of relationships with patients, and third factor related with items about the importance of following ethical and directive rules; section 2 showed a general factor about the features you valued most in the other health professional group; and, finally, in section 3, the first factor was related with items about satisfaction with the work environment and the second factor with items about satisfaction with professional career. The PREPARE instrument has the basic requirements of a valid and reliable measurement of a scale to describe medical doctors and nurses representations and practices about the decision regarding retirement.

|keywords=* Aging
* Job satisfaction
* Retirement
* Scale
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6806742
}}
==CIT==

{{medline-entry
|title=The Relationship Between the Striatal Dopaminergic Neuronal and Cognitive Function With Aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32184717
|abstract=Both cognitive function and striatal dopamine function decline by normal aging. However, the relationship among these three factors remains unclear. The aim of this study was to elucidate the association among age-related changes in the striatal dopamine transporter (DAT) and cognitive function in healthy subjects. The 30 healthy volunteers were enrolled in this research, the age ranged from 41 to 82 (64.5 ± 11.5, mean ± SD). All subjects were scanned with both T1-weighted magnetic resonance imaging (MRI) and  I-FP-[[CIT]] single-photon emission computed tomography (SPECT) images. The Wechsler Adult Intelligence Scale-Third Edition (WAIS-III) was used to evaluate cognitive function. Six spherical regions of interest (ROI) using 10 mm in diameter on the caudate nucleus, anterior putamen and posterior putamen were manually drawn on MRI image which was applied onto SPECT image. The relationship between striatal occipital ratio (SOR) values and WAIS-III subscore were analyzed by multiple regression analysis. Subscores which was significant were further analyzed by path analyses. Full intelligence quotient (IQ), verbal IQ, verbal comprehension were all positively correlated with age-adjusted striatal DAT binding ([i]P[/i] < 0.01). Multiple regression analyses revealed that the coding digit symbol correlated with all striatal regions except for the left caudate ([i]P[/i] < 0.04). Picture completion and right caudate, similarities and left caudate also showed a positive correlation ([i]P[/i] < 0.04). Path analysis found that the right caudate and picture completion; the left caudate and similarities were correlated independently from age, whereas the models of coding digit symbol were not significant. These results suggest that age-based individual diversity of striatal DAT binding was associated with verbal function, and the caudate nucleus plays an important role in this association.

|keywords=* SPECT
* Wechsler Adult Intelligence Scale
* aging
* cognitive function
* dopamine transporter
* verbal function
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7058549
}}
==COPE==

{{medline-entry
|title=Patterns and characteristics of cognitive functioning in older patients approaching end stage kidney disease, the [[COPE]]-study.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32272897
|abstract=The prevalence of impaired cognitive functioning in older patients with end stage kidney disease (ESKD) is high. We aim to describe patterns of memory, executive function or psychomotor speed and to identify nephrologic, geriatric and neuroradiologic characteristics associated with cognitive impairment in older patients approaching ESKD who have not yet started with renal replacement therapy (RRT). The [[COPE]]-study (Cognitive Decline in Older Patients with ESRD) is a prospective cohort study including 157 participants aged 65 years and older approaching ESKD (eGFR ≤20 ml/min/1.73 m ) prior to starting with RRT. In addition to routinely collected clinical parameters related to ESKD, such as vascular disease burden and parameters of metabolic disturbance, patients received a full geriatric assessment, including extensive neuropsychological testing. In a subgroup of patients (n = 93) a brain MRI was performed. The median age was 75.3 years. Compared to the normative data of neuropsychological testing participants memory performance was in the 24th percentile, executive function in the 18th percentile and psychomotor speed in the 20th percentile. Independent associated characteristics of impairment in memory, executive and psychomotor speed were high age, low educational level and low functional status (all p-values < 0.003). A history of vascular disease (p = 0.007) and more white matter hyperintensities on brain MRI (p = 0.013) were associated with a lower psychomotor speed. Older patients approaching ESKD have a high prevalence of impaired memory, executive function and psychomotor speed. The patterns of cognitive impairment and brain changes on MRI are suggestive of vascular cognitive impairment. These findings could be of potentially added value in the decision-making process concerning patients with ESKD.

|keywords=* Cognitive function
* End stage renal disease
* Geriatric assessment
* Geriatrics
* Older patients
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7147053
}}
==CPM==

{{medline-entry
|title=Age does not affect sex effect of conditioned pain modulation of pressure and thermal pain across 2 conditioning stimuli.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32072094
|abstract=Conditioned pain modulation ([[CPM]]) is a laboratory test resulting in pain inhibition through activation of descending inhibitory mechanisms. Older adults consistently demonstrate reduced [[CPM]] compared with younger samples; however, studies of sex differences in younger cohorts have shown mixed results. This study tested for sex differences in [[CPM]] within samples of younger and older adults. Participants were 67 younger adults (mean age = 25.4 years) and 50 older adults (66.4 years). Study conditioning paradigms were the cold-pressor test and contact heat pain administered in separate sessions. Pressure pain threshold and ramping suprathreshold heat were the test stimuli across three time points after presentation of the conditioning stimuli (CS). Significant inhibition was observed during both testing sessions. The hypothesis for sex differences across both age cohorts was supported only for ∆PPTh. However, sex differences did not reach significance for either paradigm using ascending suprathreshold heat as the test stimuli. The overall trend was that younger males experienced the strongest [[CPM]] and older females the weakest. From a methodological perspective, duration differences were seen in [[CPM]], with inhibition decaying more quickly for PPTh than for suprathreshold heat pain. Furthermore, there were no differences in inhibition induced by cold-pressor test and contact heat pain as CS. Sex differences were similar across both age cohorts with males experiencing greater inhibition than females. Cross-sectional associations were also demonstrated between [[CPM]] inhibition and measures of recent pain, further supporting [[CPM]] as an experimental model with clinical utility.

|keywords=* Aging
* CPM duration
* Conditioned pain modulation
* Conditioning stimulus
* Sex differences
* Test stimulus
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7004505
}}
==CRABP2==

{{medline-entry
|title=Preconception resveratrol intake against infertility: Friend or foe?
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32273814
|abstract=Resveratrol is an antiaging, antioxidant, anti-inflammatory, and insulin-sensitizing natural polyphenolic compound. Growing evidence indicates that resveratrol has potential therapeutic effects in infertile women with diminished ovarian function, polycystic ovary syndrome (PCOS), or endometriosis. However, only one clinical trial in women undergoing in vitro fertilization (IVF) cycles using resveratrol has ever been reported. This review focuses on the potential therapeutic effects of resveratrol on pregnancy and on its advantages and disadvantages in pregnancy outcomes during infertility treatment. We performed a literature review to describe the known impacts of resveratrol on the ovary and endometrium. Resveratrol upregulates sirtuin (SIRT)1 expression in ovaries, which is associated with protection against oxidative stress. It leads to the activation of telomerase activity and mitochondrial function, improving ovarian function. In the endometrium, resveratrol downregulates the [[CRABP2]]-RAR pathway leading to suppressing decidual and senescent changes of endometrial cells, which is essential for embryo implantation and placentation. Moreover, resveratrol may also induce deacetylation of important decidual-related genes. Resveratrol has potential therapeutic effects for improving ovarian function; however, it also has anti-deciduogenic actions in uterine endometrium. In addition, its teratogenicity has not yet been ruled out; thus, resveratrol should be avoided during the luteal phase and pregnancy.

|keywords=* aging
* assisted reproductive technology
* infertility
* resveratrol
* sirtuin
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7138940
}}
==CRP==

{{medline-entry
|title=The Impact of Age on the Prevalence of Sarcopenic Obesity in Bariatric Surgery Candidates.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32249368
|abstract=Sarcopenia pre-dating bariatric surgery (BS) has been suggested as concern for the use of BS in older-adults with morbid obesity. To evaluate the impact of age on the prevalence of sarcopenic obesity (SO) in BS-candidates. Cross-sectional study including 1370 consecutive BS-candidates aged ≥18, and grouped according to age: 18-39 (reference group), 40-49, 50-59 and ≥ 60 years. From body composition analysis data obtained using bioelectrical impedance, skeletal muscle mass (SMM), SMM index (SMMI=SMM/height ), and percentage of SMM (%SMM = SMM/BW*100) were calculated. Class I or class II SO was adjudicated, respectively, when a value between > - 1 and - 2, or > -2 standard deviations from the regression line from the gender-specific distribution of the relationship between BMI and SMMI or the %SMM in the reference group was encountered. According to the SMMI distribution, prevalence of class I and class II SO in the whole cohort was respectively 16.4% and 4.6%. SO was more prevalent in females (p < 0.005). Proportion of subjects with SO positively correlated with older age category in females (Tau-c = 0.149, p < 0.001) but not in males. In females aged ≥60, class I SO was present in 29.1%, and class II in 12.8%. Similar results were obtained when %SMM was used (Cohen's k-coefficient = 0.886, p < 0.001). Age and female gender were identified as independent preditors of SO, whereas [[CRP]] or the presence of obesity-associated comorbidities were not. Age is a risk factor for SO in BS-candidates. SO is fairly common in female subjects aged >60 years that are candidates to BS.

|keywords=* Aging
* Bariatric surgery
* Elderly
* Obesity
* Sarcopenia
|full-text-url=https://sci-hub.do/10.1007/s11695-019-04198-4
}}
{{medline-entry
|title=Intake of dietary advanced glycation end products influences inflammatory markers, immune phenotypes, and antiradical capacity of healthy elderly in a little-studied population.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32148813
|abstract=Dietary advanced glycation end products (dAGE) have profound negative effects on overall health, and their intake must be assessed. In this cross-sectional study, we investigated dAGE intake of 337 adult participants (180/157:M/F; age range 50-73 years). Data were collected on anthropometrics, body composition, dietary intake, selected blood biochemistry, immunological parameters, and antiradical capacity (50% hemolysis time; HT ). From the dietary data, dAGEs and phytochemical index (PI) were calculated. Mean BMI, % body fat (%BF), and fasting plasma glucose were all within the accepted normal range. Subjects with high dAGE intake had higher %BF, higher energy intake, and lower PI. They tended to have lower CD4/CD8 ratios and higher proportions of B cells and NK cells, but had significantly higher hs-[[CRP]] levels and lower HT  values. Results on HT  suggested that being >60 years of age enhanced dAGE-associated impairment of defense capacity in both those with low and high HT  compared with those <60 years of age. Thus, overall dAGE consumption was high, but elderly participants had lower dAGE intake than younger adults. Indicators of nutritional status and immunological parameters of the subjects were found to be associated with dAGE intake, suggesting a potential impact on health.

|keywords=* CRP
* advanced glycationed end products
* aging
* dAGE
* immunity
* inflammation
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7020308
}}
{{medline-entry
|title=Intentional Switching Between Bimanual Coordination Patterns in Older Adults: Is It Mediated by Inhibition Processes?
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32132919
|abstract=The study investigated the consequences of age-related decline in inhibition processes on intentional switching between bimanual coordination patterns. Fifteen young (24±2.8 years) and 20 older adults (69±5.3 years) performed Stroop tasks and bimanual coordination tasks. Stroop tasks included neutral, congruent, and incongruent conditions. Response time and error rate were measured. Bimanual coordination tasks consisted of performing in-phase (IP) and anti-phase (AP) patterns. Participants were requested to switch as quickly as possible from one pattern to the other, resulting in two different switching directions (AP to IP; IP to AP). Mean and standard deviation (SD) of the continuous relative phase ([[CRP]]) were calculated pre- and post-switching for each participant. Total switching time (TST) was measured. The switching phase was also decomposed into reaction time (RT) and reversal time (REvT). Pearson correlation analyses were performed to test for correlations between: (i) SD of [[CRP]] and response time in Stroop tasks, and (ii) switching times (TST, RT, RevT) and response time in Stroop task, respectively. In addition, parallel mediation analyses were conducted. Results showed that: (i) the AP pattern was less stable than the IP pattern in both young and older adults, (ii) coordination patterns were less stable in older adults, (iii) response times in Stroop task were longer in the incongruent condition, and (iv) RespTs were longer in older than in young participants, whatever the condition. In the bimanual coordination task, RT, RevT, and TST increased with age. The stability of the IP pattern was correlated with the response times observed in neutral and congruent conditions, while the stability of the AP pattern was correlated with response time observed in the incongruent condition. Correlation and mediation analyses showed that, in the AP to IP switching direction, RT and RevT were both significantly correlated with response times observed in the incongruent condition of Stroop task. These findings suggest that inhibition processes are involved in switching between bimanual coordination patterns, at least to trigger the early phase of switching. They also support the hypothesis that inhibition processes are more involved in maintaining the AP pattern and switching to the IP pattern. Finally, age-related changes in switching times seem to be prominently mediated by alterations of inhibition processes.

|keywords=* Stroop task
* aging
* bimanual coordination
* inhibition
* mediation analysis
* switching
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7041435
}}
{{medline-entry
|title=Shorter Telomere Length in Peripheral Blood Leukocytes Is Associated with Post-Traumatic Chronic Osteomyelitis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32125944
|abstract= This study investigated the association between post-traumatic chronic osteomyelitis (COM) and peripheral leukocyte telomere length (PLTL) and explored factors associated with PLTL in COM.   A total of 56 patients with post-traumatic COM of the extremity and 62 healthy control subjects were recruited. The PLTL was measured by real-time PCR. Binary logistic regression analysis was used to identify factors in correlation with telomere length. Sex, age, white blood cell (WBC) count, erythrocyte sedimentation rate (ESR), C-reactive protein ([[CRP]]), and infection duration were included as independent variables in the logistic regression model.   Post-traumatic COM patients had significantly shorter PLTLs (5.39 ± 0.40) than healthy control subjects (5.69 ± 0.46; p < 0.001). Binary logistic regression analysis showed that PLTL had a statistically significant association with age ([i]B[/i] = -0.072; p = 0.013) and [[CRP]] ([i]B[/i] = -0.061; p = 0.033). The logistic regression model was statistically significant and explained 31.4% (Nagelkerke R ) of the change in telomere length and correctly classified 69.6% of the cases.   Patients with post-traumatic COM have shorter PLTLs than healthy subjects. The PLTL erosion of post-traumatic COM was partially explained by age and [[CRP]].

|keywords=* aging
* post-traumatic chronic osteomyelitis
* telomere
|full-text-url=https://sci-hub.do/10.1089/sur.2019.326
}}
==CTSB==

{{medline-entry
|title=Myocardial cathepsin D is downregulated in sudden cardiac death.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32176724
|abstract=Cathepsins are the major lysosomal proteases that maintain intracellular homeostasis. Herein, we investigated the alterations in myocardial cathepsin expression during aging, cardiac hypertrophy, and sudden cardiac death (SCD). Cardiac tissue and blood were sampled from autopsy cases. Subjects were classified into three groups: SCD with cardiac hypertrophy (SCH), compensated cardiac hypertrophy (CCH), and control. Immunoblotting was performed for the major cardiac cathepsins and their targets: cathepsin B, D, and L ([[CTSB]]/D/L), p62, ATP synthase subunit c (ATPSC), and α-synuclein (ASNC). Immunohistochemical analysis and ELISA using serum samples were performed for CTSD. Cardiac [[CTSB]] and CTSD were upregulated with age (r = 0.63 and 0.60, respectively), whereas the levels of CTSL, p62, ATPSC, and ASNC remained unchanged. In age-matched groups, cardiac CTSD was significantly downregulated in SCH (p = 0.006) and CTSL was moderately downregulated in CCH (p = 0.021); however, p62, ATPSC, and ASNC were not upregulated in cardiac hypertrophy. Immunohistochemistry also revealed decreased myocardial CTSD levels in SCH, and serum CTSD levels were relatively lower in SCH cases. Overall, these results suggest that upregulation of cardiac [[CTSB]] and CTSD with age may compensate for the elevated proteolytic demand, and that downregulation of CTSD is potentially linked to SCH.
|mesh-terms=* Adult
* Aged
* Aged, 80 and over
* Aging
* Cathepsin D
* Death, Sudden, Cardiac
* Down-Regulation
* Female
* Humans
* Male
* Middle Aged
* Myocardium
* Substrate Specificity
|keywords=#f
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7075574
}}
==CX3CR1==

{{medline-entry
|title=Monocytes present age-related changes in phospholipid concentration and decreased energy metabolism.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32107839
|abstract=Age-related changes at the cellular level include the dysregulation of metabolic and signaling pathways. Analyses of blood leukocytes have revealed a set of alterations that collectively lower their ability to fight infections and resolve inflammation later in life. We studied the transcriptomic, epigenetic, and metabolomic profiles of monocytes extracted from younger adults and individuals over the age of 65 years to map major age-dependent changes in their cellular physiology. We found that the monocytes from older persons displayed a decrease in the expression of ribosomal and mitochondrial protein genes and exhibited hypomethylation at the HLA class I locus. Additionally, we found elevated gene expression associated with cell motility, including the [[CX3CR1]] and ARID5B genes, which have been associated with the development of atherosclerosis. Furthermore, the downregulation of two genes, PLA2G4B and ALOX15B, which belong to the arachidonic acid metabolism pathway involved in phosphatidylcholine conversion to anti-inflammatory lipoxins, correlated with increased phosphatidylcholine content in monocytes from older individuals. We found age-related changes in monocyte metabolic fitness, including reduced mitochondrial function and increased glycose consumption without the capacity to upregulate it during increased metabolic needs, and signs of increased oxidative stress and DNA damage. In conclusion, our results complement existing findings and elucidate the metabolic alterations that occur in monocytes during aging.

|keywords=* DNA methylation
* aging
* glucose metabolism
* monocytes
* phosphatidylcholines
* transcriptome
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189998
}}
{{medline-entry
|title=Muscle Injury Induces Postoperative Cognitive Dysfunction.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32066806
|abstract=Postoperative cognitive dysfunction (POCD) is a major complication affecting patients of any age undergoing surgery. This syndrome impacts everyday life up to months after hospital discharge, and its pathophysiology still remains unclear. Translational research focusing on POCD is based on a wide variety of rodent models, such as the murine tibial fracture, whose severity can limit mouse locomotion and proper behavioral assessment. Besides, influence of skeletal muscle injury, a lesion encountered in a wide range of surgeries, has not been explored in POCD occurrence. We propose a physical model of muscle injury in [[CX3CR1]]  mice (displaying green fluorescent microglial cells) to study POCD, with morphological, behavioral and molecular approaches. We highlighted: alteration of short- and long-term memory after muscle regeneration, wide microglial reactivity in the brain, including hippocampus area, 24 hours after muscle injury, and an alteration of central brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) balance, 28 days after muscle injury. Our results suggest for the first time that muscle injury can have early as well as late impacts on the brain. Our [[CX3CR1]]  model can also facilitate microglial investigation, more specifically their pivotal role in neuroinflammation and synaptic plasticity, in the pathophysiology of POCD.
|mesh-terms=* Aging
* Animals
* Brain
* Brain-Derived Neurotrophic Factor
* CX3C Chemokine Receptor 1
* Cytokines
* Disease Models, Animal
* Hippocampus
* Humans
* Male
* Mice
* Microglia
* Muscle, Skeletal
* Nerve Growth Factor
* Postoperative Cognitive Complications
* Postoperative Complications
|keywords=#f
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7026159
}}
==CYP2E1==

{{medline-entry
|title=DNA methylation and histone acetylation changes to cytochrome P450 2E1 regulation in normal aging and impact on rates of drug metabolism in the liver.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32221779
|abstract=Aging is associated with reduced liver function that may increase the risk for adverse drug reactions in older adults. We hypothesized that age-related changes to epigenetic regulation of genes involved in drug metabolism may contribute to this effect. We reviewed published epigenome-wide studies of human blood and identified the cytochrome P450 2E1 ([[CYP2E1]]) gene as a top locus exhibiting epigenetic changes with age. To investigate potential functional changes with age in the liver, the primary organ of drug metabolism, we obtained liver tissue from mice aged 4-32 months from the National Institute on Aging. We assayed global DNA methylation (5-methylcytosine, 5mC), hydroxymethylation (5-hydroxymethylcytosine, 5hmC), and locus-specific 5mC and histone acetylation changes around mouse Cyp2e1. The mouse livers exhibit significant global decreases in 5mC and 5hmC with age. Furthermore, 5mC significantly increased with age at two regulatory regions of Cyp2e1 in tandem with decreases in its gene and protein expressions. H3K9ac levels also changed with age at both regulatory regions of Cyp2e1 investigated, while H3K27ac did not. To test if these epigenetic changes are associated with varying rates of drug metabolism, we assayed clearance of the [[CYP2E1]]-specific probe drug chlorzoxazone in microsome extracts from the same livers. [[CYP2E1]] intrinsic clearance is associated with DNA methylation and H3K9ac levels at the Cyp2e1 locus but not with chronological age. This suggests that age-related epigenetic changes may influence rates of hepatic drug metabolism. In the future, epigenetic biomarkers could prove useful to guide dosing regimens in older adults.

|keywords=* Aging
* Cyp2e1
* DNA methylation
* Drug metabolism
* Histone acetylation
* Pharmacokinetics
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7287002
}}
==DCX==

{{medline-entry
|title=Doublecortin and IGF-1R protein levels are reduced in spite of unchanged DNA methylation in the hippocampus of aged rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32236698
|abstract=The aim of the current study was to investigate whether doublecortin ([[DCX]]), insulin-like growth factor receptor 1 (IGF-1R) and metabotropic glutamate receptor 5 (mGluR5) levels are indeed modified in the aging rat hippocampal individual subareas (rather than total hippocampal tissue as in previous reports) at the protein and mRNA level and whether the methylation status contributes to these changes. Since the aging population is not homogeneous in terms of spatial memory performance, we examined whether changes in [[DCX]], IGF-1R and mGluR5 are linked to cognitive aging. Aged (22 months) male Sprague Dawley rats were trained in the hole-board, a spatial memory task, and were subdivided according to performance to aged impaired and aged unimpaired groups. Age- and memory performance-dependent changes in mRNA steady-state levels, protein levels and DNA methylation status of [[DCX]], IGF-1R and mGluR5 were evaluated by RT-PCR, immunoblotting and bisulfite pyrosequencing. Extending previous findings, we detected decreased [[DCX]] protein and mRNA levels in dentate gyrus (DG) of aged animals. IGF-1 signaling is a key event and herein we show that mRNA levels for IGF-1R were unchanged although reduced at the protein level. This finding may simply reflect that these protein levels are regulated at the level of protein synthesis as well as protein degradation. We provide evidence that promoter methylation is not involved in regulation of mRNA and protein levels of [[DCX]], IGF-1R and mGluR5 during aging. Moreover, there was no significant difference between aged rats with impaired and aged rats with unimpaired memory at the protein and mRNA level. Findings propose that changes in the abovementioned protein levels may not be relevant for performance in the spatial memory task used in aged rats.

|keywords=* Aging
* DNA methylation
* Doublecortin
* Hippocampus
* IGF-1R
* mGluR5
|full-text-url=https://sci-hub.do/10.1007/s00726-020-02834-3
}}
==DKC1==

{{medline-entry
|title=Successful liver transplantation in short telomere syndromes without bone marrow failure due to [[DKC1]] mutation.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32166868
|abstract=Short telomere syndromes are a heterogenous spectrum of disorders leading to premature cellular aging. These may involve bone marrow failure, adult-onset idiopathic pulmonary fibrosis, and liver disease, and classical entities such as dyskeratosis congenita. We report a patient who presented with common variable immunodeficiency at 3 years of age and autoimmune cytopenias at 8 years of age. He was found to have short telomeres, and genetic testing confirmed a hemizygous mutation NM_001363.4: c.-142C > G in [[DKC1]] gene. He subsequently developed cirrhosis with severe portal hypertension and hepatopulmonary syndrome, prompting liver transplantation at 11 years of age. He remains well 10 years after transplant with no progression of bone marrow failure or progressive lung disease. In conclusion, short telomere syndromes should be considered as a potential cause of pediatric liver disease of unknown etiology, and in severe cases, isolated liver transplantation may be both appropriate and successful.

|keywords=* DKC1
* cell death: senescence
* cirrhosis
* hepatopulmonary syndrome
* liver transplantation
* short telomere syndromes
|full-text-url=https://sci-hub.do/10.1111/petr.13695
}}
==DMD==

{{medline-entry
|title=Aldehyde dehydrogenases contribute to skeletal muscle homeostasis in healthy, aging, and Duchenne muscular dystrophy patients.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32157826
|abstract=Aldehyde dehydrogenases (ALDHs) are key players in cell survival, protection, and differentiation via the metabolism and detoxification of aldehydes. ALDH activity is also a marker of stem cells. The skeletal muscle contains populations of ALDH-positive cells amenable to use in cell therapy, whose distribution, persistence in aging, and modifications in myopathic context have not been investigated yet. The Aldefluor® (ALDEF) reagent was used to assess the ALDH activity of muscle cell populations, whose phenotypic characterizations were deepened by flow cytometry. The nature of ALDH isoenzymes expressed by the muscle cell populations was identified in complementary ways by flow cytometry, immunohistology, and real-time PCR ex vivo and in vitro. These populations were compared in healthy, aging, or Duchenne muscular dystrophy ([[DMD]]) patients, healthy non-human primates, and Golden Retriever dogs (healthy vs. muscular dystrophic model, Golden retriever muscular dystrophy [GRMD]). ALDEF  cells persisted through muscle aging in humans and were equally represented in several anatomical localizations in healthy non-human primates. ALDEF  cells were increased in dystrophic individuals in humans (nine patients with [[DMD]] vs. five controls: 14.9 ± 1.63% vs. 3.6 ± 0.39%, P = 0.0002) and dogs (three GRMD dogs vs. three controls: 10.9 ± 2.54% vs. 3.7 ± 0.45%, P = 0.049). In [[DMD]] patients, such increase was due to the adipogenic ALDEF  /CD34  populations (11.74 ± 1.5 vs. 2.8 ± 0.4, P = 0.0003), while in GRMD dogs, it was due to the myogenic ALDEF  /CD34  cells (3.6 ± 0.6% vs. 1.03 ± 0.23%, P = 0.0165). Phenotypic characterization associated the ALDEF  /CD34  cells with CD9, CD36, CD49a, CD49c, CD49f, CD106, CD146, and CD184, some being associated with myogenic capacities. Cytological and histological analyses distinguished several ALDH isoenzymes (ALDH1A1, 1A2, 1A3, 1B1, 1L1, 2, 3A1, 3A2, 3B1, 3B2, 4A1, 7A1, 8A1, and 9A1) expressed by different cell populations in the skeletal muscle tissue belonging to multinucleated fibres, or myogenic, endothelial, interstitial, and neural lineages, designing them as potential new markers of cell type or of metabolic activity. Important modifications were noted in isoenzyme expression between healthy and [[DMD]] muscle tissues. The level of gene expression of some isoenzymes (ALDH1A1, 1A3, 1B1, 2, 3A2, 7A1, 8A1, and 9A1) suggested their specific involvement in muscle stability or regeneration in situ or in vitro. This study unveils the importance of the ALDH family of isoenzymes in the skeletal muscle physiology and homeostasis, suggesting their roles in tissue remodelling in the context of muscular dystrophies.

|keywords=* Aging
* Aldehyde dehydrogenase
* Dog model
* Duchenne muscular dystrophy
* Human
* Myogenic
* Non-human primate
* Skeletal muscle
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432589
}}
{{medline-entry
|title=Life expectancy at birth in Duchenne muscular dystrophy: a systematic review and meta-analysis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32107739
|abstract=Several studies indicate that prognosis for survival in Duchenne muscular dystrophy ([[DMD]]) has improved in recent decades. However, published evidence is inconclusive and some estimates may be obsolete due to improvements in standards of care, in particular the routine use of mechanical ventilatory support in advanced stages of the disease. In this systematic review and meta-analysis (PROSPERO identifier: CRD42019121800), we searched MEDLINE (through PubMed), CINAHL, Embase, PsycINFO, and Web of Science for studies published from inception up until December 31, 2018, reporting results of life expectancy in [[DMD]]. We pooled median survival estimates from individual studies using the median of medians, and weighted median of medians, methods. Risk of bias was established with the Newcastle-Ottawa Scale. Results were stratified by ventilatory support and risk of bias. We identified 15 publications involving 2662 patients from 12 countries from all inhabited continents except Africa. Median life expectancy without ventilatory support ranged between 14.4 and 27.0 years (pooled median: 19.0 years, 95% CI 18.0-20.9; weighted pooled median: 19.4 years, 18.2-20.1). Median life expectancy with ventilatory support, introduced in most settings in the 1990s, ranged between 21.0 and 39.6 years (pooled median: 29.9 years, 26.5-30.8; weighted pooled median: 31.8 years, 29.3-36.2). Risk of bias had little impact on pooled results. In conclusion, median life expectancy at birth in [[DMD]] seems to have improved considerably during the last decades. With current standards of care, many patients with [[DMD]] can now expect to live into their fourth decade of life.
|mesh-terms=* Female
* Humans
* Life Expectancy
* Male
* Muscular Dystrophy, Duchenne
* Parturition
* Pregnancy
* Prognosis
* Quality of Life
* Respiration, Artificial
* Survival
|keywords=* Mechanical ventilation
* Mortality
* Prognosis
* Survival
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7387367
}}
==DNAJB9==

{{medline-entry
|title=[[DNAJB9]] Inhibits p53-Dependent Oncogene-Induced Senescence and Induces Cell Transformation.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32264658
|abstract=[i][[DNAJB9]][/i] is known to be a member of the molecular chaperone gene family, whose cellular function has not yet been fully characterized. Here, we investigated the cellular function of [[DNAJB9]] under strong mitogenic signals. We found that [[DNAJB9]] inhibits p53-dependent oncogene-induced senescence (OIS) and induces neoplastic transformation under oncogenic RAS activation in mouse primary fibroblasts. In addition, we observed that [[DNAJB9]] interacts physically with p53 under oncogenic RAS activation and that the p53-interacting region of [[DNAJB9]] is critical for the inhibition of p53-dependent OIS and induction of neoplastic transformation by [[DNAJB9]]. These results suggest that [[DNAJB9]] induces cell transformation under strong mitogenic signals, which is attributable to the inhibition of p53-dependent OIS by physical interactions with p53. This study might contribute to our understanding of the cellular function of [[DNAJB9]] and the molecular basis of cell transformation.

|keywords=* DNAJB9
* RAS
* p53
* senescence
* transformation
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191047
}}
==DNMT3L==

{{medline-entry
|title=Transient [[DNMT3L]] Expression Reinforces Chromatin Surveillance to Halt Senescence Progression in Mouse Embryonic Fibroblast.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32195249
|abstract=Global heterochromatin reduction, which is one of the hallmarks of senescent cells, is associated with reduced transposable element repression and increased risk of chromatin instability. To ensure genomic integrity, the irreparable cells in a population exit permanently from the cell cycle, and this process is termed "senescence." However, senescence only blocks the expansion of unwanted cells, and the aberrant chromatin of senescent cells remains unstable. Serendipitously, we found that the transient ectopic expression of a repressive epigenetic modulator, DNA methyltransferase 3-like ([[DNMT3L]]) was sufficient to delay the premature senescence progression of late-passage mouse embryonic fibroblasts (MEFs) associated with a tightened global chromatin structure. [[DNMT3L]] induces more repressive H3K9 methylation on endogenous retroviruses and downregulates the derepressed transposons in aging MEFs. In addition, we found that a pulse of ectopic [[DNMT3L]] resulted in the reestablishment of H3K27me3 on polycomb repressive complex 2 (PRC2)-target genes that were derepressed in old MEFs. We demonstrated that ectopic [[DNMT3L]] interacted with PRC2 in MEFs. Our data also suggested that ectopic [[DNMT3L]] might guide PRC2 to redress deregulated chromatin regions in cells undergoing senescence. This study might lead to an epigenetic reinforcement strategy for overcoming aging-associated epimutation and senescence.

|keywords=* DNA methyltransferase 3-like (DNMT3L)
* chromatin surveillance
* epigenetics
* polycomb repressive complex 2 (PRC2)
* senescence
* transposable element (TE)
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064442
}}
==DOCK11==

{{medline-entry
|title=[Immunosenescence: The Forefront of Infection and Trophic Control].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115558
|abstract=Recently, aging is becoming an important social problem in many developed countries including Japan. It is socially and universally important to unveil the impact of aging and extend healthy life expectancy. Here we show our recent finding that dedicator of cytokinesis 11 ([[DOCK11]], also known as Zizimin2) may be involved in immunosenescence of B cells. [[DOCK11]] was identified as a guanine nucleotide exchange factor for a small GTPase called cell division cycle 42. Expression of [[DOCK11]] is restricted to lymphoid tissues, and becomes downregulated with age. Thus we examined the involvement of [[DOCK11]] in immunosenescence of B-1a B cells as an example. B-1a cells are the main source of antibodies at steady state, and function as the first line of defense against infection. Although [[DOCK11]] was expressed by B-1a cells, the expression levels declined with age. Furthermore, production of anti-pneumococcal immunoglobulin M antibodies was suppressed in aged mice, and was recovered by adoptive transfer with B-1a cells in a [[DOCK11]]-dependent manner. Thus [[DOCK11]] may be involved in immunosenescence of B-1a cells.
|mesh-terms=* Aging
* Animals
* B-Lymphocytes
* Cytokinesis
* Gene Expression
* Guanine Nucleotide Exchange Factors
* Humans
* Immunoglobulin M
* Immunosenescence
* Mice
* Nutritional Status
* Streptococcus pneumoniae
|keywords=* B-1a B cell
* dedicator of cytokinesis 11
* immunosenescence
|full-text-url=https://sci-hub.do/10.1248/yakushi.19-00193-3
}}
==DPP4==

{{medline-entry
|title=Dipeptidyl peptidase-4 inhibition improves endothelial senescence by activating AMPK/SIRT1/Nrf2 signaling pathway.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32251672
|abstract=Dipeptidyl peptidase-4 ([[DPP4]]) is elevated in numerous cardiovascular pathological processes and [[DPP4]] inhibition is associated with reduced inflammation and oxidative stress. The aim of this study was to examine the role of [[DPP4]] in endothelial senescence. Sprague-Dawley rats (24 months) were orally administrated saxagliptin (10 mg·kg ·d ), a [[DPP4]] inhibitor, for 12 weeks in drinking water. Body weight, heart rate, blood glucose, and blood pressure were measured and vascular histological experiments were performed. In vitro studies were performed using H O -induced senescent human umbilical vein endothelial cells. Both in vivo and in vitro studies confirmed the elevation of [[DPP4]] in senescent vascular endothelium, and inhibition or knockdown of [[DPP4]] ameliorated endothelial senescence. In addition, [[DPP4]] inhibition or silencing reduced endothelial oxidative stress levels in aging vasculature and senescent endothelial cells. Moreover, [[DPP4]] inhibition or knockdown normalized the expression and phosphorylation of AMP-activated protein kinase-α (AMPKα) and sirtuin 1 (SIRT1) expression. Furthermore, the beneficial effects of [[DPP4]] inhibition or knockdown on endothelial cell senescence were at least partly dependent on SIRT1 and Nrf2 activation. In conclusion, our study demonstrated that [[DPP4]] inhibition or silencing ameliorated endothelial senescence both in vivo and in vitro by regulating AMPK/SIRT1/Nrf2. [[DPP4]] may be a new therapeutic target to combat endothelial senescence.

|keywords=* Aging
* Dipeptidyl peptidase-4
* Endothelium
* Oxidative stress
* Vascular
|full-text-url=https://sci-hub.do/10.1016/j.bcp.2020.113951
}}
==DST==

{{medline-entry
|title=Ancestral germen/soma distinction in microbes: Expanding the disposable soma theory of aging to all unicellular lineages.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32268207
|abstract=Life has persisted for about 3.5 billion years (Gy) despite fluctuating environmental pressures and the aging and mortality of individuals. The disposable soma theory ([[DST]]) notoriously contributes to explain this persistence for lineages with a clear soma/germen distinction. Beyond such lineages however, the phylogenetic scope of application of the [[DST]] is less obvious. Typically, the [[DST]] is not expected to explain the survival of microbial species that comprise single-celled organisms apparently lacking a germen/soma distinction. Here, we present an evolutionary argument that generalizes the explanatory scope of [[DST]] to the entire microbial world and provides a novel characterization of the deep molecular and evolutionary roots supporting this expanded disposable soma theory of aging. Specifically, we argue that the germen/soma distinction arose early in evolution and identify DNA semi-conservative replication as a critical process through which two forms of rejuvenation could have evolved in the first microbes. Our hypothesis has fundamental and practical implications. First, whereas unicellular organisms were long thought of as potentially immortal, we suggest instead that all unicellular individuals (prokaryotes or protists alike) are very likely to age, either replicatively or physiologically, or both. Second, our theory introduces a profound reconsideration of microbial individuality, whereby, all microbial individuals, as seen by natural selection, present an obligate transient germen/soma distinction during their life cycles. Third, our work promotes the study of cellular division in prokaryotes and in protist mitosis to illuminate the evolutionary origin of the soma and germen division, traditionally studied in animals. These ideas set the stage for progress in the evolutionary theory of aging from a heretofore overlooked microbial perspective.
|mesh-terms=* Aging
* Animals
* Biological Evolution
* DNA Replication
* Humans
* Phylogeny
|keywords=* Aging
* Asymmetric cell division
* DNA replication
* Disposable Soma Theory
* Epigenetics
* Evolution
* Germen/Soma
* Prokaryotes
* Protists
* Rejuvenation
* Unicellular
|full-text-url=https://sci-hub.do/10.1016/j.arr.2020.101064
}}
==EGF==

{{medline-entry
|title=Insulin Signaling in Intestinal Stem and Progenitor Cells as an Important Determinant of Physiological and Metabolic Traits in [i]Drosophila[/i].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32225024
|abstract=The insulin-IGF-1 signaling (IIS) pathway is conserved throughout multicellular organisms and regulates many traits, including aging, reproduction, feeding, metabolism, stress resistance, and growth. Here, we present evidence of a survival-sustaining role for IIS in a subset of gut cells in [i]Drosophila melanogaster[/i], namely the intestinal stem cells (ISCs) and progenitor cells. Using RNAi to knockdown the insulin receptor, we found that inhibition of IIS in ISCs statistically shortened the lifespan of experimental flies compared with non-knockdown controls, and also shortened their survival under starvation or malnutrition conditions. These flies also showed decreased reproduction and feeding, and had lower amounts of glycogen and glucose in the body. In addition, increased expression was observed for the [i]Drosophila[/i] transcripts for the insulin-like peptides [i]dilp2[/i], [i]dilp5[/i], and [i]dilp6.[/i] This may reflect increased insulin signaling in peripheral tissues supported by up-regulation of the target of the brain insulin gene ([i]tobi[/i]). In contrast, activation of IIS (via knockdown of the insulin pathway inhibitor PTEN) in intestinal stem and progenitor cells decreased fly resistance to malnutrition, potentially by affecting adipokinetic hormone signaling. Finally, [i]Pten[/i] knockdown to enhance IIS also activated JAK-STAT signaling in gut tissue by up-regulation of [i]upd2[/i], [i]upd3[/i], and [i]soc36[/i] genes, as well as genes encoding the [[EGF]] receptor ligands [i]spitz[/i] and [i]vein[/i]. These results clearly demonstrate that manipulating insulin levels may be used to modulate various fly traits, which are important determinants of organismal survival.

|keywords=* ISC
* fruit fly
* insulin signaling pathway
* lifespan
* metabolism
* midgut
* progenitor cells
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7226132
}}
==EGFR==

{{medline-entry
|title=Comparative effectiveness and cost-effectiveness of three first-line [[EGFR]]-tyrosine kinase inhibitors: Analysis of real-world data in a tertiary hospital in Taiwan.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32267879
|abstract=Comparison of the effectiveness and cost-effectiveness of three first-line [[EGFR]]-tyrosine kinase inhibitors (TKIs) would improve patients' clinical benefits and save costs. Using real-world data, this study attempted to directly compare the effectiveness and cost-effectiveness of first-line afatinib, erlotinib, and gefitinib. During May 2011-December 2017, all patients with non-small cell lung cancer (NSCLC) visiting a tertiary center were invited to fill out the EuroQol five-dimension (EQ-5D) questionnaires and World Health Organization Quality of Life, brief version (WHOQOL-BREF), and received follow-ups for survival and direct medical costs. A total of 379 patients with [[EGFR]] mutation-positive advanced NSCLC under first-line TKIs were enrolled for analysis. After propensity score matching for the patients receiving afatinib (n = 48), erlotinib (n = 48), and gefitinib (n = 96), we conducted the study from the payers' perspective with a lifelong time horizon. Patients receiving afatinib had the worst lifetime psychometric scores, whereas the differences in quality-adjusted life expectancy (QALE) were modest. Considering 3 treatments together, afatinib was dominated by erlotinib. Erlotinib had an incremental cost-effectiveness of US$17,960/life year and US$12,782/QALY compared with gefitinib. Acceptability curves showed that erlotinib had 58.6% and 78.9% probabilities of being cost-effective given a threshold of 1 Taiwanese per capita GDP per life year and QALY, respectively. Erlotinib appeared to be cost-effective. Lifetime psychometric scores may provide additional information for effectiveness evaluation.
|mesh-terms=* Afatinib
* Aged
* Carcinoma, Non-Small-Cell Lung
* Cost-Benefit Analysis
* Erlotinib Hydrochloride
* Female
* Gefitinib
* Humans
* Life Expectancy
* Lung Neoplasms
* Male
* Propensity Score
* Protein Kinase Inhibitors
* Quality of Life
* Survival Rate
* Taiwan
* Tertiary Care Centers
|keywords=#f
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7141611
}}
{{medline-entry
|title=An Optogenetic Method to Study Signal Transduction in Intestinal Stem Cell Homeostasis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32201167
|abstract=Homeostasis in adult organs involves replacement of cells from a stem cell pool maintained in specialized niches regulated by extracellular signals. This cell-to-cell communication employs signal transduction pathways allowing cells to respond with a variety of behaviors. To study these cellular behaviors, signaling must be perturbed within tissues in precise patterns, a technique recently made possible by the development of optogenetic tools. We developed tools to study signal transduction in vivo in an adult fly midgut stem cell model where signaling was regulated by the application of light. Activation was achieved by clustering of membrane receptors [[EGFR]] and Toll, while inactivation was achieved by clustering the downstream activators ERK/Rolled and NFκB/Dorsal in the cytoplasm, preventing nuclear translocation and transcriptional activation. We show that both pathways contribute to stem and transit amplifying cell numbers and affect the lifespan of adult flies. We further present new approaches to overcome overexpression phenotypes and novel methods for the integration of optogenetics into the already-established genetic toolkit of Drosophila.
|mesh-terms=* Animals
* Cell Communication
* Cell Proliferation
* Cells, Cultured
* Drosophila Proteins
* Drosophila melanogaster
* Gene Expression Regulation
* Gene Regulatory Networks
* Homeostasis
* Intestinal Mucosa
* Light
* Longevity
* Optogenetics
* Signal Transduction
* Stem Cells
|keywords=* Drosophila
* EGFR
* Toll
* optogenetics
* stem cells
|full-text-url=https://sci-hub.do/10.1016/j.jmb.2020.03.019
}}
==EHF==

{{medline-entry
|title=Extended high frequency hearing and speech perception implications in adults and children.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32111404
|abstract=Extended high frequencies ([[EHF]]), above 8 kHz, represent a region of the human hearing spectrum that is generally ignored by clinicians and researchers alike. This article is a compilation of contributions that, together, make the case for an essential role of [[EHF]] in both normal hearing and auditory dysfunction. We start with the fundamentals of biological and acoustic determinism - humans have [[EHF]] hearing for a purpose, for example, the detection of prey, predators, and mates. [[EHF]] hearing may also provide a boost to speech perception in challenging conditions and its loss, conversely, might help explain difficulty with the same task. However, it could be that [[EHF]] are a marker for damage in the conventional frequency region that is more related to speech perception difficulties. Measurement of [[EHF]] hearing in concert with otoacoustic emissions could provide an early warning of age-related hearing loss. In early life, when [[EHF]] hearing sensitivity is optimal, we can use it for enhanced phonetic identification during language learning, but we are also susceptible to diseases that can prematurely damage it. [[EHF]] audiometry techniques and standardization are reviewed, providing evidence that they are reliable to measure and provide important information for early detection, monitoring and possible prevention of hearing loss in populations at-risk. To better understand the full contribution of [[EHF]] to human hearing, clinicians and researchers can contribute by including its measurement, along with measures of speech in noise and self-report of hearing difficulties and tinnitus in clinical evaluations and studies.

|keywords=* Aging
* Development
* Extended high frequency audiometry
* Otitis media
* Ototoxicity
* Speech in noise
* Speech perception
* Tinnitus
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431381
}}
==ERCC1==

{{medline-entry
|title=Local endothelial DNA repair deficiency causes aging-resembling endothelial-specific dysfunction.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32202295
|abstract=We previously identified genomic instability as a causative factor for vascular aging. In the present study, we determined which vascular aging outcomes are due to local endothelial DNA damage, which was accomplished by genetic removal of [[ERCC1]] (excision repair cross-complementation group 1) DNA repair in mice (EC-knockout (EC-KO) mice). EC-KO showed a progressive decrease in microvascular dilation of the skin, increased microvascular leakage in the kidney, decreased lung perfusion, and increased aortic stiffness compared with wild-type (WT). EC-KO showed expression of DNA damage and potential senescence marker p21 exclusively in the endothelium, as demonstrated in aorta. Also the kidney showed p21-positive cells. Vasodilator responses measured in organ baths were decreased in aorta, iliac and coronary artery EC-KO compared with WT, of which coronary artery was the earliest to be affected. Nitric oxide-mediated endothelium-dependent vasodilation was abolished in aorta and coronary artery, whereas endothelium-derived hyperpolarization and responses to exogenous nitric oxide (NO) were intact. EC-KO showed increased superoxide production compared with WT, as measured in lung tissue, rich in endothelial cells (ECs). Arterial systolic blood pressure (BP) was increased at 3 months, but normal at 5 months, at which age cardiac output (CO) was decreased. Since no further signs of cardiac dysfunction were detected, this decrease might be an adaptation to prevent an increase in BP. In summary, a selective DNA repair defect in the endothelium produces features of age-related endothelial dysfunction, largely attributed to loss of endothelium-derived NO. Increased superoxide generation might contribute to the observed changes affecting end organ perfusion, as demonstrated in kidney and lung.
|mesh-terms=* Age Factors
* Aging
* Animals
* Capillary Permeability
* Cellular Senescence
* Cyclin-Dependent Kinase Inhibitor p21
* DNA Damage
* DNA Repair
* DNA-Binding Proteins
* Endonucleases
* Endothelial Cells
* Endothelium, Vascular
* Mice, Inbred C57BL
* Mice, Knockout
* Nitric Oxide
* Nitric Oxide Synthase Type III
* Superoxides
* Vascular Stiffness
* Vasodilation
|keywords=* DNA damage
* aging
* endothelial dysfunction
* endothelium-dependent dilation
* nitric oxide
|full-text-url=https://sci-hub.do/10.1042/CS20190124
}}
==F3==

{{medline-entry
|title=Multigenerational exposure to TiO  nanoparticles in soil stimulates stress resistance and longevity of survived C. elegans via activating insulin/IGF-like signaling.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32203849
|abstract=With increasing release of nanoparticles (NPs) into the environment, soil organisms likely suffer from high dose and long duration of NPs contamination, while the effect of NPs across multiple generations in soil is rarely studied. Herein, we investigated how multigenerational exposure to different crystal forms (anatase, rutile, and their mixture) of TiO  NPs (nTiO ) affected the survival, behavior, physiological and biochemical traits, and lifespan of nematodes (C. elegans) in a paddy soil. The soil property changed very slightly after being spiked with nTiO , and the toxicities of three nTiO  forms were largely comparable. The nTiO  exposure adversely influenced the survival and locomotion of nematodes, and increased intracellular reactive oxygen species (ROS) generation. Interestingly, the toxic effect gradually attenuated and the lifespan of survived nematodes increased from the P0 to [[F3]] generation, which was ascribed to the survivor selection and stimulatory effect. The lethal effect and the increased oxidative stress may continuously screen out offspring possessing stronger anti-stress capabilities. Moreover, key genes (daf-2, age-1, and skn-1) in the insulin/IGF-like signaling (IIS) pathway actively responded to the nTiO  exposure, which further optimized the selective expression of downstream genes, increased the antioxidant enzyme activities and antioxidant contents, and thereby increased the stress resistance and longevity of survived nematodes across successive generations. Our findings highlight the crucial role of bio-responses in the progressively decreased toxicity of nTiO , and add new knowledge on the long-term impact of soil nTiO  contamination.
|mesh-terms=* Animals
* Caenorhabditis elegans
* Caenorhabditis elegans Proteins
* Insulin
* Longevity
* Nanoparticles
* Oxidative Stress
* Soil
* Titanium
|keywords=* Insulin/IGF-like signaling
* Longevity
* Multigenerational toxicity
* Nanomaterial
* Soil nematode
|full-text-url=https://sci-hub.do/10.1016/j.envpol.2020.114376
}}
==FAAH==

{{medline-entry
|title=Endocannabinoid genetic variation enhances vulnerability to THC reward in adolescent female mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32095523
|abstract=Adolescence represents a developmental period with the highest risk for initiating cannabis use. Little is known about whether genetic variation in the endocannabinoid system alters mesolimbic reward circuitry to produce vulnerability to the rewarding properties of the exogenous cannabinoid Δ -tetrahydrocannabinol (THC). Using a genetic knock-in mouse model ([[FAAH]] ) that biologically recapitulates the human polymorphism associated with problematic drug use, we find that in adolescent female mice, but not male mice, this [[FAAH]] polymorphism enhances the mesolimbic dopamine circuitry projecting from the ventral tegmental area (VTA) to the nucleus accumbens (NAc) and alters cannabinoid receptor 1 (CB R) levels at inhibitory and excitatory terminals in the VTA. These developmental changes collectively increase vulnerability of adolescent female [[FAAH]]  mice to THC preference that persists into adulthood. Together, these findings suggest that this endocannabinoid genetic variant is a contributing factor for increased susceptibility to cannabis dependence in adolescent females.
|mesh-terms=* Aging
* Amidohydrolases
* Animals
* Axons
* Choice Behavior
* Dronabinol
* Endocannabinoids
* Female
* Genetic Variation
* Male
* Mice, Inbred C57BL
* Nerve Net
* Nucleus Accumbens
* Polymorphism, Single Nucleotide
* Receptor, Cannabinoid, CB1
* Reward
* Tyrosine 3-Monooxygenase
* Ventral Tegmental Area
|keywords=#f
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7015690
}}
==FAS==

{{medline-entry
|title=Inhibition of USP7 activity selectively eliminates senescent cells in part via restoration of p53 activity.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32064756
|abstract=The accumulation of senescent cells (SnCs) is a causal factor of various age-related diseases as well as some of the side effects of chemotherapy. Pharmacological elimination of SnCs (senolysis) has the potential to be developed into novel therapeutic strategies to treat these diseases and pathological conditions. Here we show that ubiquitin-specific peptidase 7 (USP7) is a novel target for senolysis because inhibition of USP7 with an inhibitor or genetic depletion of USP7 by RNA interference induces apoptosis selectively in SnCs. The senolytic activity of USP7 inhibitors is likely attributable in part to the promotion of the human homolog of mouse double minute 2 (MDM2) ubiquitination and degradation by the ubiquitin-proteasome system. This degradation increases the levels of p53, which in turn induces the pro-apoptotic proteins PUMA, NOXA, and [[FAS]] and inhibits the interaction of BCL-XL and BAK to selectively induce apoptosis in SnCs. Further, we show that treatment with a USP7 inhibitor can effectively eliminate SnCs and suppress the senescence-associated secretory phenotype (SASP) induced by doxorubicin in mice. These findings suggest that small molecule USP7 inhibitors are novel senolytics that can be exploited to reduce chemotherapy-induced toxicities and treat age-related diseases.

|keywords=* MDM2
* Senescence
* USP7
* apoptosis
* p53
* senolytics
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059172
}}
==FES==

{{medline-entry
|title=A Single Question as a Screening Tool to Assess Fear of Falling in Young-Old Community-Dwelling Persons.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32165062
|abstract=Fear of falling (FOF) is common in older persons and related to negative outcomes. This study aimed to investigate the relationship between 2 FOF measures: the Falls Efficacy Scale-International ([[FES]]-I) and the single question on FOF and activity restriction (SQ-FAR). Factors associated with disagreement between the 2 measures were further examined. Cross-sectional study. Participants (N = 1359) were community-dwelling persons aged 65 to 70 years who were enrolled in the Lausanne cohort 65+. Data included demographic, functional, cognitive, affective, and health status. FOF was measured with [[FES]]-I and the 3-level SQ-FAR (no FOF, FOF without activity restriction (AR, FOF with AR). [[FES]]-I concern about falling was categorized as low (score 16-19), moderate (score 20-27), and high (score 28-64). Weighted agreement between the [[FES]]-I and the SQ-FAR was 87.8% (Kappa = 0.57). Using the [[FES]]-I as gold standard, the performance of SQ-FAR was good (specificity 86%; sensitivity 74%, negative predicting value 89%, positive predicting value 69%). Among participants with moderate/high FOF according to [[FES]]-I, male sex (P = .011) and the absence of previous falls (P < .001) were associated with disagreement between the 2 tools. Among participants with low FOF, female sex (P = .005), falls history (P < .001), and pre-frailty/frailty status (P = .050) were associated with disagreement. The SQ-FAR has a moderate agreement with [[FES]]-I and might be used as a screening tool. The results also may help design a step-by-step strategy to evaluate and address FOF in the clinical setting.

|keywords=* FES-I
* elderly
* fear of falling
* healthy aging
* older adults
|full-text-url=https://sci-hub.do/10.1016/j.jamda.2020.01.101
}}
==FEV==

{{medline-entry
|title=Current Bronchodilator Responsiveness Criteria Underestimate Asthma in Older Adults.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32071132
|abstract=Asthma is common in older adults and is confirmed by demonstration of variable expiratory air-flow limitations, typically evaluated by spirometric assessment of bronchodilator responsiveness. However, many patients with clinically suspected asthma and documented air-flow obstruction do not exhibit a post-bronchodilator response that meets or exceeds current established guidelines. We investigated if extending the time from bronchodilator administration to assessment of bronchodilator response increases the yield of spirometry for the diagnosis of asthma in older adults. This was a cross-sectional study. The subjects were non-smokers, ≥ 60 y old, and with suspected asthma. Subjects were characterized as (1) those with a positive bronchodilator response on the 30-min post-bronchodilator spirometry, (2) those with a positive bronchodilator response on the 60-min post-bronchodilator spirometry, and (3) those without a positive bronchodilator response but with a positive methacholine challenge test. Factors associated with a late response to bronchodilator were evaluated by using bivariate analysis and by multivariate analysis by using a logistic regression model. This study enrolled 165 subjects. Of these, 81 (49.1%) had a positive bronchodilator response on 30-min post-bronchodilator spirometry; 25 (15.2%) had a positive bronchodilator response on the 1-h post-bronchodilator spirometry; and 59 (35.8%) had no positive bronchodilator response but had a positive methacholine challenge test. On multivariable regression analysis, those with a higher baseline percentage of predicted [[FEV]] , higher scores on a standard asthma control test, and wheezing and/or cough after exercise were more likely to either have a late bronchodilator response or no bronchodilator response. Our study showed that a late positive response to bronchodilator use was more common than previously presumed in older subjects with suspected asthma. Pulmonary function testing laboratories should consider routinely reassessing spirometry at 1 h after bronchodilator use if the earlier assessment did not reveal a significant response.

|keywords=* aging
* albuterol
* asthma
* bronchodilator effect
* lung diseases
* older adult
* spirometry
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7538007
}}
==FGF19==

{{medline-entry
|title=Bile acid receptor agonists in primary biliary cholangitis: Regulation of the cholangiocyte secretome and downstream T cell differentiation.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32123836
|abstract=Primary biliary cholangitis (PBC) is a chronic autoimmune liver disease. Approximately 30% of patients do not respond to therapy with ursodeoxycholic acid (UDCA). Previous studies have implicated increased senescence of cholangiocytes in patients who do not respond to UDCA. This may increase the release of cytokines which drive pathogenic T cell polarization. As FXR agonists are beneficial in treating UDCA non-responsive patients, the current study was designed to model the interactions between cholangiocytes and CD4+ T cells to investigate potential immunomodulatory mechanisms of bile acid receptor agonists. Human cholangiocytes were co-cultured with CD4+ T cells to model the biliary stress response. Senescent cholangiocytes were able to polarize T cells toward a Th17 phenotype and suppressed expression of FoxP3 ([i]P[/i] = 0.0043). Whilst FXR and TGR5 receptor agonists were unable directly to alter cholangiocyte cytokine expression, [[FGF19]] was capable of significantly reducing IL-6 release ([i]P[/i] = 0.044). Bile acid receptor expression was assessed in PBC patients with well-characterized responsiveness to UDCA therapy. A reduction in FXR staining was observed in both cholangiocytes and hepatocytes in PBC patients without adequate response to UDCA. Increased IL-6 expression by senescent cholangiocytes represents a potential mechanism by which biliary damage in PBC could contribute to excessive inflammation.

|keywords=* FGF19
* FXR
* TGR5
* autoimmunity
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996327
}}
==FGFR1==

{{medline-entry
|title=Satellite cell-specific ablation of Cdon impairs integrin activation, FGF signalling, and muscle regeneration.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32103583
|abstract=Perturbation in cell adhesion and growth factor signalling in satellite cells results in decreased muscle regenerative capacity. Cdon (also called Cdo) is a component of cell adhesion complexes implicated in myogenic differentiation, but its role in muscle regeneration remains to be determined. We generated inducible satellite cell-specific Cdon ablation in mice by utilizing a conditional Cdon allele and Pax7   . To induce Cdon ablation, mice were intraperitoneally injected with tamoxifen (tmx). Using cardiotoxin-induced muscle injury, the effect of Cdon depletion on satellite cell function was examined by histochemistry, immunostaining, and 5-ethynyl-2'-deoxyuridine (EdU) incorporation assay. Isolated myofibers or myoblasts were utilized to determine stem cell function and senescence. To determine pathways related to Cdon deletion, injured muscles were subjected to RNA sequencing analysis. Satellite cell-specific Cdon ablation causes impaired muscle regeneration with fibrosis, likely attributable to decreased proliferation, and senescence, of satellite cells. Cultured Cdon-depleted myofibers exhibited 32 ± 9.6% of EdU-positive satellite cells compared with 58 ± 4.4% satellite cells in control myofibers (P < 0.05). About 32.5 ± 3.7% Cdon-ablated myoblasts were positive for senescence-associated β-galactosidase (SA-β-gal) while only 3.6 ± 0.5% of control satellite cells were positive (P < 0.001). Transcriptome analysis of muscles at post-injury Day 4 revealed alterations in genes related to mitogen-activated protein kinase signalling (P < 8.29 e  ) and extracellular matrix (P < 2.65 e  ). Consistent with this, Cdon-depleted tibialis anterior muscles had reduced phosphorylated extracellular signal-regulated kinase (p-ERK) protein levels and expression of ERK targets, such as Fos (0.23-fold) and Egr1 (0.31-fold), relative to mock-treated control muscles (P < 0.001). Cdon-depleted myoblasts exhibited impaired ERK activation in response to basic fibroblast growth factor. Cdon ablation resulted in decreased and/or mislocalized integrin β1 activation in satellite cells (weak or mislocalized integrin1 in tmx = 38.7 ± 1.9%, mock = 21.5 ± 6%, P < 0.05), previously linked with reduced fibroblast growth factor (FGF) responsiveness in aged satellite cells. In mechanistic studies, Cdon interacted with and regulated cell surface localization of [[FGFR1]] and FGFR4, likely contributing to FGF responsiveness of satellite cells. Satellite cells from a progeria model, Zmpste24  myofibers, showed decreased Cdon levels (Cdon-positive cells in Zmpste24  = 63.3 ± 11%, wild type = 90 ± 7.7%, P < 0.05) and integrin β1 activation (weak or mislocalized integrin β1 in Zmpste24  = 64 ± 6.9%, wild type = 17.4 ± 5.9%, P < 0.01). Cdon deficiency in satellite cells causes impaired proliferation of satellite cells and muscle regeneration via aberrant integrin and FGFR signalling.

|keywords=* Cdon
* Cellular senescence
* FGFR
* Growth factor signalling
* Muscle regeneration
* Satellite cell
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432598
}}
==FH==

{{medline-entry
|title=Macroscopic hematuria as a risk factor for hypertension in ageing people with hemophilia and a family history of hypertension.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32118768
|abstract=Ageing people with hemophilia (PWH) have a higher prevalence of hypertension than the general population. This study aimed to determine whether macroscopic hematuria was associated with hypertension in PWH in a post hoc analysis using data from a cross-sectional study conducted by the ADVANCE Working Group (the H3 study), which included PWH ≥ 40 years of age. Data from 16 contributing centers, located in 13 European countries and Israel, were analyzed using logistic regression models. Of 532 recruited PWH in the H3 study, 117 had hypertension and a positive family history of hypertension (hypertension [[FH]]+), 75 had hypertension and a negative family history of hypertension (hypertension [[FH]]-), 290 had no diagnosis of hypertension, and the remaining 50 had missing hypertension data. Logistic regressions showed that macroscopic hematuria was associated with hypertension [[FH]]+, both in the univariate (OR = 1.84 [1.17-2.90], P = .01) and in the multivariate model (OR = 1.80 [1.03-3.16], P = .04). Macroscopic hematuria was not associated with hypertension [[FH]]-. Moreover, in a multivariate logistic regression the odds of hypertension [[FH]]+ were increased with the number of macroscopic hematuria episodes. The association between macroscopic hematuria and hypertension was significant for PWH with a family history of hypertension.
|mesh-terms=* Adult
* Aged
* Aged, 80 and over
* Aging
* Cross-Sectional Studies
* Female
* Hematuria
* Hemophilia A
* Humans
* Hypertension
* Israel
* Logistic Models
* Male
* Middle Aged
* Risk Factors
|keywords=#f
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7478422
}}
==FOS==

{{medline-entry
|title=Muscle atrophy-related myotube-derived exosomal microRNA in neuronal dysfunction: Targeting both coding and long noncoding RNAs.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32233025
|abstract=In mammals, microRNAs can be actively secreted from cells to blood. miR-29b-3p has been shown to play a pivotal role in muscle atrophy, but its role in intercellular communication is largely unknown. Here, we showed that miR-29b-3p was upregulated in normal and premature aging mouse muscle and plasma. miR-29b-3p was also upregulated in the blood of aging individuals, and circulating levels of miR-29b-3p were negatively correlated with relative appendicular skeletal muscle. Consistently, miR-29b-3p was observed in exosomes isolated from long-term differentiated atrophic C2C12 cells. When C2C12-derived miR-29b-3p-containing exosomes were uptaken by neuronal SH-SY5Y cells, increased miR-29b-3p levels in recipient cells were observed. Moreover, miR-29b-3p overexpression led to downregulation of neuronal-related genes and inhibition of neuronal differentiation. Interestingly, we identified HIF1α-AS2 as a novel c-[[FOS]] targeting lncRNA that is induced by miR-29b-3p through down-modulation of c-[[FOS]] and is required for miR-29b-3p-mediated neuronal differentiation inhibition. Our results suggest that atrophy-associated circulating miR-29b-3p may mediate distal communication between muscle cells and neurons.

|keywords=* HIF-1α-AS2
* aging
* lncRNAs
* miR-29b-3p
* muscle atrophy
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7253071
}}
==FOSL2==

{{medline-entry
|title=LncRNA GUARDIN suppresses cellular senescence through a LRP130-PGC1α-FOXO4-p21-dependent signaling axis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32149459
|abstract=The long noncoding RNA GUARDIN functions to protect genome stability. Inhibiting GUARDIN expression can alter cell fate decisions toward senescence or apoptosis, but the underlying molecular signals are unknown. Here, we show that GUARDIN is an essential component of a transcriptional repressor complex involving LRP130 and PGC1α. GUARDIN acts as a scaffold to stabilize LRP130/PGC1α heterodimers and their occupancy at the FOXO4 promotor. Destabilizing this complex by silencing of GUARDIN, LRP130, or PGC1α leads to increased expression of FOXO4 and upregulation of its target gene p21, thereby driving cells into senescence. We also found that GUARDIN expression was induced by rapamycin, an agent that suppresses cell senescence. FOS-like antigen 2 ([[FOSL2]]) acts as a transcriptional repressor of GUARDIN, and lower [[FOSL2]] levels in response to rapamycin correlate with increased levels of GUARDIN. Together, these results demonstrate that GUARDIN inhibits p21-dependent senescence through a LRP130-PGC1α-FOXO4 signaling axis, and moreover, GUARDIN contributes to the anti-aging activities of rapamycin.

|keywords=* 
GUARDIN

* LRP130-PGC1α
* cellular senescence
* lncRNAs
* p21
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7132339
}}
==FSHR==

{{medline-entry
|title=[[FSHR]] ablation induces depression-like behaviors.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32203083
|abstract=Alteration in reproductive hormones profile is associated with the increasing risk of menopausal depression in women. Serum follicle-stimulating hormone (FSH) level is changed during the menopause transition, while the effect of FSH on menopausal depression has remained undefined. In this study we investigated whether or how FSH affected menopausal depression in postmenopausal (ovariectomized) [[FSHR]] knockout mice (Fshr ). We found that Fshr  mice displayed aggravated depression-like behaviors, accompanied by severe oxidative stress in the whole brain, resulted from significantly reduced glutamate cysteine ligase modifier subunit (GCLm) in glutathione synthesis and glucose-6-phosphate dehydrogenase (G6PD) in NADP/NADPH transition. Importantly, administration of ROS scavenger N-acetyl cysteine (NAC, 150 mg · kg  · d , i.p. for 12 weeks) attenuated the depression-like behaviors of Fshr  mice. Consistent with these in vivo experiment results, we found that pretreatment with FSH (50, 100 ng/mL) dose-dependently increased protein levels of GCLm and G6PD, and decreased the ROS production in N2a mouse neuroblastoma cells. These findings demonstrate that FSH signaling is involved in pathogenesis of menopausal depression, and likely to maintain the redox-optimized ROS balance in neurons.

|keywords=* FSH
* ROS
* aging
* antioxidants
* depression
* metabolism
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7468367
}}
==GAP43==

{{medline-entry
|title=HDAC inhibition leads to age-dependent opposite regenerative effect upon PTEN deletion in rubrospinal axons after SCI.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32171589
|abstract=Epigenetic changes associated with aging have been linked to functional and cognitive deficits in the adult CNS. Histone acetylation is involved in the control of the transcription of plasticity and regeneration-associated genes. The intrinsic axon growth capacity in the CNS is negatively regulated by phosphatase and tensin homolog (Pten). Inhibition of Pten is an effective method to stimulate axon growth following an injury to the optic nerve, corticospinal tract (CST), and rubrospinal tract (RST). Our laboratory has previously demonstrated that the deletion of Pten in aged animals diminishes the regenerative capacity in rubrospinal neurons. We hypothesize that changes in the chromatin structure might contribute to this age-associated decline. Here, we assessed whether Trichostatin A (TSA), a histone deacetylases (HDACs) inhibitor, reverses the decline in regeneration in aged Pten  mice. We demonstrate that HDAC inhibition induces changes in the expression of [[GAP43]] in both young and aged Pten  mice. The regenerative capacity of the RST did not improve significantly in young mice, neither their motor function on the horizontal ladder or cylinder test after TSA treatment for 7 days. Interestingly, TSA treatment in the aged mice worsened their motor function deficits, suggesting that the systemic treatment with TSA might have an overall adverse effect on motor recovery after SCI in aged animals.
|mesh-terms=* Aging
* Animals
* Axons
* GAP-43 Protein
* Gene Deletion
* Gene Expression
* Histone Deacetylase Inhibitors
* Histone Deacetylases
* Hydroxamic Acids
* Mice, Transgenic
* Motor Activity
* Nerve Regeneration
* PTEN Phosphohydrolase
* Recovery of Function
* Spinal Cord
* Spinal Cord Injuries
|keywords=* Aging
* Epigenetics
* Histone deacetylase
* Pten
* Regeneration
* Spinal cord injury
|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.02.006
}}
==GC==

{{medline-entry
|title=Physicochemical characterization of a polysaccharide from Agrocybe aegirita and its anti-ageing activity.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32172871
|abstract=The aim of the present study is to characterize the structure of a novel natural polysaccharide from Agrocybe aegirita (AAPS) and evaluate its anti-aging activity. The MALLS and [[GC]]-MS analysis indicated that the AAPS with molecular weights of 1.81 × 10  Da was mainly composed by rhamnose, fucose, mannose, and glucose in a molar ratio of 2.90:10.25:3.70:38.27. The FT-IR and NMR analysis showed that the backbone of AAPS was α-L-Rhap-(1→6)-β-D-Glcp-(1→2)-α-L-Fucp-(1→6)-α-D-Glcp-(1→5)-α-L-Araf-(1→4)-β-D-GlcpA-(1→5)-α-L-Araf-(1→6)-α-D-Manp-(1→6)-α-D-Manp-(1→2)-α-L-Fucp-(1→6)-β-D-Glap-(1→2)-α-L-Rhap-(1→6)-β-D-Galp-(1→, which linked with two side chains α-L-Fucp-(1→6)-β-D-Glcp-(1→6)-β-D-Manp-(1→ and α-D-Xylp-(1→2)-α-L-Fucp-(1→5) -α-D-Araf-(1→6)-β-D-Galp-(1→ at O  at H-4-arabinose and the terminal Galp residues, respectively. The MRC-5 cells induced by H O  were used to explore the anti-ageing effect and its underlying mechanism of AAPS. It showed a potent anti-ageing activity, representing by the increased cell viability and β-Gal viability, prevented G1-phase cell-cycle arrest, and decreased mitochondrial membrane potential. The polysaccharides extracted from A. aegirita might be applied in functional food as anti-ageing ingredient.
|mesh-terms=* Aging
* Agrocybe
* Antioxidants
* Carbohydrate Sequence
* Cell Line
* Chemical Phenomena
* G1 Phase Cell Cycle Checkpoints
* Humans
* Membrane Potential, Mitochondrial
* Mitochondria
* Polysaccharides
|keywords=* Agrocybe aegirita polysaccharide
* Anti-ageing
* Cell cycle
* Mitochondrial membrane potential
* Structure
|full-text-url=https://sci-hub.do/10.1016/j.carbpol.2020.116056
}}
{{medline-entry
|title=Structural characteristics, antioxidant properties and antiaging activities of galactan produced by Mentha haplocalyx Briq.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32070549
|abstract=An antioxidant-active polysaccharide (WMP) with a molecular weight of 26.91 kDa was isolated from Mentha haplocalyx Briq by water extraction, ethanol precipitation and gel filtration. According to HPLC, methylation, [[GC]]-MS, and 1D/2D nuclear magnetic resonance spectroscopy, WMP is a heteropolysaccharide composed of Gal (84.2 %), Glc (9.8 %), Man (2.8 %) and Ara (3.2 %) with (1→6)-α-d-Galp and (1→4, 6)-α-d-Galp residues in the backbone and (1→6)-α-d-Galp and (1→6)-α-d-Glcp residues in the branch. The branch point was located at C-4 of (1→4, 6)-α-d-Galp residue with a branching degree of 19.71 %. WMP showed remarkably high scavenging ability for 1, 1-diphenyl-2-picrylhydrazyl (DPPH) and hydroxyl radicals, ferrous ion chelating activity and ferric reducing powder in vitro. In vivo result showed that WMP oral administration substantially increased the activities of antioxidant enzymes, including SOD, GSH-Px and CAT, and decreased MDA levels in the serum and liver of d-Gal-induced aging mice. Therefore, WMP can be an effective natural antioxidant.
|mesh-terms=* Aging
* Animals
* Antioxidants
* Biphenyl Compounds
* Carbohydrate Conformation
* Galactans
* Male
* Mentha
* Mice
* Mice, Inbred Strains
* Particle Size
* Picrates
* Surface Properties
|keywords=* Anti-aging activity
* Antioxidant activity
* Mentha haplocalyx Briq
* Polysaccharides
|full-text-url=https://sci-hub.do/10.1016/j.carbpol.2020.115936
}}
==GDF11==

{{medline-entry
|title=Targeted Approach to Distinguish and Determine Absolute Levels of GDF8 and [[GDF11]] in Mouse Serum.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32104967
|abstract=Growth differentiation factor 11 ([[GDF11]]) is a TGF-β superfamily circulating factor that regulates cardiomyocyte size in rodents, sharing 90% amino acid sequence identity in the active domains with myostatin (GDF8)-the major determinant of skeletal muscle mass. Conflicting data on age-related changes in circulating levels have been reported mainly due to the lack of specific detection methods. More recently, liquid chromatography tandem mass spectrometry (LC-MS/MS) based assay showed that the circulating levels of [[GDF11]] do not change significantly throughout human lifespan, but GDF8 levels decrease with aging in men. Here a novel detection method is demonstrated based on parallel reaction monitoring LC-MS/MS assay combined with immunoprecipitation to reliably distinguish [[GDF11]] and GDF8 as well as determine their endogenous levels in mouse serum. The data indicate that both [[GDF11]] and GDF8 circulating levels significantly decline with aging in female mice.

|keywords=* GDF11
* aging
* immunoprecipitation
* myostatin/GDF8
* serum
* targeted-quantitative proteomics
|full-text-url=https://sci-hub.do/10.1002/pmic.201900104
}}
==GFAP==

{{medline-entry
|title=Meta-analysis of human prefrontal cortex reveals activation of [[GFAP]] and decline of synaptic transmission in the aging brain.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32138778
|abstract=Despite ongoing research efforts, mechanisms of brain aging are still enigmatic and need to be elucidated for a better understanding of age-associated cognitive decline. The aim of this study is to investigate aging in the prefrontal cortex region of human brain in a meta-analysis of transcriptome datasets. We analyzed 591 gene expression datasets pertaining to female and male human prefrontal cortex biopsies of distinct ages. We used hierarchical clustering and principal component analysis (PCA) to determine the influence of sex and age on global transcriptome levels. In sex-specific analysis we identified genes correlating with age and differentially expressed between groups of young, middle-aged and aged. Pathways and gene ontologies (GOs) over-represented in the resulting gene sets were calculated. Potential causal relationships between genes and between GOs were explored employing the Granger test of gene expression time series over the range of ages. The most outstanding results were the age-related decline of synaptic transmission and activated expression of glial fibrillary acidic protein ([[GFAP]]) in both sexes. We found an antagonistic relationship between calcium/calmodulin dependent protein kinase IV (CAMK4) and [[GFAP]] which may include regulatory mechanisms involving cAMP responsive element binding protein (CREB) and mitogen-activated protein kinase (MAPK, alias ERK). Common to both sexes was a decline in synaptic transmission, neurogenesis and an increased base-level of inflammatory and immune-related processes. Furthermore, we detected differences in dendritic spine morphogenesis, catecholamine signaling and cellular responses to external stimuli, particularly to metal (Zinc and cadmium) ions which were higher in female brains.

|keywords=* Aging
* Meta-analysis
* Prefrontal cortex
* Sex-specific
* Transcriptome
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059712
}}
==GHRH==

{{medline-entry
|title=Transcriptomic and metabolomic profiling of long-lived growth hormone releasing hormone knock-out mice: evidence for altered mitochondrial function and amino acid metabolism.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32091406
|abstract=Numerous genetic manipulations that extend lifespan in mice have been discovered over the past two decades, the most robust of which has arguably been the down regulation of growth hormone (GH) signaling. However, while decreased GH signaling has been associated with improved health and lifespan, many of the underlying physiological changes and molecular mechanisms associated with GH signaling have yet to be elucidated. To this end, we have completed the first transcriptomic and metabolomic study on long-lived growth hormone releasing hormone knockout ([[GHRH]]-KO) and wild-type mice in brown adipose tissue (transcriptomics) and blood serum (metabolomics). We find that [[GHRH]]-KO mice have increased transcript levels of mitochondrial and amino acid genes with decreased levels of extracellular matrix genes. Concurrently, mitochondrial metabolites are differentially regulated in [[GHRH]]-KO. Furthermore, we find a strong signal of genotype-by-sex interactions, suggesting the sexes have differing physiological responses to GH deficiency. Overall, our results point towards a strong influence of mitochondrial metabolism in [[GHRH]]-KO mice which potentially is tightly intertwined with their extended lifespan phenotype.

|keywords=* aging
* growth hormone
* metabolite
* mouse
* transcriptomics
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066919
}}
==GREM1==

{{medline-entry
|title=[[GREM1]] inhibits osteogenic differentiation, senescence and BMP transcription of adipose-derived stem cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32151168
|abstract=: Adipose-derived stem cells (ADSCs) are ideal for cell-based therapies to support bone regeneration. It is vital to understand the critical genes and molecular mechanisms involved in the functional regulation of ADSCs for enhancing bone regeneration. In the present study, we investigated the Gremlin 1 ([[GREM1]]) effect on ADSCs osteogenic differentiation and senescence. : The [i]in vitro[/i] ADSCs osteogenic differentiation potential was evaluated by determining alkaline phosphatase (ALP) activity, mineralization ability, and the expression of osteogenic markers. Cell senescence is determined by SA-β-gal staining, telomerase assay, and the expression of aging markers. : [[GREM1]] overexpression in ADSCs reduced ALP activity and mineralization, inhibited the expression of osteogenic related genes [i]OCN, OPN, DSPP, DMP1[/i], and [i]BSP[/i], and key transcription factors, [i]RUNX2[/i] and [i]OSX[/i]. [[GREM1]] knockdown in ADSCs enhanced ALP activity and mineralization, promoted the expression of [i]OCN, OPN, DSPP, DMP1, BSP, RUNX2[/i], and [i]OSX[/i]. [[GREM1]] overexpression in ADSCs reduced the percent SA-β-Gal positive cells, [i]P16[/i] and [i]P53[/i] expressions, and increased telomerase activity. [[GREM1]] knockdown in ADSCs increased the percentage of SA-β-Gal positive cells, [i]P16[/i] and [i]P53[/i] expressions, and reduced telomerase activity. Furthermore, [[GREM1]] reduced the mRNA expression levels of BMP2, BMP6, and BMP7. : In summary, our findings suggested that [[GREM1]] inhibited ADSCs senescence and osteogenic differentiation and antagonized BMP transcription.

|keywords=* BMP
* GREM1
* adipose-derived stem cells (ADSCs)
* osteogenic differentiation
* senescence
|full-text-url=https://sci-hub.do/10.1080/03008207.2020.1736054
}}
==GRID1==

{{medline-entry
|title=Gene discovery for high-density lipoprotein cholesterol level change over time in prospective family studies.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109663
|abstract=Several genes are known to contribute to the levels and metabolism of HDL-C, however, their protective effects in cardiovascular disease (CVD), healthy aging, and longevity are complex and poorly understood. It is also unclear if these genes predict longitudinal HDL-C change. We aimed to identify loci influencing HDL-C change. We performed a genome-wide association study (GWAS) with harmonized HDL-C and imputed genotype in three family-based studies recruited for exceptional survival (Long Life Family Study), from community-based (Framingham Heart Study) and enriched for CVD (Family Heart Study). In 7738 individuals with at least 2 visits, we employed a growth curve model to estimate the random linear trajectory parameter of age-sex-adjusted HDL-C for each person. GWAS was performed using a linear regression model on HDL-C change accounting for kinship correlations, population structure, and differences among studies. We identified a novel association for HDL-C with [[GRID1]] (p = 5.43 × 10 ), which encodes a glutamate receptor channel subunit involved in synaptic plasticity. Seven suggestive novel loci (p < 1.0 × 10 ; MBOAT2, LINC01876-NR4A2, NTNG2, CYSLTR2, SYNE2, CTXND1-LINC01314, and CYYR1) and a known lipid gene (ABCA10) showed associations with HDL-C change. Two additional sex-specific suggestive loci were identified in women (DCLK2 and KCNJ2). Several of these genetic variants are associated with lipid-related conditions influencing cardiovascular and metabolic health, have predictive regulatory function, and are involved in lipid-related pathways. Modeling longitudinal HDL-C in prospective studies, with differences in healthy aging, longevity and CVD risk, contributed to gene discovery and provided insights into mechanisms of HDL-C regulation.

|keywords=* GWAS
* HDL-C metabolism
* Healthy aging
* Longevity
* Longitudinal HDL-C change
|full-text-url=https://sci-hub.do/10.1016/j.atherosclerosis.2020.02.005
}}
==GRK2==

{{medline-entry
|title=Loss of dynamic regulation of G protein-coupled receptor kinase 2 by nitric oxide leads to cardiovascular dysfunction with aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32216616
|abstract=Nitric oxide (NO) and [i]S[/i]-nitrosothiol (SNO) are considered cardio- and vasoprotective substances. We now understand that one mechanism in which NO/SNOs provide cardiovascular protection is through their direct inhibition of cardiac G protein-coupled receptor (GPCR) kinase 2 ([[GRK2]]) activity via [i]S[/i]-nitrosylation of [[GRK2]] at cysteine 340 (C340). This maintains GPCR homeostasis, including β-adrenergic receptors, through curbing receptor [[GRK2]]-mediated desensitization. Previously, we have developed a knockin mouse ([[GRK2]]-C340S) where endogenous [[GRK2]] is resistant to dynamic [i]S[/i]-nitrosylation, which led to increased [[GRK2]] desensitizing activity. This unchecked regulation of cardiac [[GRK2]] activity resulted in significantly more myocardial damage after ischemic injury that was resistant to NO-mediated cardioprotection. Although young adult [[GRK2]]-C340S mice show no overt phenotype, we now report that as these mice age, they develop significant cardiovascular dysfunction due to the loss of SNO-mediated [[GRK2]] regulation. This pathological phenotype is apparent as early as 12 mo of age and includes reduced cardiac function, increased cardiac perivascular fibrosis, and maladaptive cardiac hypertrophy, which are common maladies found in patients with cardiovascular disease (CVD). There are also vascular reactivity and aortic abnormalities present in these mice. Therefore, our data demonstrate that a chronic and global increase in [[GRK2]] activity is sufficient to cause cardiovascular remodeling and dysfunction, likely due to [[GRK2]]'s desensitizing effects in several tissues. Because [[GRK2]] levels have been reported to be elevated in elderly CVD patients, [[GRK2]]-C340 mice can give insight into the aged-molecular landscape leading to CVD.  Research on G protein-coupled receptor kinase 2 ([[GRK2]]) in the setting of cardiovascular aging is largely unknown despite its strong established functions in cardiovascular physiology and pathophysiology. This study uses a mouse model of chronic [[GRK2]] overactivity to further investigate the consequences of long-term [[GRK2]] on cardiac function and structure. We report for the first time that chronic [[GRK2]] overactivity was able to cause cardiac dysfunction and remodeling independent of surgical intervention, highlighting the importance of GRK activity in aged-related heart disease.
|mesh-terms=* Aging
* Animals
* Female
* G Protein-Coupled Inwardly-Rectifying Potassium Channels
* Heart
* Heart Diseases
* Homeostasis
* Male
* Mice
* Mutation
* Myocardium
* Nitric Oxide
|keywords=* S-nitrosylation
* cardiac hypertrophy
* heart disease
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7346533
}}
==GRM3==

{{medline-entry
|title=Profiling gene expression in the human dentate gyrus granule cell layer reveals insights into schizophrenia and its genetic risk.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32203495
|abstract=Specific cell populations may have unique contributions to schizophrenia but may be missed in studies of homogenate tissue. Here laser capture microdissection followed by RNA sequencing (LCM-seq) was used to transcriptomically profile the granule cell layer of the dentate gyrus (DG-GCL) in human hippocampus and contrast these data to those obtained from bulk hippocampal homogenate. We identified widespread cell-type-enriched aging and genetic effects in the DG-GCL that were either absent or directionally discordant in bulk hippocampus data. Of the ~9 million expression quantitative trait loci identified in the DG-GCL, 15% were not detected in bulk hippocampus, including 15 schizophrenia risk variants. We created transcriptome-wide association study genetic weights from the DG-GCL, which identified many schizophrenia-associated genetic signals not found in transcriptome-wide association studies from bulk hippocampus, including [[GRM3]] and CACNA1C. These results highlight the improved biological resolution provided by targeted sampling strategies like LCM and complement homogenate and single-nucleus approaches in human brain.
|mesh-terms=* Adolescent
* Adult
* Aged
* Aged, 80 and over
* Aging
* Bipolar Disorder
* Dentate Gyrus
* Depressive Disorder, Major
* Female
* Gene Expression Profiling
* Genetic Predisposition to Disease
* Genome-Wide Association Study
* Humans
* Male
* Middle Aged
* Neurons
* Quantitative Trait Loci
* Schizophrenia
* Transcriptome
* Young Adult
|keywords=#f
|full-text-url=https://sci-hub.do/10.1038/s41593-020-0604-z
}}
==GUK1==

{{medline-entry
|title=Characterization of the impact of GMP/GDP synthesis inhibition on replicative lifespan extension in yeast.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32232569
|abstract=Slowing down aging-associated accumulation of molecular damage or its prevention represents a promising therapeutic paradigm to combat aging-related disease and death. While several chemical compounds extend lifespan in model organisms, their mechanism of action is often unknown, reducing their therapeutic potential. Using a systematic approach, here we characterize the impact of the GMP pathway on yeast lifespan and elucidate GMP synthesis inhibition as a lifespan extension mechanism. We further discover that proteasome activation extends lifespan in part through the GMP pathway. GMP synthesis inhibition exerts its lifespan extension effect independently of the canonical nutrient-sensing pathway regulating lifespan. Exposing longitudinally aging yeast cells to GMP pathway inhibition in an age-dependent manner, we demonstrate that the lifespan extension is facilitated by slowing, rather than reversing, the aging process in cells. Using a [[GUK1]] mutant with lower GMP-to-GDP conversion activity, we observe lifespan extension, suggesting that reduced GDP level by itself can also extend yeast lifespan. These findings elucidate the involvement of nucleotide metabolism in the aging process. The existence of clinically-approved GMP pathway inhibitors elicits the potential of a new class of therapeutics for aging-related disorders.

|keywords=* Aging
* GDP
* GMP
* Mycophenolic acid
* Proteasome
* Replicative lifespan
* Yeast
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7367712
}}
==H2AX==

{{medline-entry
|title=Guanine Deaminase Stimulates Ultraviolet-induced Keratinocyte Senescence in Seborrhoeic Keratosis via Guanine Metabolites.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32215662
|abstract=DNA damage and oxidative stress play a critical role in photoageing. Seborrhoeic keratosis (SK) affects sunlight-exposed sites in aged individuals. This study examined the mechanism of photoageing in SK. The guanine deaminase gene, which is involved in purine metabolism, was upregulated with uric acid levels and p21 in SK. Guanine deaminase was detectable in keratinocytes. Repeated exposure to ultraviolet (UV) increased levels of guanine deaminase, together with DNA damage, such as γ-[[H2AX]] and cyclobutane pyrimidine dimer formation, generation of reactive oxygen species, and keratinocyte senescence, which were reversed by guanine deaminase knockdown. However, guanine deaminase overexpression and H2O2 formed γ-[[H2AX]], but not cyclobutane pyrimidine dimer. Loss-of-function guanine deaminase mutants reduced the metabolic end-product uric acid, which was increased by exposure to exogenous xanthine. Repeated exposure to UV increased levels of uric acid. Exogenous uric acid increased cellular senescence, reactive oxygen species, and γ-[[H2AX]], similar to guanine deaminase. Overall, guanine deaminase upregulation increased UV-induced keratinocyte senescence in SK, via uric acid mediated by reactive oxygen species followed by DNA damage.

|keywords=*  DNA damage
*  UV-induced keratinocyte senescence
*  guanine deaminase
*  reactive oxygen species
*  uric acid
* seborrhoeic keratosis
|full-text-url=https://sci-hub.do/10.2340/00015555-3473
}}
==HCN1==

{{medline-entry
|title=Protein expression changes of [[HCN1]] and HCN2 in hippocampal subregions of gerbils during the normal aging process.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32128096
|abstract=Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels play essential roles in various hippocampal functions, including regulation of long-term potentiation, synaptic plasticity, and hippocampal-dependent cognitive process. The objective of this study was to investigate age-related changes in [[HCN1]] and HCN2 protein expressions in gerbil hippocampus at various ages. In this study, the protein expressions of [[HCN1]] and HCN2 were compared in the hippocampus at the ages of 1, 3, 12, and 24 months using Western blot analysis and immunohistochemistry. Immunoreactivity of both [[HCN1]] and HCN2 was shown primarily in cells of the pyramidal cell layer in the hippocampus proper and in cells of the granule cell layer in the dentate gyrus. [[HCN1]] and HCN2 protein expression levels and immunoreactivity were significantly increased at three months (3 M) of age compared with those at 1 M of age. After that, both [[HCN1]] and HCN2 expression levels in the hippocampus were gradually decreased with age. Our results show that the normal aging process affects the expression levels of [[HCN1]] and HCN2 in hippocampal cells in gerbils. There are marked reductions in [[HCN1]] and HCN2 expressions in the aged hippocampus compared to the young hippocampus. Such reductions might be related to aging in the hippocampus.

|keywords=* Aging
* Dentate gyrus
* Granule cells
* HCN channel
* Hippocampus proper
* Pyramidal cells
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7038419
}}
==HDC==

{{medline-entry
|title=Induced pluripotency and spontaneous reversal of cellular aging in supercentenarian donor cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115145
|abstract=Supercentenarians (≥110-year-old, SC) are a uniquely informative population not only because they surpass centenarians in age, but because they appear to age more slowly with fewer incidences of chronic age-related disease than centenarians. We reprogramed donor B-lymphoblastoid cell lines (LCL) derived from a 114-year-old (SC), a 43-year-old healthy disease-free control ([[HDC]]) and an 8-year-old with a rapid aging disease (Hutchinson-Gilford progeria syndrome (HGPS)) and compared SC-iPSC to [[HDC]]-iPSC and HGPS-iPSCs. Reprogramming to pluripotency was confirmed by pluripotency marker expression and differentiation to 3 germ-layers. Each iPSC clone differentiated efficiently to mesenchymal progenitor cells (MPC) as determined by surface marker expression and RNAseq analysis. We identified supercentenarian and HGPS associated gene expression patterns in the differentiated MPC lines that were not evident in the parental iPSC lines. Importantly, telomere length resetting occurred in iPSC from all donors albeit at a lower incidence in supercentenarian iPSCs. These data indicate the potential to use reprogramming to reset both developmental state and cellular age in the "oldest of the old." We anticipate that supercentenarian iPSC and their differentiated derivatives will be valuable tools for studying the underlying mechanisms of extreme longevity and disease resistance.
|mesh-terms=* Adult
* Aged, 80 and over
* Cell Differentiation
* Cell Line
* Cellular Reprogramming
* Cellular Senescence
* Child
* Clone Cells
* Gene Expression Regulation
* Humans
* Induced Pluripotent Stem Cells
* Mesenchymal Stem Cells
* Telomere Homeostasis
* Tissue Donors
* Transcriptome
|keywords=* Aging
* Longevity
* Reprogramming
* Supercentenarian
* Telomere
* iPSC
|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2020.02.092
}}
==HGF==

{{medline-entry
|title=Phenytoin sodium-ameliorated gingival fibroblast aging is associated with autophagy.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32281104
|abstract=Human gingival fibrolasts aging is an important cause of periodontal disease. Phenytoin sodium (phenytoin) has a side effect of gingival hyperplasia and an effect on the autophagy progress. This study investigated whether the effect of phenytoin on aging gingival fibroblast is related to the autophagy pathway. The aging model of gingival fibroblast cell line [[HGF]]-1 was induced by hydrogen peroxide (H  O  ), and the treatment of phenytoin and 3-methyladenine (3-MA) was performed simultaneously. Cell viability, cell cycle, and intracellular calcium ion were measured by flow cytometry. Changes in expression of basic fibroblast growth factor (bFGF), P16  , P21  , and bFGF, P16  , P21  , LC3II, p62, and Beclin were tested by using reverse transcription polymerase chain reaction, western blot, and immunofluorescence staining. The results showed that aging [[HGF]]-1 proliferation was inhibited by H  O  , gene, protein expression of bFGF, P16  , and P21  were decreased, autophagy-related proteins LC3II, p62, and Becline were decreased, and the proportion of G0/G1 phase and intracellular calcium ion of cell cycle was increased. Phenytoin treatment could recovery above changes, but the effect of phenytoin could be blocked by 3-MA. We propose that phenytoin alleviates the aging of gingival fibroblasts induced by H  O  . This condition is related to the enhancement of autophagy pathway.

|keywords=* aging
* autophagy
* gingival fibroblast
* phenytoin sodium
|full-text-url=https://sci-hub.do/10.1111/jre.12750
}}
{{medline-entry
|title=Impaired integrin α  /β  -mediated hepatocyte growth factor release by stellate cells of the aged liver.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32157808
|abstract=Hepatic blood flow and sinusoidal endothelial fenestration decrease during aging. Consequently, fluid mechanical forces are reduced in the space of Disse where hepatic stellate cells (HSC) have their niche. We provide evidence that integrin α  /β  is an important mechanosensor in HSC involved in shear stress-induced release of hepatocyte growth factor ([[HGF]]), an essential inductor of liver regeneration which is impaired during aging. The expression of the integrin subunits α  and β  decreases in liver and HSC from aged rats. CRISPR/Cas9-mediated integrin α  and β  knockouts in isolated HSC lead to lowered [[HGF]] release and impaired cellular adhesion. Fluid mechanical forces increase integrin α  and laminin gene expression whereas integrin β  remains unaffected. In the aged liver, laminin β2 and γ1 protein chains as components of laminin-521 are lowered. The integrin α  knockout in HSC reduces laminin expression via mechanosensory mechanisms. Culture of HSC on nanostructured surfaces functionalized with laminin-521 enhances Hgf expression in HSC, demonstrating that these ECM proteins are critically involved in HSC function. During aging, HSC acquire a senescence-associated secretory phenotype and lower their growth factor expression essential for tissue repair. Our findings suggest that impaired mechanosensing via integrin α  /β  in HSC contributes to age-related reduction of ECM and [[HGF]] release that could affect liver regeneration.

|keywords=* aging
* hepatic stellate cells
* integrins
* laminins
* mechanobiology
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189994
}}
==HMGA2==

{{medline-entry
|title=4D Genome Rewiring during Oncogene-Induced and Replicative Senescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32220303
|abstract=To understand the role of the extensive senescence-associated 3D genome reorganization, we generated genome-wide chromatin interaction maps, epigenome, replication-timing, whole-genome bisulfite sequencing, and gene expression profiles from cells entering replicative senescence (RS) or upon oncogene-induced senescence (OIS). We identify senescence-associated heterochromatin domains (SAHDs). Differential intra- versus inter-SAHD interactions lead to the formation of senescence-associated heterochromatin foci (SAHFs) in OIS but not in RS. This OIS-specific configuration brings active genes located in genomic regions adjacent to SAHDs in close spatial proximity and favors their expression. We also identify DNMT1 as a factor that induces SAHFs by promoting [[HMGA2]] expression. Upon DNMT1 depletion, OIS cells transition to a 3D genome conformation akin to that of cells in replicative senescence. These data show how multi-omics and imaging can identify critical features of RS and OIS and discover determinants of acute senescence and SAHF formation.
|mesh-terms=* Cells, Cultured
* Cellular Senescence
* Chromatin Assembly and Disassembly
* DNA (Cytosine-5-)-Methyltransferase 1
* DNA Methylation
* Fibroblasts
* Genome, Human
* Heterochromatin
* Humans
* In Situ Hybridization, Fluorescence
* Oncogenes
|keywords=* 3D genome architecture
* DNMT1
* Hi-C
* chromatin compartments
* gene regulation
* oncogene-induced senescence
* replicative senescence
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7208559
}}
{{medline-entry
|title=The protective effects of [[HMGA2]] in the senescence process of bone marrow-derived mesenchymal stromal cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32068957
|abstract=Bone marrow-derived mesenchymal stromal cells (MSCs) have been wildly applied to cell-based strategies for tissue engineering and regenerative medicine; however, they have to undergo the senescence process and thus appeared to be less therapeutic effective. [[HMGA2]], a protein belonged to high mobility group A (HMGA) family, exhibits an inverse expression level related to embryonic development and acts as a developmental regulator in stem cell self-renewal progression. Therefore, we performed senescence-associated β-galactosidase (SA-β-gal) staining, transwell assay, to examine the changes of MSCs in different stages and then over-expressed [[HMGA2]] in MSCs by lentivirus transfection. We found the percentage of SA-β-gal staining positive cells in MSCs from 24-month-old Sprague-Dawley (SD) rats (O-MSCs) was significantly higher compared with MSCs from 2-week-old SD rats (Y-MSCs), and the expression levels of P21 and P53, two senescence-related molecules, were also significantly up-regulated in O-MSCs than in Y-MSCs. In contrast, the [[HMGA2]] expression level in O-MSCs was dramatically down-regulated in contrast to Y-MSCs. In additional, the migration ability in O-MSCs was significantly attenuated than in Y-MSCs. After successfully over-expressed [[HMGA2]] in O-MSCs, the percentage of SA-β-gal staining positive cells and the expression levels of P21 and P53 were reduced, and the migration ability was improved compared with O-MSCs without treatment. Further, mRNA sequencing analysis revealed that overexpression of [[HMGA2]] changed the expression of genes related to cell proliferation and senescence, such as Lyz2, Pf4, Rgs2, and Mstn. Knockdown of Rgs2 in [[HMGA2]] overexpression O-MSCs could antagonize the protective effect of [[HMGA2]] in the senescence process of O-MSCs.

|keywords=* bone marrow derived mesenchymal stromal cells (MSCs)
* high-mobility group AT-hook 2 (HMGA2)
* regulator of G protein signaling 2 (Rgs2)
* senescence
|full-text-url=https://sci-hub.do/10.1002/term.3023
}}
==HP==

{{medline-entry
|title=Beta Human Papillomavirus 8E6 Attenuates LATS Phosphorylation after Failed Cytokinesis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32238586
|abstract=Beta genus human papillomaviruses (β-[[HP]]Vs) cause cutaneous squamous cell carcinomas (cSCCs) in a subset of immunocompromised patients. However, β-[[HP]]Vs are not necessary for tumor maintenance in the general population. Instead, they may destabilize the genome in the early stages of cancer development. Supporting this idea, β-[[HP]]V's 8E6 protein attenuates p53 accumulation after failed cytokinesis. This paper offers mechanistic insight into how β-[[HP]]V E6 causes this change in cell signaling. An [i]in silico[/i] screen and characterization of HCT 116 cells lacking p300 suggested that the histone acetyltransferase is a negative regulator of Hippo pathway ([[HP]]) gene expression. [[HP]] activation restricts growth in response to stimuli, including failed cytokinesis. Loss of p300 resulted in increased [[HP]] gene expression, including proproliferative genes associated with [[HP]] inactivation. β-[[HP]]V 8E6 expression recapitulates some of these phenotypes. We used a chemical inhibitor of cytokinesis (dihydrocytochalasin B [H2CB]) to induce failed cytokinesis. This system allowed us to show that β-[[HP]]V 8E6 reduced activation of large tumor suppressor kinase (LATS), an [[HP]] kinase. LATS is required for p53 accumulation following failed cytokinesis. These phenotypes were dependent on β-[[HP]]V 8E6 destabilizing p300 and did not completely attenuate the [[HP]]. It did not alter H2CB-induced nuclear exclusion of the transcription factor YAP. β-[[HP]]V 8E6 also did not decrease [[HP]] activation in cells grown to a high density. Although our group and others have previously described inhibition of DNA repair, to the best of our knowledge, this marks the first time that a β-[[HP]]V E6 protein has been shown to hinder [[HP]] signaling.  β-[[HP]]Vs contribute to cSCC development in immunocompromised populations. However, it is unclear if these common cutaneous viruses are tumorigenic in the general population. Thus, a more thorough investigation of β-[[HP]]V biology is warranted. If β-[[HP]]V infections do promote cSCCs, they are hypothesized to destabilize the cellular genome. [i]In vitro[/i] data support this idea by demonstrating the ability of the β-[[HP]]V E6 protein to disrupt DNA repair signaling events following UV exposure. We show that β-[[HP]]V E6 more broadly impairs cellular signaling, indicating that the viral protein dysregulates the [[HP]]. The [[HP]] protects genome fidelity by regulating cell growth and apoptosis in response to a myriad of deleterious stimuli, including failed cytokinesis. After failed cytokinesis, β-[[HP]]V 8E6 attenuates phosphorylation of the [[HP]] kinase (LATS). This decreases some, but not all, [[HP]] signaling events. Notably, β-[[HP]]V 8E6 does not limit senescence associated with failed cytokinesis.
|mesh-terms=* Apoptosis
* Cell Cycle Proteins
* Cell Line, Tumor
* Cell Proliferation
* Cell Survival
* Cytochalasin B
* Cytokinesis
* DNA Repair
* E1A-Associated p300 Protein
* Gene Expression Regulation
* HCT116 Cells
* Host-Pathogen Interactions
* Humans
* Keratinocytes
* Oncogene Proteins, Viral
* Osteoblasts
* Papillomaviridae
* Phenotype
* Phosphorylation
* Primary Cell Culture
* Protein-Serine-Threonine Kinases
* Signal Transduction
* Transcription Factors
* Tumor Suppressor Protein p53
|keywords=* Hippo signaling pathway
* apoptosis
* cancer
* cytokinesis
* human papillomavirus
* senescence
* skin cancer
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7307087
}}
==HPSE==

{{medline-entry
|title=Distribution of heparan sulfate correlated with the expression of heparanase-1 and matrix metalloproteinase-9 in an ovariectomized rats skin.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32159248
|abstract=There are few studies on heparan sulfate (HS) in the skin, during aging, when estrogen is suppressed. The enzyme heparanase-1 ([[HPSE]]-1), has its 17β-estrogen-regulated expression in pathological conditions such as cancer and chronic inflammatory diseases. [[HPSE]]-1 is correlated with the matrix metalloproteinase-9 (MMP-9), an endopeptidase that also undergoes estrogen action. We investigated the distribution of HS, expression [[HPSE]]-1 and MMP-9 in the skin of adult rats at different ages and in the age-matched ovariectomized rats to evaluate the influence of low estrogen on the distribution of HS. Thirty female Wistar rats were used. Rats underwent to a sham surgery (ctr, n = 15) or to a bilateral ovariectomy (ovx, n = 15) and were euthanized after 45, 75, and 90 days after ovariectomy. Morphological, morphometric, biochemical, and reverse transcriptase polymerase chain reaction (RT-PCR) methodologies were used. A significant decrease (P < 0.001) in total skin thickness was observed in the ctr and ovx animals, being higher in the older animals. The thickness of the epidermis and dermis decreased; however, the proportion in the total skin remained similar comparing ctr and ovx. An increase of HS with increasing age and ovariectomy was observed. The expression of the [[HPSE]]-1 and MMP-9 enzymes decreased, being higher in old animals. A correlation between the increase of HS and the decrease of the [[HPSE]]-1 was demonstrated in both groups. Overall, these data suggested that estrogen acts in the regulation of the expression of the [[HPSE]]-1, not only in pathological states, as already established, but also in aging.

|keywords=* aging
* estrogen
* extracellular matrix
* heparan sulfate
* heparanase-1
* matrix metalloproteinase-9
|full-text-url=https://sci-hub.do/10.1002/cbin.11339
}}
==HR==

{{medline-entry
|title=Physical activity trajectories, mortality, hospitalization, and disability in the Toledo Study of Healthy Aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32163233
|abstract=Physical activity (PA) is a recognized contributor to healthy aging. However, the majority of studies exploring its associations with adverse outcomes in cohorts of older adults use single-time PA estimates, which do not consider its dynamic nature. The aim of the present study is to explore the presence of different PA trajectories in the Toledo Study of Healthy Aging and their association with adverse outcomes. Our hypothesis is that prospectively maintaining or increasing PA is associated with a reduced risk of adverse outcomes. We used data from 1679 participants enrolled in the Toledo Study of Healthy Aging. Trajectories based on the Physical Activity Scale for the Elderly were identified using group-based trajectory modelling. Cox and logistic regression were used to investigate associations between PA trajectories and mortality and hospitalization, and incident and worsening disability, respectively. Mortality was ascertained by linkage to the Spanish National Death Index; disability was evaluated through the Katz Index; and hospitalization was defined as the first admission to Toledo Hospital. Models were adjusted by age, sex, smoking, Charlson Index, education, cognitive impairment, polypharmacy, and Katz Index at Wave 2. We found four PA-decreasing and one PA-increasing trajectories: high PA-consistent (n = 566), moderate PA-mildly decreasing (n = 392), low PA-increasing (n = 237), moderate PA-consistent (n = 191), and low PA-decreasing (n = 293). Belonging to the high PA-consistent trajectory group was associated with reduced risks of mortality as compared with the low PA-decreasing group [hazard ratio ([[HR]]) 1.68; 95% confidence interval (CI) = 1.21-2.31] and hospitalization compared with the low PA-increasing and low PA-decreasing trajectory groups ([[HR]] 1.24; 95% CI = 1.004-1.54 and [[HR]] 1.25; 95% CI = 1.01-1.55, respectively) and with lower rates of incident [odds ratio (OR) 3.14; 95% CI = 1.59-6.19] and worsening disability (OR 2.16; 95% CI = 1.35-3.45) in relation to the low PA-decreasing trajectory group and at follow-up. Increasing PA during late life (low PA-increasing group) was associated with lower incident disability rates (OR 0.38; 95% CI = 0.19-0.82) compared with decreasing PA (low PA-decreasing group), despite similar baseline PA. Our results suggest that sustaining higher PA levels during aging might lead to healthy aging, characterized by a reduction in adverse outcomes. Our study supports the need for enhancing PA participation among older populations, with the goal of reducing personal and economic burden in a worldwide aging population.

|keywords=* Adverse outcomes
* Healthy aging
* Mortality
* Older adults
* Physical activity
* Trajectories
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432572
}}
{{medline-entry
|title=U-Shaped Association of Plasma Testosterone, and no Association of Plasma Estradiol, with Incidence of Fractures in Men.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32155267
|abstract=Whether androgens, distinct from estrogen, maintain bone health during male aging has implications for understanding osteoporosis. We assessed associations of different sex hormones with incidence of any bone fracture or hip fracture in older men. Analysis of 3307 community-dwelling men aged 76.8 ± 3.5 years, median follow-up period of 10.6 years. Plasma testosterone (T), dihydrotestosterone (DHT), and estradiol (E2) assayed by mass spectrometry, sex hormone-binding globulin (SHBG), and luteinizing hormone (LH) using immunoassay. Incident fractures determined via data linkage. We analyzed probability of fracture and performed Cox regression adjusted for age, medical comorbidities, and frailty. Incident fractures occurred in 330 men, including 144 hip fractures. Probability plots suggested nonlinear relationships between hormones and risk of any fracture and hip fracture, with higher risk at lower and higher plasma T, lower E2, higher SHBG, and higher LH. In fully adjusted models, there was a U-shaped association of plasma T with incidence of any fracture (Quartile 2 [Q2] versus Q1: fully adjusted hazard ratio [[[HR]]] = 0.69, 95% confidence interval [CI] 0.51-0.94, P = .020; Q3: [[HR]] 0.59, 95% CI 0.42-0.83, P = .002) and hip fracture (Q2 versus Q1: [[HR]] 0.60, 95% CI 0.37-0.93, P = .043; Q3: [[HR]] 0.52, 95% CI 0.31-0.88, P = .015). DHT, E2, and LH were not associated with fracture. Higher SHBG was associated with hip fracture (Q4 versus Q1: [[HR]] 1.76, 95% CI 1.05-2.96, P = .033). Midrange plasma T was associated with lower incidence of any fracture and hip fracture, and higher SHBG with increased risk of hip fracture. Circulating androgen rather than estrogen represents a biomarker for hormone effects on bone driving fracture risk.

|keywords=* estradiol
* fracture
* male aging
* osteoporosis
* sex hormone-binding globulin
* testosterone
|full-text-url=https://sci-hub.do/10.1210/clinem/dgaa115
}}
{{medline-entry
|title=Pregnancy-Related Bone Mineral and Microarchitecture Changes in Women Aged 30 to 45 Years.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32119748
|abstract=At birth, the neonatal skeleton contains 20 to 30 g calcium (Ca). It is hypothesized maternal bone mineral may be mobilized to support fetal skeletal development, although evidence of pregnancy-induced mineral mobilization is limited. We recruited healthy pregnant (n = 53) and non-pregnant non-lactating (NPNL; n = 37) women aged 30 to 45 years (mean age 35.4 ± 3.8 years) and obtained peripheral quantitative computed tomography (pQCT) and high-resolution pQCT ([[HR]]-pQCT) scans from the tibia and radius at 14 to 16 and 34 to 36 weeks of pregnancy, with a similar scan interval for NPNL. Multiple linear regression models were used to assess group differences in change between baseline and follow-up; differences are expressed as standard deviation scores (SDS) ± SEM. Decreases in volumetric bone mineral density (vBMD) outcomes were found in both groups; however, pregnancy-related decreases for pQCT total and trabecular vBMD were -0.65 ± 0.22 SDS and -0.50 ± 0.23 SDS greater (p < .05). [[HR]]-pQCT total and cortical vBMD decreased compared with NPNL by -0.49 ± 0.24 SDS and -0.67 ± 0.23 SDS, respectively; trabecular vBMD decreased in both groups to a similar magnitude. Pregnancy-related changes in bone microarchitecture significantly exceeded NPNL change for trabecular number (0.47 ± 0.23 SDS), trabecular separation (-0.54 ± 0.24 SDS), cortical thickness (-1.01 ± 0.21 SDS), and cortical perimeter (0.78 ± 0.23 SDS). At the proximal radius, cortical vBMD and endosteal circumference increased by 0.50 ± 0.23 SDS and 0.46 ± 0.23 SDS, respectively, compared with NPNL, whereas cortical thickness decreased -0.50 ± 0.22 SDS. Pregnancy-related decreases in total and compartment-specific vBMD exceed age-related change at the distal tibia. Changes at the radius were only evident with pQCT at the cortical-rich proximal site and suggest endosteal resorption. Although the magnitude of these pregnancy-related changes in the appendicular skeleton are small, if they reflect global changes across the skeleton at large, they may contribute substantially to the Ca requirements of the fetus. © 2020 Crown copyright. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR). This article is published with the permission of the Controller of HMSO and the Queen's Printer for Scotland.

|keywords=* AGING
* ANALYSIS/QUANTITATION OF BONE
* BONE QCT/μCT
* EPIDEMIOLOGY
* GENERAL POPULATION STUDIES
|full-text-url=https://sci-hub.do/10.1002/jbmr.3998
}}
==HRAS==

{{medline-entry
|title=How do combinations of unhealthy behaviors relate to attitudinal factors and subjective health among the adult population in the Netherlands?
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32245376
|abstract=Health behaviours like smoking, nutrition, alcohol consumption and physical activity (SNAP) are often studied separately, while combinations can be particularly harmful. This study aims to contribute to a better understanding of lifestyle choices by studying the prevalence of (combinations of) unhealthy SNAP behaviours in relation to attitudinal factors (time orientation, risk attitude) and subjective health (self-rated health, life expectancy) among the adult Dutch population. In total 1006 respondents, representative of the Dutch adult population (18-75 years) in terms of sex, age, and education, were drawn from a panel in 2016. They completed an online questionnaire. Groups comparisons and logistic regression analyses (crude and adjusted) were applied to analyse (combinations of) SNAP behaviours in relation to time orientation (using the Consideration of Future Consequences scale comprising Immediate (CFC-I) and Future (CFC-F) scales) and risk attitude (Health-Risk Attitude Scale; [[HRAS]]-6), as well as subjective health (visual analogue scale and subjective life expectancy). In the analyses, 989 respondents (51% men, average 52 years, 22% low, 48% middle, and 30% high educated) were included. About 8% of respondents engaged in four unhealthy SNAP behaviours and 18% in none. Self-rated health varied from 5.5 to 7.6 in these groups, whilst subjective life expectancy ranged between 73.7 and 85.5 years. Logistic regression analyses, adjusted for socio-demographic variables, showed that smoking, excessive drinking and combining two or more unhealthy SNAP behaviours were significantly associated with CFC-I scores, which increased the odds by 30%, 18% and 19%, respectively. Only physical inactivity was significantly associated with CFC-F scores, which increased the odds by 20%. Three out of the four SNAP behaviours were significantly associated with [[HRAS]]-6, which increased the odds between 6% and 12%. An unhealthy diet, excessive drinking, and physical inactivity were significantly associated with SRH, which decreased the odds by 11%. Only smoking was significantly associated with subjective life expectancy, which decreased the odds by 3%. Our findings suggest that attitudinal factors and subjective health are relevant in the context of understanding unhealthy SNAP behaviours and their clustering. This emphasizes the relevance of a holistic approach to health prevention rather than focusing on a single unhealthy SNAP behaviour.
|mesh-terms=* Adult
* Alcohol Drinking
* Attitude to Health
* Cluster Analysis
* Diagnostic Self Evaluation
* Diet, Healthy
* Exercise
* Female
* Health Risk Behaviors
* Humans
* Life Expectancy
* Life Style
* Logistic Models
* Male
* Middle Aged
* Netherlands
* Prevalence
* Sedentary Behavior
* Smoking
* Surveys and Questionnaires
* Young Adult
|keywords=* Clustering risk attitude
* Health behaviours
* Subjective health
* Time orientation
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7126128
}}
==IHH==

{{medline-entry
|title=Indian Hedgehog regulates senescence in bone marrow-derived mesenchymal stem cell through modulation of ROS/mTOR/4EBP1, p70S6K1/2 pathway.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32235006
|abstract=Premature senescence of bone marrow-derived mesenchymal stem cells (BMSC) remains a major concern for their application clinically. Hedgehog signaling has been reported to regulate aging-associated markers and MSC skewed differentiation. Indian Hedgehog ([[IHH]]) is a ligand of Hedgehog intracellular pathway considered as an inducer in chondrogenesis of human BMSC. However, the role of [[IHH]] in the aging of BMSC is still unclear. This study explored the role [[IHH]] in the senescence of BMSC obtained from human samples and senescent mice. Isolated BMSC were transfected with [[IHH]] siRNA or incubated with exogenous [[IHH]] protein and the mechanisms of aging and differentiation investigated. Moreover, the interactions between [[IHH]], and mammalian target of rapamycin (mTOR) and reactive oxygen species (ROS) were evaluated using the corresponding inhibitors and antioxidants. BMSC transfected with [[IHH]] siRNA showed characteristics of senescence-associated features including increased senescence-associated β-galactosidase activity (SA-β-gal), induction of cell cycle inhibitors (p53/p16), development of senescence-associated secretory phenotype (SASP), activation of ROS and mTOR pathways as well as the promotion of skewed differentiation. Interestingly, BMSC treatment with [[IHH]] protein reversed the senescence markers and corrected biased differentiation. Moreover, [[IHH]] shortage-induced senescence signs were compromised after mTOR and ROS inhibition. Our findings presented anti-aging activity for [[IHH]] in BMSC through down-regulation of ROS/mTOR pathways. This discovery might contribute to increasing the therapeutic, immunomodulatory and regenerative potency of BMSC and introduce a novel remedy in the management of aging-related diseases.

|keywords=* Indian hedgehog
* aging
* differentiation
* mammalian target of rapamycin
* mesenchymal stem cell
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185126
}}
==IL15==

{{medline-entry
|title=Moderate physical activity associated with a higher naïve/memory T-cell ratio in healthy old individuals: potential role of [[IL15]].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32221610
|abstract=ageing is accompanied by impairments in immune responses due to remodelling of the immune system (immunesenescence). Additionally, a decline in habitual physical activity has been reported in older adults. We have recently published that specific features of immunesenescence, such as thymic involution and naïve/memory T-cell ratio, are prevented by maintenance of a high level of physical activity. This study compares immune ageing between sedentary and physically active older adults. a cross-sectional study recruited 211 healthy older adults (60-79 years) and assessed their physical activity levels using an actigraph. We compared T- and B-cell immune parameters between relatively sedentary (n = 25) taking 2,000-4,500 steps/day and more physically active older adults (n = 25) taking 10,500-15,000 steps/day. we found a higher frequency of naïve CD4 (P = 0.01) and CD8 (P = 0.02) and a lower frequency of memory CD4 cells (P = 0.01) and CD8 (P = 0.04) T cells in the physically active group compared with the sedentary group. Elevated serum IL7 (P = 0.03) and [[IL15]] (P = 0.003), cytokines that play an essential role in T-cell survival, were seen in the physically active group. Interestingly, a positive association was observed between [[IL15]] levels and peripheral CD4 naïve T-cell frequency (P = 0.023). we conclude that a moderate level of physical activity may be required to give a very broad suppression of immune ageing, though 10,500-15,000 steps/day has a beneficial effect on the naïve T-cell pool.

|keywords=* T cells
* ageing
* immune senescence
* older people
* physical activity
|full-text-url=https://sci-hub.do/10.1093/ageing/afaa035
}}
==IMPACT==

{{medline-entry
|title=Using Video Telehealth to Deliver Patient-Centered Collaborative Care: The G-[[IMPACT]] Pilot.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32228299
|abstract=: This pilot project aimed to explore a new model of healthcare delivery to older adult medically complex Veterans by combining telehealth technology with an interdisciplinary medical team operating in real time. : The Geriatric-Interdisciplinary Mobile Patient Access Team (G-[[IMPACT]]) was comprised of a field team including a nurse practitioner and technology assistant who visited enrolled patients in their homes using synchronous video to link to a suite of geriatric specialists in a video-enabled room at a Veterans Affairs hospital. Clinicians interacted with patients, caregivers, and each other to develop mutually agreed upon treatment plans that were then immediately implemented in the field. : 11 total visits were conducted with 9 Veteran patients aged 55-91 (mean = 75.3 years). Both patients and clinicians reported a high level of satisfaction across multiple metrics, including visit quality, and positive indirect indicators of effectiveness were apparent from qualitative data. : Nurse practitioner facilitated video visits allowed geriatric patients to meet with multiple specialists simultaneously with both high patient satisfaction and increased real-time care coordination. : This project identified challenges and opportunities afforded by this type of real-time telehealth care delivery and can inform the development of future interdisciplinary mobile medical teams.

|keywords=* Telehealth
* aging
* care coordination
* home care
* interdisciplinary
* medicine
* older adult
* video
|full-text-url=https://sci-hub.do/10.1080/07317115.2020.1738000
}}
==IQGAP1==

{{medline-entry
|title=Hyaluronan-binding protein 1 (HABP1) overexpression triggers induction of senescence in fibroblasts cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32068317
|abstract=Hyaluronan-binding protein 1 (HABP1), a multi-compartmental, multi-functional protein has a wide range of functions, which can be attributed to its ability to associate with a variety of cellular ligands. Earlier we have reported that HABP1 overexpression in rat normal fibroblasts (F-HABP07) shows chronic generation of reactive oxygen species (ROS), induction of autophagy, and apoptosis. However, a significant proportion of cells remained viable after the majority went through apoptosis from 60 to 72 h. In this study, an attempt has been made to delineate the cellular events in the declined population of surviving cells. It has been elucidated here that, these cells at later time points of growth, that is, 72 and 84 h, not only appeared to shrink but also are devoid of autophagic vacuoles and displayed polyploidy. F-HABP07 cells exhibited an altered cytoskeletal structure from their parental cell line F111, assumed to be caused upon inhibition of actin polymerization and decrease in IQ motif-containing GTPase activating protein 1 ([[IQGAP1]]), a key protein associated with maintenance of cytoskeletal integrity. Enhanced expression and nuclear localization of AKT observed in F-HABP07 cells appears to be contributing toward the maintenance of high ROS levels in these cells and also potentially modulating the [[IQGAP1]] activity. These observations, in fact have been considered to result in sustained DNA damage, which then leads to increased expression of p53 and activation of p21 and carry out the cellular events responsible for senescence. Subsequent assessment of the presence of positive β-gal staining and enhanced expression of p16  in F-HABP07, confirmed that HABP1 overexpressing fibroblasts undergo senescence.

|keywords=* F-HABP07
* HABP1
* IQGAP1
* senescence
|full-text-url=https://sci-hub.do/10.1002/cbin.11326
}}
==JAK1==

{{medline-entry
|title=Irradiation-induced senescence of bone marrow mesenchymal stem cells aggravates osteogenic differentiation dysfunction via paracrine signaling.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32233952
|abstract=The role of cellular senescence induced by radiation in bone loss has attracted much attention. As one of the common complications of anticancer radiotherapy, irradiation-induced bone deterioration is common and clinically significant, but the pathological mechanism has not been elucidated. This study was performed to explore the cellular senescence and senescence-associated secretory phenotype (SASP) induction of bone marrow-derived mesenchymal stem cells (BMSCs) by irradiation and its role in osteogenic differentiation dysfunction. It was observed that irradiated BMSCs lost typical fibroblast-like morphology, exhibited suppressed viability and differentiation potential accompanied with senescence phenotypes, including an increase in senescence-associated β-galactosidase (SA-β-gal) staining-positive cells, and upregulated senescence-related genes [i]p53/p21[/i], whereas no changes happened to [i]p16[/i]. Additionally, DNA damage γ-H2AX foci, G0/G1 phase of cell cycle arrest, and cellular and mitochondrial reactive oxygen species (ROS) increased in an irradiation dose-dependent manner. Meanwhile, the [[JAK1]]/STAT3 pathway was activated and accompanied by an increase in SASP secretion, such as IL-6, IL-8, and matrix metalloproteinase-9 (MMP9), whereas 0.8 μM [[JAK1]] inhibitor (JAKi) treatment effectively inhibited the JAK pathway and SASP production. Furthermore, conditioned medium (CM) from irradiation-induced senescent (IRIS) BMSCs exhibited a markedly reduced ability in osteogenic differentiation and marker gene expression of osteoblasts, whereas CM with JAKi intervention may effectively improve these deterioration effects. In conclusion, irradiation could provoke BMSC senescence and SASP secretion and further aggravate osteogenic differentiation dysfunction via paracrine signaling, whereas SASP targeting may be a possible intervention strategy for alleviating irradiation-induced bone loss.
|mesh-terms=* Bone Resorption
* Cell Cycle Checkpoints
* Cell Differentiation
* Cell Proliferation
* Cellular Senescence
* DNA Damage
* Gene Expression Regulation, Developmental
* Histones
* Humans
* Janus Kinase 1
* Mesenchymal Stem Cells
* Mitochondria
* Osteogenesis
* Paracrine Communication
* Radiation
* Reactive Oxygen Species
* STAT3 Transcription Factor
* Signal Transduction
|keywords=* SASP
* bone marrow mesenchymal stem cells
* cellular senescence
* irradiation
* osteogenic differentiation
|full-text-url=https://sci-hub.do/10.1152/ajpcell.00520.2019
}}
==KDM2B==

{{medline-entry
|title=Identification of Structural Elements of the Lysine Specific Demethylase 2B CxxC Domain Associated with Replicative Senescence Bypass in Primary Mouse Cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32270414
|abstract=Lysine specific demethylase 2B, [[KDM2B]], regulates genes that participate in cellular development, morphogenesis, differentiation and metabolism as a component of the polycomb repressive complex 1 (PRC1). The CxxC finger of [[KDM2B]] is responsible for the DNA binding capacity of this epigenetic regulator, acting as a sampling mechanism across chromatin for gene repression OBJECTIVES: The molecular determinants of the CxxC-DNA interaction remain largely unknown, revealing a significant knowledge gap to be explored. Our goal was to elucidate the key residues of the CxxC domain that contribute to its function as well as to further elaborate on the significance of this domain in the [[KDM2B]] role METHODS: By using electrophoresis mobility swift assay, we identified structural elements of CxxC domain that participate in the DNA recognition. We created mouse embryonic fibroblasts overexpressing different truncated and point-mutated mouse [[KDM2B]] variants to examine the contribution of the [[KDM2B]] domains in replicative senescence bypass RESULTS: In this study, we show that only the CxxC finger is essential for the ability of m[[KDM2B]] to bypass replicative senescence in primary cells by ink4A-Arf-ink4B locus repression, and that this is mediated by specific interactions of residues R585, K608 and K616 with non-methylated CpG containing DNA CONCLUSIONS: These results provide new structural insights into the molecular interactions of CxxC and could serve as a stepping-stone for developing domain-specific inhibitors for [[KDM2B]].

|keywords=* Lysine demethylase
* Non-methylated CpG
* Oncogene
* Polycomb repressive complex
* Replicative senescence
* Zn-finger
|full-text-url=https://sci-hub.do/10.1007/s10930-020-09895-z
}}
==KIT==

{{medline-entry
|title=Prediction of ovarian aging using ovarian expression of BMP15, GDF9, and C-[[KIT]].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32223330
|abstract=Ovarian aging is becoming a more important issue in terms of fertility preservation and infertility treatment. Serum anti-Mullerian hormone (AMH) level and antral follicle count (AFC) are being practically used as markers of ovarian aging as well as ovarian reserve in human. However, these factors have some drawbacks in assessing ovarian aging and reserve. Therefore, the identification of ovarian expressions of BMP15, GDF9, and C-[[KIT]] according to female could be applied as a potent predictor of ovarian aging. This work provides new information on the development of diagnosis and treatment strategy of age-related fertility decline and premature ovarian insufficiency.

|keywords=* BMP15
* C-KIT
* GDF9
* Ovarian aging
* biomarkers
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7221484
}}
==KRAS==

{{medline-entry
|title=Senescence-Induced Vascular Remodeling Creates Therapeutic Vulnerabilities in Pancreas Cancer.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32234521
|abstract=[[KRAS]] mutant pancreatic ductal adenocarcinoma (PDAC) is characterized by a desmoplastic response that promotes hypovascularity, immunosuppression, and resistance to chemo- and immunotherapies. We show that a combination of MEK and CDK4/6 inhibitors that target [[KRAS]]-directed oncogenic signaling can suppress PDAC proliferation through induction of retinoblastoma (RB) protein-mediated senescence. In preclinical mouse models of PDAC, this senescence-inducing therapy produces a senescence-associated secretory phenotype (SASP) that includes pro-angiogenic factors that promote tumor vascularization, which in turn enhances drug delivery and efficacy of cytotoxic gemcitabine chemotherapy. In addition, SASP-mediated endothelial cell activation stimulates the accumulation of CD8  T cells into otherwise immunologically "cold" tumors, sensitizing tumors to PD-1 checkpoint blockade. Therefore, in PDAC models, therapy-induced senescence can establish emergent susceptibilities to otherwise ineffective chemo- and immunotherapies through SASP-dependent effects on the tumor vasculature and immune system.
|mesh-terms=* Aging
* Animals
* CD8-Positive T-Lymphocytes
* Carcinoma, Pancreatic Ductal
* Cell Line, Tumor
* Cell Proliferation
* Cyclin-Dependent Kinase 4
* Cyclin-Dependent Kinase 6
* Gene Expression Regulation, Neoplastic
* Genes, ras
* Humans
* Immunotherapy
* MAP Kinase Signaling System
* Mice
* Pancreatic Neoplasms
* Retinoblastoma Protein
* Signal Transduction
* Tumor Microenvironment
* Vascular Remodeling
|keywords=* T cells
* chemotherapy resistance
* endothelial cell activation
* immunotherapy
* pancreatic cancer
* senescence
* senescence-associated secretory phenotype
* targeted therapy
* tumor microenvironment
* vascular biology
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7278897
}}
==LBP==

{{medline-entry
|title=Aging-related liver degeneration is associated with increased bacterial endotoxin and lipopolysaccharide binding protein levels.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32090603
|abstract=Aging is a risk factor in the development of many diseases, including liver-related diseases. The two aims of the present study were [i]1[/i]) to determine how aging affects liver health in mice in the absence of any interventions and [i]2[/i]) if degenerations observed in relation to blood endotoxin levels are critical in aging-associated liver degeneration. Endotoxin levels and markers of liver damage, mitochondrial dysfunction, insulin resistance, and apoptosis as well as the Toll-like receptor 4 (Tlr-4) signaling cascade were studied in liver tissue and blood, respectively, of 3- and 24-mo-old male C57BL/6J mice. In a second set of experiments, 3- to 4-mo-old and 14-mo-old female lipopolysaccharide-binding protein ([[LBP]])  mice and littermates fed standard chow, markers of liver damage, insulin resistance, and mitochondrial dysfunction were assessed. Plasma activity of aspartate aminotransferase and histological signs of hepatic inflammation and fibrosis were significantly higher in old C57BL/6J mice than in young animals. The number of neutrophils, CD8α-positive cells, and mRNA expression of markers of apoptosis were also significantly higher in livers of old C57BL/6J mice compared with young animals, being also associated with a significant induction of hepatic Tlr-4 and [[LBP]] expression as well as higher endotoxin levels in peripheral blood. Compared with age-matched littermates, [[LBP]]  mice display less signs of senescence in liver. Taken together, our data suggest that, despite being fed standard chow, old mice developed liver inflammation and beginning fibrosis and that bacterial endotoxin may play a critical role herein.  Old age in mice is associated with marked signs of liver degeneration, hepatic inflammation, and fibrosis. Aging-associated liver degeneration is associated with elevated bacterial endotoxin levels and an induction of lipopolysaccharide-binding protein ([[LBP]]) and Toll-like receptor 4-dependent signaling cascades in liver tissue. Furthermore, in old aged [[LBP]]  mice, markers of senescence seem to be lessened, supporting the hypothesis that bacterial endotoxin levels might be critical in aging-associated decline of liver.
|mesh-terms=* Acute-Phase Proteins
* Aging
* Animals
* Apoptosis
* Biomarkers
* Carrier Proteins
* Endotoxins
* Female
* Gene Expression Regulation
* Glucose
* Inflammation
* Insulin Receptor Substrate Proteins
* Liver
* Liver Cirrhosis
* Malate Dehydrogenase
* Male
* Membrane Glycoproteins
* Mice
* Mice, Inbred C57BL
* Mice, Knockout
* RNA, Messenger
* Receptor, Insulin
* Toll-Like Receptor 4
|keywords=* Tlr-4 signaling
* aging
* bacterial endotoxin
* lipopolysaccharide binding protein
* liver degeneration
|full-text-url=https://sci-hub.do/10.1152/ajpgi.00345.2018
}}
==LBR==

{{medline-entry
|title=The impact of age beyond ploidy: outcome data from 8175 euploid single embryo transfers.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32173784
|abstract=The rate of embryonic aneuploidy increases with increasing female age and is the primary cause of lower pregnancy and live birth rates ([[LBR]]) in older reproductive age women. This retrospective cohort study evaluates single euploid embryo transfers to determine whether an age-related decline in reproductive efficiency persists. A total of 8175 non-donor single embryo transfers (SET) after pre-implantation testing for aneuploidy (PGT-A) and cryopreservation were included. These were divided into five groups by patient age: < 35 years old (n = 3789 embryos transferred), 35-37 (n = 2200), 38-40 (n = 1624), 41-42 (n = 319), and > 42 (n = 243). Implantation rate (IR), clinical pregnancy rate (CPR), and [[LBR]] were calculated for each group as a percentage of embryos transferred and compared. CPR was also analyzed as a percentage of implanted pregnancies, and [[LBR]] as a percentage of clinical pregnancies, to determine when age has the greatest impact. These results were then adjusted for confounding variables via a multivariate logistic regression model. Implantation rates negatively correlated with age. After adjusting for confounders, women 38 years or older had a significantly lower IR than those under 35 (OR 0.85, 95%CI 0.73-0.99 for 38-40 years old; 0.69, 0.53-0.91 for 41-42, and 0.69, 0.51-0.94 for > 42). These differences are also apparent in CPR and [[LBR]]. The rates of progression to clinical pregnancy and live birth did not differ significantly by age group. Other factors observed to affect IR independently were anti-Müllerian hormone (AMH), day of embryo transfer, and embryo morphology. While selection of euploid embryos may be effective in overcoming a significant proportion of the age-related decline in reproductive efficiency, a decrease in IR, CPR, and [[LBR]] persists even when analyzing only euploid embryo transfers. The observed impact of aging is, therefore, independent of ploidy, as well as of other variables that affect reproductive efficiency. These results indicate that factors other than aneuploidy contribute to reproductive senescence.

|keywords=* Aneuploidy
* Pregestational genetic testing
* Reproductive aging
* Single embryo transfer
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7125286
}}
{{medline-entry
|title=The role of lamin B receptor in the regulation of senescence-associated secretory phenotype (SASP).
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32126237
|abstract=Cellular senescence is a phenomenon of irreversible growth arrest of mammalian somatic cells. Senescent cells increase the production of secretory proteins such as inflammatory cytokines, a phenomenon termed senescence-associated secretory phenotype (SASP). SASP is known to have profound effects on organismal health and aging; however, the molecular mechanisms of SASP are not precisely understood. In our previous studies, we have shown that senescent cells show decreased function of lamin B receptor ([[LBR]]), a nuclear membrane protein that regulates heterochromatin organization. Here we examined the implication of [[LBR]] in the regulation of SASP because senescent cells show altered heterochromatin organization, which would affect gene expression. We found that knock-down of [[LBR]] up-regulated the expression of the SASP factors such as IL-6, IL-8, and MMP1 in HeLa cells, even though cellular senescence was not induced by [[LBR]] knock-down. Conversely, enforced expression of [[LBR]] suppressed their up-regulated expression in senescent cells induced by excess thymidine. Further, our gene expression profile analysis also showed that many secretory proteins were up-regulated by [[LBR]] knock-down. We then analyzed the regulatory mechanisms of the expression of SASP factors by [[LBR]], and found that the promoters of these SASP factors associated with [[LBR]] in normally growing cells, but dissociated from it in senescent cells. Additionally, we found that enforced expression of [[LBR]] decreased the generation of cytoplasmic DNA, which could be involved in SASP, in senescent cells. These findings suggested that [[LBR]] would play crucial roles in the regulation of SASP.

|keywords=* Gene expression
* LBR
* SAHF
* SASP
* Senescence
|full-text-url=https://sci-hub.do/10.1016/j.yexcr.2020.111927
}}
==LMNA==

{{medline-entry
|title=The JAK1/2 inhibitor ruxolitinib delays premature aging phenotypes.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32196928
|abstract=Hutchinson-Gilford progeria syndrome (HGPS) is caused by an [[LMNA]] mutation that results in the production of the abnormal progerin protein. Children with HGPS display phenotypes of premature aging and have an average lifespan of 13 years. We found earlier that the targeting of the transmembrane protein PLA2R1 overcomes senescence and improves phenotypes in a mouse model of progeria. PLA2R1 is regulating the JAK/STAT signaling, but we do not yet know whether targeting this pathway directly would influence cellular and in vivo progeria phenotypes. Here, we show that JAK1/2 inhibition with ruxolitinib rescues progerin-induced cell cycle arrest, cellular senescence, and misshapen nuclei in human normal fibroblasts expressing progerin. Moreover, ruxolitinib administration reduces several premature aging phenotypes: bone fractures, bone mineral content, grip strength, and a trend to increase survival in a mouse model of progeria. Thus, we propose that ruxolitinib, an FDA-approved drug, should be further evaluated as a drug candidate in HGPS therapy.

|keywords=* JAK/STAT pathway
* cellular senescence
* progeria
* ruxolitinib
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189991
}}
==LOX==

{{medline-entry
|title=12-[[LOX]] catalyzes the oxidation of 2-arachidonoyl-lysolipids in platelets generating eicosanoid-lysolipids that are attenuated by iPLA γ knockout.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32161117
|abstract=The canonical pathway of eicosanoid production in most mammalian cells is initiated by phospholipase A -mediated release of arachidonic acid, followed by its enzymatic oxidation resulting in a vast array of eicosanoid products. However, recent work has demonstrated that the major phospholipase in mitochondria, iPLA γ (patatin-like phospholipase domain containing 8 (PNPLA8)), possesses [i]sn[/i]-1 specificity, with polyunsaturated fatty acids at the [i]sn[/i]-2 position generating polyunsaturated [i]sn[/i]-2-acyl lysophospholipids. Through strategic chemical derivatization, chiral chromatographic separation, and multistage tandem MS, here we first demonstrate that human platelet-type 12-lipoxygenase (12-[[LOX]]) can directly catalyze the regioselective and stereospecific oxidation of 2-arachidonoyl-lysophosphatidylcholine (2-AA-LPC) and 2-arachidonoyl-lysophosphatidylethanolamine (2-AA-LPE). Next, we identified these two eicosanoid-lysophospholipids in murine myocardium and in isolated platelets. Moreover, we observed robust increases in 2-AA-LPC, 2-AA-LPE, and their downstream 12-[[LOX]] oxidation products, 12([i]S[/i])-HETE-LPC and 12([i]S[/i])-HETE-LPE, in calcium ionophore (A23187)-stimulated murine platelets. Mechanistically, genetic ablation of iPLA γ markedly decreased the calcium-stimulated production of 2-AA-LPC, 2-AA-LPE, and 12-HETE-lysophospholipids in mouse platelets. Importantly, a potent and selective 12-[[LOX]] inhibitor, ML355, significantly inhibited the production of 12-HETE-LPC and 12-HETE-LPE in activated platelets. Furthermore, we found that aging is accompanied by significant changes in 12-HETE-LPC in murine serum that were also markedly attenuated by iPLA γ genetic ablation. Collectively, these results identify previously unknown iPLA γ-initiated signaling pathways mediated by direct 12-[[LOX]] oxidation of 2-AA-LPC and 2-AA-LPE. This oxidation generates previously unrecognized eicosanoid-lysophospholipids that may serve as biomarkers for age-related diseases and could potentially be used as targets in therapeutic interventions.

|keywords=* 2-arachidonoyl-lysophospholipids
* aging
* calcium
* eicosanoid
* iPLA2γ
* lysophospholipid
* myocardium
* platelet
* platelet-type 12-lipoxygenase (12-LOX)
* polyunsaturated fatty acids (PUFAs)
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7170522
}}
==LPA==

{{medline-entry
|title=Does sedentary time increase in older adults in the days following participation in intense exercise?
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32130714
|abstract=Older adults have the highest sedentary time across all age groups, and only a small portion is meeting the minimum recommendations for weekly physical activity. Little research to date has looked at how changes in one of these behaviours influences the other. To assess changes in 24-h movement behaviours (sedentary time, light intensity physical activity ([[LPA]]), moderate-vigorous PA (MVPA) and sleep) over three consecutive days, following acute bouts of exercise of varying intensity in older adults. Participants (n = 28, 69.7 ± 6.5 years) completed a maximal exercise test and the following exercise protocols in random order: moderate continuous exercise (MOD), high-intensity interval exercise (HI) and sprint interval exercise (SPRT). A thigh-worn device (ActivPAL™) was used to measure movement behaviours at baseline and the 3 days following each exercise session. Repeated measures analysis of variance indicated that compared to baseline, participants decreased MVPA in the 3 days following all exercise sessions and decreased [[LPA]] following HI and SPRT (p < 0.05). Over half of the sample had clinically meaningful increases in sedentary time (30 min/day) in the days following exercise participation. Older adults who compensate for exercise participation by reducing physical activity and increasing sedentary time in subsequent days may require behavioural counseling to ensure that incidental and recreational physical activities are not reduced. It appears that older adults compensate for acute exercise by decreasing MVPA and [[LPA]], and increasing sedentary time in the days following exercise. Future research is needed to determine whether compensation persists with regular engagement.
|mesh-terms=* Accelerometry
* Aged
* Exercise
* Exercise Test
* Humans
* Sedentary Behavior
* Sleep
|keywords=* Aging
* Compensation
* High intensity
* Movement behaviours
|full-text-url=https://sci-hub.do/10.1007/s40520-020-01502-6
}}
{{medline-entry
|title=Association of Long-term Exposure to Elevated Lipoprotein(a) Levels With Parental Life Span, Chronic Disease-Free Survival, and Mortality Risk: A Mendelian Randomization Analysis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32108890
|abstract=Elevated lipoprotein(a) (Lp[a]) levels are associated with atherosclerotic cardiovascular diseases. The association between high Lp(a) levels and human longevity phenotypes is, however, controversial. To examine whether genetically determined Lp(a) levels are associated with parental life span and chronic disease-free survival (health span) and the association between Lp(a) levels and long-term, all-cause mortality risk. In this genetic association study, cross-sectional mendelian randomization (UK Biobank [2006-2010] and LifeGen Consortium) and prospective analyses (European Prospective Investigation Into Cancer and Nutrition (EPIC)-Norfolk [1993-1997, with patients followed up to 2016]) were conducted using individual-level data on 139 362 participants. The association between a weighted genetic risk score of 26 independent single-nucleotide polymorphisms at the [[LPA]] locus on parental life span using individual participant data from the UK Biobank, as well as with summary statistics of a genome-wide association study of more than 1 million life spans (UK Biobank and LifeGen), were examined. The association between these single-nucleotide polymorphisms and the age at the end of the health span was tested using summary statistics of a previous genome-wide association study in the UK Biobank. The association between Lp(a) levels and all-cause mortality in the EPIC-Norfolk study was also investigated. Data were analyzed from December 2018 to December 2019. Genetically determined and measured Lp(a) levels. Parental life span, health span, and all-cause mortality. In 139 362 white British participants (mean [SD] age, 62.8 [3.9] years; 52% women) from the UK Biobank, increases in the genetic risk score (weighted for a 50-mg/dL increase in Lp[a] levels) were inversely associated with a high parental life span (odds ratio, 0.92; 95% CI, 0.89-0.94; P = 2.7 × 10-8). Using the Egger-mendelian randomization method, a negative association between [[LPA]] single-nucleotide polymorphisms and parental life span (mean [SD] Egger-mendelian randomization slope, -0.0019 [0.0002]; P = 2.22 × 10-18) and health span (-0.0019 [0.0003]; P = 3.00 × 10-13) was noted. In 18 720 participants from EPIC-Norfolk (5686 cases), the mortality risk for those with Lp(a) levels equal to or above the 95th percentile was equivalent to being 1.5 years older in chronologic age (β coefficient [SE], 0.194 [0.064]). The results of this study suggest a potential causal effect of absolute Lp(a) levels on human longevity as defined by parental life span, health span, and all-cause mortality. The results also provide a rationale for trials of Lp(a)-lowering therapy in individuals with high Lp(a) levels.
|mesh-terms=* Aged
* Case-Control Studies
* Cross-Sectional Studies
* Female
* Humans
* Lipoprotein(a)
* Longevity
* Male
* Mendelian Randomization Analysis
* Middle Aged
* Parents
* Phenotype
* Prospective Studies
* Risk Factors
|keywords=#f
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7049087
}}
==LPO==

{{medline-entry
|title=[Features of the changes in lipid peroxidation and activity of Na+/K+-ATPase in the brain of the aged rats in the conditions of two-vessel cerebral ischemia/reperfusion.]
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32160433
|abstract=The success of preclinical neuroprotection studies depends on the model used in animal research. The methodological approaches developed on young animals and widely used for modeling cerebral ischemia/reperfusion injury may not be so effective or not suitable for its modeling on senescent animals, which usage is recommended for preclinical trials. The aim of this study was to investigate the age-related features on the effect of brain reperfusion with different duration (1 and 3 h) after 2-vessel forebrain ischemia on the level of lipid peroxidation ([[LPO]]) products and on the activity of Na+/K+-ATPase in the cerebral cortex of rats aged 22-24 months. We found a later accumulation of [[LPO]] products (3 h instead of 1 h after blood recirculation), specifically triene conjugates and Schiff bases, and a decrease in the activity of Na+/K+-ATPase in the cerebral cortex of aged rats compared to young animals. The data obtained reveal the difference in the molecular and physiological mechanisms of the development of disorders in the brain during ischemia/reperfusion in aged and young animals. The revealed differences in these mechanisms should be consider in developing and testing compounds, which will be further used for the treatment of elderly patients with stroke and ischemic brain damage.
|mesh-terms=* Aging
* Animals
* Brain Ischemia
* Disease Models, Animal
* Lipid Peroxidation
* Rats
* Reperfusion Injury
* Sodium-Potassium-Exchanging ATPase
|keywords=* Na+/K+-ATPase
* aging
* brain
* lipid peroxidation
* oxidative stress
* stroke

}}
==LRP1==

{{medline-entry
|title=Drug Targeting of Plasminogen Activator Inhibitor-1 Inhibits Metabolic Dysfunction and Atherosclerosis in a Murine Model of Metabolic Syndrome.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32268785
|abstract=Enhanced expression of PAI-1 (plasminogen activator inhibitor-1) has been implicated in atherosclerosis formation in humans with obesity and metabolic syndrome. However, little is known about the effects of pharmacological targeting of PAI-1 on atherogenesis. This study examined the effects of pharmacological PAI-1 inhibition on atherosclerosis formation in a murine model of obesity and metabolic syndrome. Approach and Results: LDL receptor-deficient ([i]ldlr[/i] ) mice were fed a Western diet high in cholesterol, fat, and sucrose to induce obesity, metabolic dysfunction, and atherosclerosis. Western diet triggered significant upregulation of PAI-1 expression compared with normal diet controls. Addition of a pharmacological PAI-1 inhibitor (either PAI-039 or MDI-2268) to Western diet significantly inhibited obesity and atherosclerosis formation for up to 24 weeks without attenuating food consumption. Pharmacological PAI-1 inhibition significantly decreased macrophage accumulation and cell senescence in atherosclerotic plaques. Recombinant PAI-1 stimulated smooth muscle cell senescence, whereas a PAI-1 mutant defective in [[LRP1]] (LDL receptor-related protein 1) binding did not. The prosenescent effect of PAI-1 was blocked by PAI-039 and R2629, a specific anti-[[LRP1]] antibody. PAI-039 significantly decreased visceral adipose tissue inflammation, hyperglycemia, and hepatic triglyceride content without altering plasma lipid profiles. Pharmacological targeting of PAI-1 inhibits atherosclerosis in mice with obesity and metabolic syndrome, while inhibiting macrophage accumulation and cell senescence in atherosclerotic plaques, as well as obesity-associated metabolic dysfunction. PAI-1 induces senescence of smooth muscle cells in an [[LRP1]]-dependent manner. These results help to define the role of PAI-1 in atherosclerosis formation and suggest a new plasma-lipid-independent strategy for inhibiting atherogenesis.
|mesh-terms=* Animals
* Atherosclerosis
* Cellular Senescence
* Diet, Western
* Disease Models, Animal
* Indoleacetic Acids
* Macrophages
* Metabolic Syndrome
* Mice
* Mice, Knockout
* Obesity
* Plaque, Atherosclerotic
* Plasminogen Activator Inhibitor 1
* Receptors, LDL
|keywords=* atherosclerosis
* cellular senescence
* fibrinolysis
* metabolic syndrome
* muscle, smooth
* obesity
* plasminogen activator inhibitor-1
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7255962
}}
==LRP6==

{{medline-entry
|title=Low-density lipoprotein receptor-related protein 6-mediated signaling pathways and associated cardiovascular diseases: diagnostic and therapeutic opportunities.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32076828
|abstract=Low-density lipoprotein receptor-related protein 6 ([[LRP6]]) is a member of the low-density lipoprotein receptors (LDLRs) family and accumulating evidence points to the critical role of [[LRP6]] in cardiovascular health and homeostasis. In addition to presenting the well-appreciated roles in canonical signaling regulating blood pressure, blood glucose, lipid metabolism, atherosclerosis, cardiac valve disease, cardiac development, Alzheimer's disease and tumorigenesis, [[LRP6]] also inhibits non-canonical Wnt signals that promote arterial smooth muscle cell proliferation and vascular calcification. Noticeably, the role of [[LRP6]] is displayed in cardiometabolic disease, an increasingly important clinical burden with aging and obesity. The prospect for cardiovascular diseases treatment via targeting [[LRP6]]-mediated signaling pathways may improve central blood pressure and lipid metabolism, and reduce neointima formation and myocardial ischemia-reperfusion injury. Thus, a deep and comprehensive understanding of [[LRP6]] structure, function and signaling pathways will contribute to clinical diagnosis, therapy and new drug development for [[LRP6]]-related cardiovascular diseases.
|mesh-terms=* Aging
* Animals
* Cardiovascular Diseases
* Humans
* Low Density Lipoprotein Receptor-Related Protein-6
* Muscle, Smooth, Vascular
* Myocytes, Smooth Muscle
* Obesity
* Signal Transduction
* Structure-Activity Relationship
* Vascular Calcification
* Wnt Signaling Pathway
|keywords=#f
|full-text-url=https://sci-hub.do/10.1007/s00439-020-02124-8
}}
==LRRK2==

{{medline-entry
|title=Parkinson's disease-related Leucine-rich repeat kinase 2 modulates nuclear morphology and genomic stability in striatal projection neurons during aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32075681
|abstract=Multiple missense mutations in Leucine-rich repeat kinase 2 ([[LRRK2]]) are associated with familial forms of late onset Parkinson's disease (PD), the most common age-related movement disorder. The dysfunction of dopamine transmission contributes to PD-related motor symptoms. Interestingly, [[LRRK2]] is more abundant in the dopaminoceptive striatal spiny projection neurons (SPNs) compared to the dopamine-producing nigrostriatal dopaminergic neurons. Aging is the most important risk factor for PD and other neurodegenerative diseases. However, whether [[LRRK2]] modulates the aging of SPNs remains to be determined. We conducted RNA-sequencing (RNA-seq) analyses of striatal tissues isolated from Lrrk2 knockout (Lrrk2 ) and control (Lrrk2 ) mice at 2 and 12 months of age. We examined SPN nuclear DNA damage and epigenetic modifications; SPN nuclear, cell body and dendritic morphology; and the locomotion and motor skill learning of Lrrk2  and Lrrk2  mice from 2 to 24 months of age. Considering the strength of cell cultures for future mechanistic studies, we also performed preliminary studies in primary cultured SPNs derived from the Lrrk2  and Lrrk2  mice as well as the PD-related Lrrk2 G2019S and R1441C mutant mice. Lrrk2-deficiency accelerated nuclear hypertrophy and induced dendritic atrophy, soma hypertrophy and nuclear invagination in SPNs during aging. Additionally, increased nuclear DNA damage and abnormal histone methylations were also observed in aged Lrrk2  striatal neurons, together with alterations of molecular pathways involved in regulating neuronal excitability, genome stability and protein homeostasis. Furthermore, both the PD-related Lrrk2 G2019S mutant and [[LRRK2]] kinase inhibitors caused nuclear hypertrophy, while the Lrrk2 R1441C mutant and γ-Aminobutyric acid type A receptor (GABA-AR) inhibitors promoted nuclear invagination in the cultured SPNs. On the other hand, inhibition of neuron excitability prevented the formation of nuclear invagination in the cultured Lrrk2  and R1441C SPNs. Our findings support an important physiological function of [[LRRK2]] in maintaining nuclear structure integrity and genomic stability during the normal aging process, suggesting that PD-related [[LRRK2]] mutations may cause the deterioration of neuronal structures through accelerating the aging process.

|keywords=* And aging
* Dendritic hypotrophy
* Excitability
* G2019S
* GABAA
* LRRK2
* Nuclear DNA damage
* Nuclear hypertrophy
* Nuclear invagination
* Parkinson’s disease
* R1441C
* Striatal spiny projection neuron
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031993
}}
==MBP==

{{medline-entry
|title=Demyelination associated with chronic arsenic exposure in Wistar rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32171569
|abstract=Inorganic arsenic is among the major contaminants of groundwater in the world. Worldwide population-based studies demonstrate that chronic arsenic exposure is associated with poor cognitive performance among children and adults, while research in animal models confirms learning and memory deficits after arsenic exposure. The aim of this study was to investigate the long-term effects of environmentally relevant arsenic exposure in the myelination process of the prefrontal cortex (PFC) and corpus callosum (CC). A longitudinal study with repeated follow-up assessments was performed in male Wistar rats exposed to 3 ppm sodium arsenite in drinking water. Animals received the treatment from gestation until 2, 4, 6, or 12 months of postnatal age. The levels of myelin basic protein ([[MBP]]) were evaluated by immunohistochemistry/histology and immunoblotting from the PFC and CC. As plausible alterations associated with demyelination, we considered mitochondrial mass (VDAC) and two axonal damage markers: amyloid precursor protein (APP) level and phosphorylated neurofilaments. To analyze the microstructure of the CC in vivo, we acquired diffusion-weighted images at the same ages, from which we derived metrics using the tensor model. Significantly decreased levels of [[MBP]] were found in both regions together with significant increases of mitochondrial mass and slight axonal damage at 12 months in the PFC. Ultrastructural imaging demonstrated arsenic-associated decreases of white matter volume, water diffusion anisotropy, and increases in radial diffusivity. This study indicates that arsenic exposure is associated with a significant and persistent negative impact on microstructural features of white matter tracts.
|mesh-terms=* Aging
* Amyloid beta-Protein Precursor
* Animals
* Arsenic Poisoning
* Arsenites
* Axons
* Corpus Callosum
* Demyelinating Diseases
* Diffusion Tensor Imaging
* Drinking Water
* Immunohistochemistry
* Male
* Mitochondria
* Myelin Basic Protein
* Neurofilament Proteins
* Prefrontal Cortex
* Rats
* Rats, Wistar
* Sodium Compounds
* White Matter
|keywords=* Amyloid
* Anisotropy
* Arsenic
* Axonal damage
* DTI
* Demyelination
* Development
* MRI
* Microstructure
* Mitochondria
|full-text-url=https://sci-hub.do/10.1016/j.taap.2020.114955
}}
{{medline-entry
|title=Natural killer cells as participants in pathogenesis of rat experimental autoimmune encephalomyelitis (EAE): lessons from research on rats with distinct age and strain.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32140045
|abstract=Natural killer (NK) cells, influencing dendritic cell (DC)-mediated CD4+ lymphocyte priming in draining lymph nodes (dLNs) and controlling spinal cord (SC) infiltration with encephalitogenic CD4+T lymphocytes, modulate EAE (multiple sclerosis model). This study examined their putative contribution to age-related differences in EAE development in Dark Agouti (DA) (exhibiting age-related decrease in EAE susceptibility) and Albino Oxford (AO) (becoming susceptible to EAE with aging) rats. Aging increased NK cell number in dLNs from rats of both strains. In AO rats, but not in DA ones, it also increased the numbers of IFN-γ-producing NK cells (important for DC activation) and activated/matured DCs, thereby increasing activated/matured DC/conventional Foxp3-CD4+ cell ratio and activated CD25+Foxp3-CD4+ cell number. Aging in DA rats diminished activated/matured DC/conventional Foxp3-CD4+ cell ratio and activated Foxp3-CD4+ cell number. However, [[MBP]]-stimulated CD4+ cell proliferation did not differ in dLN cell cultures from young and aged AO rats (as more favorable activated/matured DC/Foxp3-CD4+ cell ratio was abrogated by lower intrinsic CD4+ cell proliferative capacity and a greater regulatory CD25+Foxp3+CD4+ lymphocyte frequency), but was lower in those from aged compared with young DA rats. At SC level, aging shifted Foxp3-CD4+/cytotoxic CX3CR1+ NK cell ratio towards the former in AO rats, so it was less favorable in aged AO rats exhibiting prolonged neurological deficit compared with their DA counterparts. The study showed strain and age differences in number of IFN-γ-producing NK cells in EAE rat dLNs, and suggested that their pathogenetic relevance depends on frequency and/or activity of other cells involved in CD4+ T cell (auto)immune response.

|keywords=* EAE
* NK cells
* aging
* dendritic cells
* strain differences
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7050050
}}
==MDH1==

{{medline-entry
|title=Oxidative Damage to the TCA Cycle Enzyme [[MDH1]] Dysregulates Bioenergetic Enzymatic Activity in the Aged Murine Brain.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32175745
|abstract=Aging can have profound effects on the mammalian brain leading to neurodegeneration and cognitive impairment. The brain has exceptionally high-energy requirements and is particularly susceptible to damage within its bioenergetic pathways. Here, we asked how the bioenergetic proteome of the murine brain changed with age and how this might affect brain function. Using label-free LC-MS/MS proteomics for the discovery phase and quantitative multiple reaction monitoring LC-MRM-MS/MS for the validation phase, we found dysregulated expression of multiple components of the tricarboxylic acid cycle, which is key for mitochondrial energy production, including SULA2, IDH1, IDH2, SDHB, PDHB, [[MDH1]], FH1, and NDUFS3, in old murine brains. We also saw that the oxidoreductases, thioredoxin and glutaredoxin, were significantly down-regulated in the old mouse brain and showed through MS that this correlated with the accumulation of trioxidation in the key metabolic enzyme [[MDH1]] at Cys137. 3D modeling of [[MDH1]] predicted that the damaged sites were located at the protein active zone, and enzymatic kinetic analysis confirmed that [[MDH1]] function was significantly reduced in the old mouse brain. These findings identify the tricarboxylic acid cycle as a key target of degenerative protein modifications with deleterious effects on the aging brain's bioenergetic function.

|keywords=* DPM
* MRM
* TCA cycle
* aging
* brain
|full-text-url=https://sci-hub.do/10.1021/acs.jproteome.9b00861
}}
==MET==

{{medline-entry
|title=Leisure-time physical activity volume, intensity, and duration from mid- to late-life in U.S. subpopulations by race and sex. The Atherosclerosis Risk In Communities (ARIC) Study.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32170049
|abstract=Mitigating age-related disease and disability presents challenges. Physical activity (PA) may be influential for prolonging health and functioning, warranting characterization of its patterns over the life course in population-based data. With the availability of up to three self-reported assessments of past year leisure-time PA (LTPA) over multiple decades in 15,036 participants (26% African American; 55% women; mean baseline age=54; median follow-up=23 years) from the Atherosclerosis Risk in Communities (ARIC) Study sampled from four U.S. communities, race-sex-stratified trajectories of average weekly intensity (metabolic equivalent of task ([[MET]])), duration (hours), and energy expenditure or volume ([[MET]]-h) of LTPA were developed from age 45 to 90 using joint models to accommodate expected non-ignorable attrition. Declines in weekly LTPA intensity, duration, and volume from age 70 to 90 were observed in white women (2.9 to 1.2 [[MET]]; 2.5 to 0.6 h; 11.1 to 2.6 [[MET]]-h), white men (2.5 to 1.0 [[MET]]; 3.5 to 1.8 h; 15.5 to 6.4 [[MET]]-h), African American women (2.5 to 2.4 [[MET]]; 0.8 to 0.1 h; 6.7 to 6.0 [[MET]]-h), and African American men (2.3 to 1.4 [[MET]]; 1.5 to 0.6 h; 8.0 to 2.3 [[MET]]-h). These data reveal population-wide shifts towards less active lifestyles in older adulthood.

|keywords=* exercise
* healthy aging
* physical activity
* retirement
* successful aging
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7093185
}}
==MMD==

{{medline-entry
|title=Impact and Lessons From the Lifestyle Interventions and Independence for Elders (LIFE) Clinical Trials of Physical Activity to Prevent Mobility Disability.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32105353
|abstract=Walking independently is basic to human functioning. The Lifestyle Interventions and Independence for Elders (LIFE) studies were developed to assess whether initiating physical activity could prevent major mobility disability ([[MMD]]) in sedentary older adults. We review the development and selected findings of the LIFE studies from 2000 through 2019, including the planning phase, the LIFE-Pilot Study, and the LIFE Study. The planning phase and the LIFE-Pilot provided key information for the successful implementation of the LIFE Study. The LIFE Study, involving 1635 participants randomized at eight sites throughout the United States, showed that compared with health education, the physical activity program reduced the risk of the primary outcome of [[MMD]] (inability to walk 400 m: hazard ratio = 0.82; 95% confidence interval = 0.69-0.98; P = .03), and that the intervention was cost-effective. There were no significant effects on cognitive outcomes, cardiovascular events, or serious fall injuries. In addition, the LIFE studies provided relevant findings on a broad range of other outcomes, including health, frailty, behavioral outcomes, biomarkers, and imaging. To date, the LIFE studies have generated a legacy of 109 peer-reviewed publications, 19 ancillary studies, and 38 independently funded grants and clinical trials, and advanced the development of 59 early career scientists. Data and biological samples of the LIFE Study are now publicly available from a repository sponsored by the National Institute on Aging (https://agingresearchbiobank.nia.nih.gov). The LIFE studies generated a wealth of important scientific findings and accelerated research in geriatrics and gerontology, benefiting the research community, trainees, clinicians, policy makers, and the general public. J Am Geriatr Soc 68:872-881, 2020.

|keywords=* aging
* mobility disability
* multicenter trialphysical activity
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7187344
}}
==MOS==

{{medline-entry
|title=Effect of mannan oligosaccharides on the microbiota and productivity parameters of Litopenaeus vannamei shrimp under intensive cultivation in Ecuador.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32066764
|abstract=The white leg Litopenaeus vannamei shrimp is of importance to the eastern Pacific fisheries and aquaculture industry but suffer from diseases such as the recently emerged early mortality syndrome. Many bacterial pathogens have been identified but the L. vannamei microbiota is still poorly known. Using a next-generation sequencing (NGS) approach, this work evaluated the impact of the inclusion in the diet of mannan oligosaccharide, ([[MOS]], 0.5% w/w), over the L. vannamei microbiota and production behavior of L. vannamei under intensive cultivation in Ecuador. The [[MOS]] supplementation lasted for 60 days, after which the shrimp in the ponds were harvested, and the production data were collected. [[MOS]] improved productivity outcomes by increasing shrimp survival by 30%. NGS revealed quantitative differences in the shrimp microbiota between [[MOS]] and control conditions. In the treatment with inclusion of dietary [[MOS]], the predominant phylum was Actinobacteria (28%); while the control group was dominated by the phylum Proteobacteria (30%). [[MOS]] has also been linked to an increased prevalence of Lactococcus- and Verrucomicrobiaceae-like bacteria. Furthermore, under the treatment of [[MOS]], the prevalence of potential opportunistic pathogens, like Vibrio, Aeromonas, Bergeyella and Shewanella, was negligible. This may be attributable to [[MOS]] blocking the adhesion of pathogens to the surfaces of the host tissues. Together, these findings point to the fact that the performance (survival) improvements of the dietary [[MOS]] may be linked to the impact on the microbiota, since bacterial lines with pathogenic potential towards shrimps were excluded in the gut.
|mesh-terms=* Actinobacteria
* Aeromonas
* Animal Feed
* Animals
* Aquaculture
* Bacterial Adhesion
* Ecuador
* Flavobacteriaceae
* Lactococcus
* Longevity
* Mannans
* Microbiota
* Oligosaccharides
* Penaeidae
* Proteobacteria
* Seafood
* Shewanella
* Verrucomicrobia
* Vibrio
|keywords=#f
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7026423
}}
==MPHOSPH6==

{{medline-entry
|title=Genome-wide Association Analysis in Humans Links Nucleotide Metabolism to Leukocyte Telomere Length.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109421
|abstract=Leukocyte telomere length (LTL) is a heritable biomarker of genomic aging. In this study, we perform a genome-wide meta-analysis of LTL by pooling densely genotyped and imputed association results across large-scale European-descent studies including up to 78,592 individuals. We identify 49 genomic regions at a false dicovery rate (FDR) < 0.05 threshold and prioritize genes at 31, with five highlighting nucleotide metabolism as an important regulator of LTL. We report six genome-wide significant loci in or near SENP7, MOB1B, CARMIL1, PRRC2A, TERF2, and RFWD3, and our results support recently identified PARP1, POT1, ATM, and [[MPHOSPH6]] loci. Phenome-wide analyses in >350,000 UK Biobank participants suggest that genetically shorter telomere length increases the risk of hypothyroidism and decreases the risk of thyroid cancer, lymphoma, and a range of proliferative conditions. Our results replicate previously reported associations with increased risk of coronary artery disease and lower risk for multiple cancer types. Our findings substantially expand current knowledge on genes that regulate LTL and their impact on human health and disease.
|mesh-terms=* Genome-Wide Association Study
* Humans
* Leukocytes
* Nucleotides
* Telomere
|keywords=* Mendelian randomisation
* age-related disease
* biological aging
* telomere length
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7058826
}}
==MPI==

{{medline-entry
|title=Age-related decline of lymphatic drainage from the eye: A noninvasive in vivo photoacoustic tomography study.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32251650
|abstract=We aim to determine whether lymphatic drainage from the eye changes with age. Using quantitative photoacoustic tomography, groups of young and older mice were studied in the live state. 10 CD-1 mice of 2-3 months (5M/5F) were studied in addition to 13 older mice of 12-13 months (6M/7F). In each of 23 mice, near-infrared tracer (a near-infrared dye, QC-1 conjugated with Bovine Serum Albumin) was injected into the right eye, and imaging of ipsilateral cervical lymph nodes was performed with laser pulses at 11 different wavelengths prior to and 20 min, 2, 4 and 6 h after injection. Mean pixel intensities ([[MPI]]s) of nodes were calculated at each imaging session. The areas under the curves (AUC) were calculated for both groups of mice and compared using the t-test. The slopes of [[MPI]] of each region of interest were compared using the linear mixed model before and after adjusting for sex, body weight and intraocular pressure of the right eye. The mean intraocular pressure of right eyes before injection was similar in older and younger groups (12.77 ± 2.01 mmHg and 12.90 ± 2.38 mmHg, respectively; p = 0.888). In each mouse, the photoacoustic signal was detected in the right cervical lymph nodes at the 2-h time point following tracer injection into the right eye. At the 4 and 6 h imaging times, a steady increase of tracer signal was observed. Areas under the curve in the right cervical nodes were decreased significantly in older mice compared to younger mice (p = 0.007). The slopes of [[MPI]] in the nodes were significantly decreased in old mice compared to young mice both before and after adjusting for sex, body weight and intraocular pressure of the right eye (p = 0.003). In conclusion, lymphatic drainage from the eye is significantly reduced in older eyes. This finding suggests that impaired lymphatic clearance of aqueous humor, proteins and antigens from the eye may contribute to age-related disease of the eye such as glaucoma and inflammatory eye disease.

|keywords=* Age-related
* Aging
* Aqueous humor
* Drainage
* Eye
* Glaucoma
* Imaging
* In vivo
* Lymph node
* Lymphatic
* Mice
* Photoacoustic tomography
* Uveoscleral
|full-text-url=https://sci-hub.do/10.1016/j.exer.2020.108029
}}
==MSC==

{{medline-entry
|title=Human Obesity Induces Dysfunction and Early Senescence in Adipose Tissue-Derived Mesenchymal Stromal/Stem Cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32274385
|abstract=Chronic inflammatory conditions like obesity may adversely impact the biological functions underlying the regenerative potential of mesenchymal stromal/stem cells ([[MSC]]). Obesity can impair [[MSC]] function by inducing cellular senescence, a growth-arrest program that transitions cells to a pro-inflammatory state. However, the effect of obesity on adipose tissue-derived [[MSC]] in human subjects remains unclear. We tested the hypothesis that obesity induces senescence and dysfunction in human [[MSC]]. [[MSC]] were harvested from abdominal subcutaneous fat collected from obese and age-matched non-obese subjects ([i]n[/i] = 40) during bariatric or kidney donation surgeries, respectively. [[MSC]] were characterized, their migration and proliferation assessed, and cellular senescence evaluated by gene expression of cell-cycle arrest and senescence-associated secretory phenotype markers. [i]In vitro[/i] studies tested [[MSC]] effect on injured human umbilical vein endothelial cells (HUVEC) function. Mean age was 59 ± 8 years, 66% were females. Obese subjects had higher body-mass index (BMI) than non-obese. [[MSC]] from obese subjects exhibited lower proliferative capacities than non-obese-[[MSC]], suggesting decreased function, whereas their migration remained unchanged. Senescent cell burden and phenotype, manifested as [i]p16[/i], [i]p53[/i], [i]IL-6[/i], and [i]MCP-1[/i] gene expression, were significantly upregulated in obese subjects' [[MSC]]. BMI correlated directly with expression of [i]p16[/i], [i]p21[/i], and [i]IL-6[/i]. Furthermore, co-incubation with non-obese, but not with obese-[[MSC]], restored VEGF expression and tube formation that were blunted in injured HUVEC. Human obesity triggers an early senescence program in adipose tissue-derived [[MSC]]. Thus, obesity-induced cellular injury may alter efficacy of this endogenous repair system and hamper the feasibility of autologous transplantation in obese individuals.

|keywords=* adipose tissue
* cellular dysfunction
* cellular senescence
* mesenchymal stem cells
* obesity
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7113401
}}
{{medline-entry
|title=miR-155-5p inhibition rejuvenates aged mesenchymal stem cells and enhances cardioprotection following infarction.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32196916
|abstract=Aging impairs the functions of human mesenchymal stem cells ([[MSC]]s), thereby severely reducing their beneficial effects on myocardial infarction (MI). MicroRNAs (miRNAs) play crucial roles in regulating the senescence of [[MSC]]s; however, the underlying mechanisms remain unclear. Here, we investigated the significance of miR-155-5p in regulating [[MSC]] senescence and whether inhibition of miR-155-5p could rejuvenate aged [[MSC]]s (A[[MSC]]s) to enhance their therapeutic efficacy for MI. Young [[MSC]]s (Y[[MSC]]s) and A[[MSC]]s were isolated from young and aged donors, respectively. The cellular senescence of [[MSC]]s was evaluated by senescence-associated β-galactosidase (SA-β-gal) staining. Compared with Y[[MSC]]s, A[[MSC]]s exhibited increased cellular senescence as evidenced by increased SA-β-gal activity and decreased proliferative capacity and paracrine effects. The expression of miR-155-5p was much higher in both serum and [[MSC]]s from aged donors than young donors. Upregulation of miR-155-5p in Y[[MSC]]s led to increased cellular senescence, whereas downregulation of miR-155-5p decreased A[[MSC]] senescence. Mechanistically, miR-155-5p inhibited mitochondrial fission and increased mitochondrial fusion in [[MSC]]s via the AMPK signaling pathway, thereby resulting in cellular senescence by repressing the expression of Cab39. These effects were partially reversed by treatment with AMPK activator or mitofusin2-specific siRNA (Mfn2-siRNA). By enhancing angiogenesis and promoting cell survival, transplantation of anti-miR-155-5p-A[[MSC]]s led to improved cardiac function in an aged mouse model of MI compared with transplantation of A[[MSC]]s. In summary, our study shows that miR-155-5p mediates [[MSC]] senescence by regulating the Cab39/AMPK signaling pathway and miR-155-5p is a novel target to rejuvenate A[[MSC]]s and enhance their cardioprotective effects.

|keywords=* mesenchymal stem cells
* miR-155-5p
* myocardial infarction
* rejuvenation
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189985
}}
{{medline-entry
|title=Mesenchymal Stem Cell Derived Extracellular Vesicles in Aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32154253
|abstract=Aging is associated with high prevalence of chronic degenerative diseases that take a large part of the increasing burden of morbidities in a growing demographic of elderly people. Aging is a complex process that involves cell autonomous and cell non-autonomous mechanisms where senescence plays an important role. Senescence is characterized by the loss of proliferative potential, resistance to cell death by apoptosis and expression of a senescence-associated secretory phenotype (SASP). SASP includes pro-inflammatory cytokines and chemokines, tissue-damaging proteases, growth factors; all contributing to tissue microenvironment alteration and loss of tissue homeostasis. Emerging evidence suggests that the changes in the number and composition of extracellular vesicles (EVs) released by senescent cells contribute to the adverse effects of senescence in aging. In addition, age-related alterations in mesenchymal stem/stromal cells ([[MSC]]s) have been associated to dysregulated functions. The loss of functional stem cells necessary to maintain tissue homeostasis likely directly contributes to aging. In this review, we will focus on the characteristics and role of EVs isolated from senescent [[MSC]]s, the potential effect of [[MSC]]-derived EVs in aging and discuss their therapeutic potential to improve age-related diseases.

|keywords=* aging
* clinical translation
* extracellular vesicles
* mesenchymal stem cells
* regenerative medicine
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7047768
}}
{{medline-entry
|title=Molecular Mechanisms Contributing to Mesenchymal Stromal Cell Aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32098040
|abstract=Mesenchymal stem/stromal cells ([[MSC]]s) are a reservoir for tissue homeostasis and repair that age during organismal aging. Beside the fundamental in vivo role of [[MSC]]s, they have also emerged in the last years as extremely promising therapeutic agents for a wide variety of clinical conditions. [[MSC]] use frequently requires in vitro expansion, thus exposing cells to replicative senescence. Aging of [[MSC]]s (both in vivo and in vitro) can affect not only their replicative potential, but also their properties, like immunomodulation and secretory profile, thus possibly compromising their therapeutic effect. It is therefore of critical importance to unveil the underlying mechanisms of [[MSC]] senescence and to define shared methods to assess [[MSC]] aging status. The present review will focus on current scientific knowledge about [[MSC]] aging mechanisms, control and effects, including possible anti-aging treatments.

|keywords=* MSC senescence
* in vitro aging
* in vivo aging
* mesenchymal stem/stromal cells (MSC)
* rejuvenating strategies
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072652
}}
{{medline-entry
|title=Inhibition of DNA Methyltransferase by RG108 Promotes Pluripotency-Related Character of Porcine Bone Marrow Mesenchymal Stem Cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32125888
|abstract=Mesenchymal stem/stromal cells ([[MSC]]s) have been identified in almost all adult human tissues and been used in numerous clinical trials for a variety of diseases. Studies have shown that [[MSC]]s would undergo cellular senescence when cultured over a long term, which is brought on by increased epigenetic modifications, including DNA methylation. However, the mechanism of [[MSC]]s senescence is not well studied. In this study, the effects of RG108, a DNA methyltransferase inhibitor (DNMTi), on senescence, apoptosis, and pluripotency gene expressions in porcine bone marrow (pBM)-[[MSC]]s were investigated. First, we determined the optimized dose and time of RG108 treatment in pBM-[[MSC]]s to be 10 μM for 48 hours, respectively. Under these conditions, the pluripotency genes ([i]NANOG[/i], [i]POU5F1[/i]), the anti-senescence genes ([i]TERT[/i], [i]bFGF[/i]), and the anti-apoptosis gene ([i]BCL2[/i]) were increased, whereas the apoptotic gene ([i]BAX[/i]) was decreased. RG108 protected against apoptosis when pBM-[[MSC]] induces apoptosis with H O  for 1.5 hours. We also found that RG108 significantly induced the expression of [i]NANOG[/i] and [i]POU5F1[/i] by decreasing DNA methylation in gene promoter regions. These results indicate that an optimized dose of RG108 may promote the pluripotency-related character of pBM-[[MSC]]s through improving cellular anti-senescence, anti-apoptosis, and pluripotency, which provide a better cell origin for stem cell therapy.

|keywords=* RG108
* apoptosis
* pluripotency
* porcine bone marrow mesenchymal stem cells
* senescence
|full-text-url=https://sci-hub.do/10.1089/cell.2019.0060
}}
{{medline-entry
|title=Extracellular Vesicles of Stem Cells to Prevent BRONJ.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32119600
|abstract=Extracellular vesicles (EVs), several tens to hundreds of nanometers in size, are vesicles secreted by cells for intercellular communication. EVs released from mesenchymal stem cells ([[MSC]]-EVs) have the potential to treat multiple diseases. This study aimed to determine the effects of [[MSC]]-EVs on bisphosphonate-related osteonecrosis of the jaw (BRONJ), whose pathogenesis and treatment are not yet established. To this end, zoledronic acid (ZOL) was administered to bone marrow cells and fibroblasts in vitro. In vivo, a BRONJ model was produced by administering ZOL to rats and extracting teeth. Each [[MSC]]-EV-treated and nontreated group was compared histologically and molecularly. In vitro, the nontreated group showed an increased number of β-galactosidase-positive cells and expression of senescence-associated genes [i]p21, pRB[/i] and senescence-related inflammatory cytokines. Conversely, [[MSC]]-EV administration decreased the number of senescent cells and expression levels of [i]p21, pRB[/i] and inflammatory cytokines. In vivo, in the nontreated group, the socket was partially uncovered by the oral epithelium, leaving an exposed bone. Conversely, in the [[MSC]]-EV-treated group, the socket was healed. Besides, in the nontreated group, β-galactosidase-positive cells existed in the socket and colocalized with the CD90 and periostin-positive cells. However, there were few β-galactosidase-positive cells in the [[MSC]]-EV-treated group. Furthermore, gene expression of stem cell markers [i]Bmi1[/i] and [i]Hmga2[/i] and the vascular endothelial marker [i]VEGF[/i] was significantly increased in the [[MSC]]-EV-treated group, compared with that in the nontreated group. These results indicate that [[MSC]]-EVs prevent ZOL-induced senescence in stem cells, osteoblasts, and fibroblasts and reduce inflammatory cytokines. Furthermore, administration of [[MSC]]-EVs prevented senescence of cells involved in wound healing and the spread of chronic inflammation around senescent cells, thereby promoting angiogenesis and bone regeneration and preventing BRONJ.

|keywords=* bisphosphonate-associated osteonecrosis of the jaw
* cellular senescence
* exosomes
* mesenchymal stem cells
* wound healing
* zoledronic acid
|full-text-url=https://sci-hub.do/10.1177/0022034520906793
}}
==MTOR==

{{medline-entry
|title=The roles of [[MTOR]] and miRNAs in endothelial cell senescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32246301
|abstract=Accumulation of senescent cells in vascular endothelium is known to contribute to vascular aging and increases the risk of developing cardiovascular diseases. The involvement of classical pathways such as p53/p21 and p16/pRB in cellular senescence are well described but there are emerging evidence supporting the increasingly important role of mammalian target of rapamycin ([[MTOR]]) as driver of cellular senescence via these pathways or other effector molecules. MicroRNAs (miRNAs) are a highly conserved group of small non-coding RNAs (18-25 nucleotides), instrumental in modulating the expression of target genes associated with various biological and cellular processes including cellular senescence. The inhibition of [[MTOR]] activity is predominantly linked to cellular senescence blunting and prolonged lifespan in model organisms. To date, known miRNAs regulating [[MTOR]] in endothelial cell senescence remain limited. Herein, this review discusses the roles of [[MTOR]] and [[MTOR]]-associated miRNAs in regulating endothelial cell senescence, including the crosstalk between [[MTOR]] Complex 1 ([[MTOR]]C1) and cell cycle pathways and the emerging role of [[MTOR]]C2 in cellular senescence. New insights on how [[MTOR]] and miRNAs coordinate underlying molecular mechanisms of endothelial senescence will provide deeper understanding and clarity to the complexity of the regulation of cellular senescence.

|keywords=* Endothelium
* MTOR
* MicroRNAs
* Senescence
* Vascular aging
|full-text-url=https://sci-hub.do/10.1007/s10522-020-09876-w
}}
==MTR==

{{medline-entry
|title=Amide proton transfer-weighted magnetic resonance imaging of human brain aging at 3 Tesla.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32269932
|abstract=Amide proton transfer-weighted (APTw) imaging has been revealed to hold great potential in the diagnosis of several brain diseases. The purpose of this proof-of-concept study was to evaluate the feasibility and value of APTw magnetic resonance imaging (MRI) in characterizing normal brain aging. A total of 106 healthy subjects were recruited and scanned at 3.0 Tesla, with APTw and conventional magnetization transfer (MT) sequences. Quantitative image analyses were performed in 12 regions of interest (ROIs) for each subject. The APTw or MT ratio ([[MTR]]) signal differences among five age groups (young, mature, middle-aged, young-old, and middle-old) were assessed using the one-way analysis of variance, with the Benjamini-Hochberg correction for multiple comparisons. The relationship between APTw and [[MTR]] signals and the age dependencies of APTw and [[MTR]] signals were assessed using the Pearson correlation and non-linear regression. There were no significant differences between the APTw or [[MTR]] values for males and females in any of the 12 ROIs analyzed. Among the five age groups, there were significant differences in the three white matter regions in the temporal, occipital, and frontal lobes. Overall, the mean APTw values in the older group were higher than those in the younger group. Positive correlations were observed in relation to age in most brain regions, including four with significant positive correlations (r=0.2065-0.4182) and five with increasing trends. As a comparison, the mean [[MTR]] values did not appear to be significantly different among the five age groups. In addition, the mean APTw and [[MTR]] values revealed significant positive correlations in 10 ROIs (r=0.2214-0.7269) and a significant negative correlation in one ROI (entorhinal cortex, r=-0.2141). Our early results show that the APTw signal can be used as a promising and complementary imaging biomarker with which normal brain aging can be evaluated at the molecular level.

|keywords=* Aging
* amide proton transfer imaging
* biomarkers
* chemical exchange saturation transfer (CEST)
* molecular imaging
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7136735
}}
==NLRP3==

{{medline-entry
|title=Ginsenoside Rg1 ameliorates glomerular fibrosis during kidney aging by inhibiting NOX4 and [[NLRP3]] inflammasome activation in SAMP8 mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32114413
|abstract=Aging is closely related to the progress of renal fibrosis, which eventually results in renal dysfunction. Ginsenoside Rg1 (Rg1) has been reported to have an extensive anti-aging effect. However, the role and mechanism of Rg1 in aging-related renal fibrosis remain unclear. The present study aimed to evaluate the protective effect and mechanism of Rg1 in renal fibrosis during kidney aging in a model of SAMP8 mice. Taking SAMR1 mice as the control group, SAMP8 mice were administered Apocynin (50 mg/kg), Tempol (50 mg/kg), or Rg1 (5, 10 mg/kg) intragastrically for 9 weeks as treatment groups. The results showed that the elevated levels of blood urea nitrogen, serum creatinine and senescence-associated β-galactosidase (β-Gal) were markedly decreased, the glomerular mesangial proliferation was significantly alleviated and the increased levels of collagen IV and TGF-β1 were significantly downregulated by Rg1 in SAMP8 mice. In addition, the generation of ROS and the expression of NADHP oxidase 4 (NOX4) in the renal cortex were significantly reduced by Rg1 treatment. The expression levels of [[NLRP3]] inflammasome-related proteins and the inflammation-related cytokine IL-1β were also inhibited by Rg1 treatment in the SAMP8 mice. These results suggested that Rg1 could delay kidney aging and inhibit aging-related glomerular fibrosis by reducing NOX4-derived ROS generation and downregulating [[NLRP3]] inflammasome expression.

|keywords=* Ginsenoside Rg1
* Kidney aging
* NADPH oxidase 4 (NOX4)
* NLRP3 inflammasome
* Renal fibrosis
|full-text-url=https://sci-hub.do/10.1016/j.intimp.2020.106339
}}
==PC==

{{medline-entry
|title=Pacing During 200-m Competitive Masters Swimming.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32271289
|abstract=Breen, D, Powell, C, and Anderson, R. Pacing during 200-m competitive masters swimming. J Strength Cond Res 34(7): 1903-1910, 2020-Pacing strategies are key to overall performance outcome, particularly in swimming given the large resistive properties of water. However, no studies examining how swimming stroke, gender, age, or performance level affect pacing strategies during 200-m races. This study aimed to examine masters athletes pacing strategies categorized by stroke, gender, age, and performance level. Data were retrieved from World and European masters swimming championships and contained data for 4,272 performances. Performances were coded for stroke, gender, age, and performance classification ([[PC]]). Performance classification was based on comparison to the appropriate masters world record. Performances were then normalized, with split times being expressed as a percentage faster or slower than average 50-m split time to determine relative pace. Coefficient of variation (CV) of 50-m time was examined across splits. The main effect for stroke was examined at each split, whereas gender, age, and [[PC]] were examined for split-1 pace and CV. An alpha level of 0.05 was set to denote statistical significance. A main effect for stroke was identified at each split (all p < 0.001; (Equation is included in full-text article.)-split-1 = 0.292; (Equation is included in full-text article.)-split-2 = 0.040; (Equation is included in full-text article.)-split-3 = 0.058; (Equation is included in full-text article.)-split-4 = 0.162). A main effect for [[PC]] was identified for split-1 pace and CV within all strokes (all p < 0.001), except for breaststroke (both p > 0.775). Masters athletes exhibit different pacing patterns across strokes, whereas lower ranked athletes also display less even pacing and a faster relative start compared with higher-ranked athletes. Individual analyses of pacing strategies may be necessary.
|mesh-terms=* Adult
* Age Factors
* Aged
* Aged, 80 and over
* Aging
* Athletes
* Athletic Performance
* Competitive Behavior
* Female
* Humans
* Male
* Middle Aged
* Sex Factors
* Swimming
|keywords=#f
|full-text-url=https://sci-hub.do/10.1519/JSC.0000000000003621
}}
{{medline-entry
|title=Prostate cancer in Pennsylvania: The role of older age at diagnosis, aggressiveness, and environmental risk factors on treatment and mortality using data from the Pennsylvania Cancer Registry.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32212232
|abstract=To assess: (a) cancer treatment in prostate cancer survivors ([[PC]]S) by age at diagnosis (ADx) and prostate cancer ([[PC]]) aggressiveness; (b) potential impact on [[PC]] mortality; and (c) these results in the context of environmental/behavioral risk factors on [[PC]]S in Pennsylvania. Prostate cancer survivors ages ≥40 years were identified from the 2004-2014 Pennsylvania Cancer Registry ([[PC]]R). Demographic/clinical descriptors and [[PC]] treatment were extracted from [[PC]]R. Prostate cancer aggressiveness was defined by clinical/pathologic Gleason score and tumor stage. Logistic and Cox regression analyses tested associations between treatment received and [[PC]]-specific mortality. County-level data from the Pennsylvania BRFSS were used to estimate cancer-related behavioral risk factors (eg, smoking, physical inactivity, fruit/vegetable consumption [FV], alcohol use) and used as covariates. There were 90 694 [[PC]]S ages 40-105 years (mean age = 66.19 years, SD = 9.25) included. Most were non-Hispanic white men (83%). Prostate cancer survivors ≥75 years were least likely to receive any treatment but men ages 65-74 were more likely to receive combined therapies (OR = 1.47; 95% CI 1.28, 1.69) vs [[PC]]S ages 40-54 years, controlling for covariates. Prostate cancer survivors 55-75+ with aggressive [[PC]] who received any treatment vs no definitive treatment had significantly reduced mortality. Men from counties with high obesity and smoking rates were significantly less likely to receive any treatment than men living in counties with lower rates of these risk factors. Prostate cancer survivors who lived in counties with high rates of physical inactivity and had high rates of sufficient FV consumption were slightly more likely to receive cancer treatment vs no definitive treatment compared to men who lived in counties with high rates of physical activity and lower FV consumption. We observed a general age-related decline in receipt of treatment. Prostate cancer survivors ages ≥75 years were significantly less likely to get any cancer treatment compared to younger [[PC]]S. However, most men with more aggressive disease who received any treatment had greatly reduced [[PC]] mortality, regardless of age. Considering environmental/behavioral risk factors may attenuate [[PC]] risk and inform treatment options.

|keywords=* aging
* behavioral risk factors
* geriatric oncology
* healthy aging
* prostate cancer survivorship
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7221418
}}
==PCNA==

{{medline-entry
|title=[Mechanosensitive protein of Hippo regulatory pathway - transcription coactivator with PZD-binding motif (TAZ) in human skin during aging.]
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32145162
|abstract=The aim of this work was to examine the content of transcription coactivator with PZD-binding motif (TAZ) in fibroblasts and blood vessels of human dermis from the development until deep aging (from 20 weeks of pregnancy until 85 years old), and defining of a role of TAZ in age-dependent changes in the number of fibroblasts and blood vessels in the dermis. TAZ, proliferating cells nuclear antigen ([[PCNA]]), endothelial cells marker CD31 were detected with indirect immunohistochemical technique. Results showed that portion of fibroblasts with positive staining for TAZ in the dermis is decreased from 20 weeks of pregnancy to 40 years old. Percent of TAZ positive fibroblasts in dermis is increased since 41 years old until 60-85 years old group. The content of TAZ in blood vessels in the human dermis is decreased sufficiently from 20 weeks of pregnancy until 40 years old followed by an increase from 41 years old. From 61 to 85 years of life, content of TAZ in dermal vessels was not differ from those in 41-60 age group. Age-related changes in the content of TAZ in fibroblasts and blood vessels is not associated with an age-related decrease in total number and percent of [[PCNA]] positive fibroblasts, the number of blood vessels in the dermis.
|mesh-terms=* Adolescent
* Adult
* Aged
* Aged, 80 and over
* Aging
* Child
* Child, Preschool
* Dermis
* Female
* Fibroblasts
* Humans
* Infant
* Infant, Newborn
* Middle Aged
* Pregnancy
* Protein-Serine-Threonine Kinases
* Skin Aging
* Trans-Activators
* Young Adult
|keywords=* CD31
* PCNA
* TAZ
* aging
* blood vessels
* fibroblasts
* skin

}}
==PGC==

{{medline-entry
|title=[Metabolic Alteration in Aging Process: Metabolic Remodeling in White Adipose Tissue by Caloric Restriction].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115557
|abstract=Caloric restriction (CR) improves whole-body metabolism, suppresses various age-related pathophysiological changes, and extends lifespan. The beneficial actions of CR are regulated in growth hormone (GH)/insulin-like growth factor-1 (IGF-1) signal-dependent and -independent manners. To clarify the GH/IGF-1-independent mechanism, we compared gene expression profiles in white adipose tissue (WAT) between CR and GH/IGF-1 suppression, and found that CR upregulated sterol regulatory element-binding protein 1c (SREBP-1c) regulatory gene expression. To validate the impact of SREBP-1c as a beneficial mediator of CR, we compared the responses to CR between wild-type and SREBP-1c knockout (KO) mice. CR extended lifespan, upregulated gene expression involved in FA biosynthesis, activated mitochondrial biogenesis, and suppressed oxidative stress predominantly in WAT. In contrast, most of these findings were not observed in KO mice. Furthermore, SREBP-1c was implicated in CR-associated mitochondrial activation through upregulation of peroxisome proliferator-activated receptor γ coactivator-1α ([[PGC]]-1α), a master regulator of mitochondrial biogenesis. Sirtuin-3 (SIRT3) regulates mitochondrial quality and is also involved in the beneficial actions of CR. We observed that CR upregulated the mature form of SIRT3 protein and mitochondrial intermediate peptidase (MIPEP), a mitochondrial signal peptidase (MtSPase), in WAT. MIPEP cleaved precursor form of SIRT3 to mature form, and activated certain mitochondrial matrix proteins, suggesting that MIPEP might contribute to maintenance of mitochondrial quality during CR via SIRT3 activation. Taken together, CR induces SREBP-1c-dependent metabolic remodeling, including enhancement of FA biosynthesis and mitochondrial activation, via [[PGC]]-1α, and improvement of mitochondria quality via Mipep in WAT, resulting in beneficial actions.
|mesh-terms=* Adipose Tissue, White
* Aging
* Animals
* Caloric Restriction
* Gene Expression
* Humans
* Longevity
* Mice
* Organelle Biogenesis
* Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
* Sirtuin 3
* Sterol Regulatory Element Binding Protein 1
* Up-Regulation
|keywords=* caloric restriction (CR)
* fatty acid biosynthesis
* mitochondria
* white adipose tissue (WAT)
|full-text-url=https://sci-hub.do/10.1248/yakushi.19-00193-2
}}
{{medline-entry
|title=Kynurenine aminotransferase isoforms display fiber-type specific expression in young and old human skeletal muscle.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32068089
|abstract=Conversion of kynurenine (KYN) to kynurenic acid (KYNA) is the main pathway for free tryptophan degradation in skeletal muscle and has emerged as an important mechanism of how exercise is linked to promotion of mental health. Metabolism of KYN to KYNA mainly depends on the expression of kynurenine aminotransferases (KATs) that is under control of the mitochondria biogenesis regulator [[PGC]]-1α. We therefore hypothesized that expression of KATs would vary between muscle fibers that differ in mitochondrial content, i.e. oxidative type I vs more glycolytic type II muscle fibers. Moreover, we tested the hypothesis that KAT expression differs with age. Single muscle fibers were isolated from biopsies taken from the vastus lateralis muscle in young and old healthy subjects. In young and old subjects the abundance of KAT I, KAT III and KAT IV was greater in Type I than Type II fibers without age-dependent difference in the KAT isoform expressions. The link to mitochondrial content was further seen as the expression of KAT IV correlated to mitochondrial cytochrome c oxidase IV (COX IV) abundance in both fiber types. In conclusion, we describe for the first time the expression pattern of KAT isoforms with respect to specific fiber types and age in human skeletal muscle.

|keywords=* Aging
* Kynurenine aminotransferases
* Mitochondria
* Muscle fiber-type
* Skeletal muscle
|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110880
}}
==PINK1==

{{medline-entry
|title=Compression-induced senescence of nucleus pulposus cells by promoting mitophagy activation via the [[PINK1]]/PARKIN pathway.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32281308
|abstract=The current research aimed to explore the possible relationship between [[PINK1]]/PARKIN-mediated mitophagy and the compression-induced senescence of nucleus pulposus cells (NPCs). Therefore, the stages of senescence in NPCs were measured under compression lasting 0, 24 and 48 hours. The mitophagy-related markers, autophagosomes and mitochondrial membrane potential were tested to determine the levels of [[PINK1]]/PARKIN-mediated mitophagy under compression. The [[PINK1]] and PARKIN levels were also measured by immunohistochemistry of human and rat intervertebral disc (IVD) tissues taken at different degenerative stages. A specific mitophagy inhibitor, cyclosporine A (CSA) and a constructed [[PINK1]]-shRNA were used to explore the relationship between mitophagy and senescence by down-regulating the [[PINK1]]/PARKIN-mediated mitophagy levels. Our results indicated that compression significantly enhanced the senescence of NPCs in a time-dependent manner. Also, [[PINK1]]/PARKIN-mediated mitophagy was found to be activated by the extended duration of compression on NPCs as well as the increased degenerative stages of IVD tissues. After inhibition of [[PINK1]]/PARKIN-mediated mitophagy by CSA and [[PINK1]]-shRNA, the senescence of NPCs induced by compression was strongly rescued. Hence, the excessive degradation of mitochondria in NPCs by mitophagy under continuous compression may accelerate the senescence of NPCs. Regulating [[PINK1]]/PARKIN-mediated mitophagy might be a potential therapeutic treatment for IVD degeneration.

|keywords=* PARKIN pathway
* PINK1
* compression
* intervertebral disc
* mitophagy
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7214186
}}
{{medline-entry
|title=Doxorubicin-induced normal breast epithelial cellular aging and its related breast cancer growth through mitochondrial autophagy and oxidative stress mitigated by ginsenoside Rh2.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32100342
|abstract=Clinical dose of doxorubicin (100 nM) induced cellular senescence and various secretory phenotypes in breast cancer and normal epithelial cells. Herein, we reported the detailed mechanism underlying ginsenoside Rh2-mediated NF-κB inhibition, and mitophagy promotion were evaluated by antibody array assay, western blotting analysis, and immunocytostaining. Ginsenoside Rh2 suppressed the protein levels of TRAF6, p62, phosphorylated IKK, and IκB, which consequently inactivated NF-κB activity. Rh2-mediated secretory phenotype was delineated by the suppressed IL-8 secretion. Senescent epithelial cells showed increased level of reactive oxygen species (ROS), which was significantly abrogated by Rh2, with upregulation on SIRT 3 and SIRT 5 and subsequent increase in SOD1 and SOD2. Rh2 remarkably favored mitophagy by the increased expressions of [[PINK1]] and Parkin and decreased level of PGC-1α. A decreased secretion of IL-8 challenged by mitophagy inhibitor Mdivi-1 with an NF-κB luciferase system was confirmed. Importantly, secretory senescent epithelial cells promoted the breast cancer (MCF-7) proliferation while decreased the survival of normal epithelial cells demonstrated by co-culture system, which was remarkably alleviated by ginsenoside Rh2 treatment. These data included ginsenoside Rh2 regulated ROS and mitochondrial autophagy, which were in large part attributed to secretory phenotype of senescent breast epithelial cells induced by doxorubicin. These findings also suggested that ginsenoside Rh2 is a potential treatment candidate for the attenuation of aging related disease.
|mesh-terms=* Autophagy
* Breast Neoplasms
* Cell Culture Techniques
* Cell Line, Tumor
* Doxorubicin
* Drugs, Chinese Herbal
* Female
* Ginsenosides
* Humans
* Mitochondria
* Oxidative Stress
|keywords=* ROS
* cancer growth
* cellular senescence
* chemotherapy
* ginsenoside Rh2
* mitophagy
|full-text-url=https://sci-hub.do/10.1002/ptr.6636
}}
==PLK4==

{{medline-entry
|title=A novel lncRNA [[PLK4]] up-regulated by talazoparib represses hepatocellular carcinoma progression by promoting YAP-mediated cell senescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32243714
|abstract=A growing number of studies recognize that long non-coding RNAs (lncRNAs) are essential to mediate multiple tumorigenic processes, including hepatic tumorigenesis. However, the pathological mechanism of lncRNA-regulated liver cancer cell growth remains poorly understood. In this study, we identified a novel function lncRNA, named polo-like kinase 4 associated lncRNA (lncRNA [[PLK4]], GenBank Accession No. RP11-50D9.3), whose expression was dramatically down-regulated in hepatocellular carcinoma (HCC) tissues and cells. Interestingly, talazoparib, a novel and highly potent poly-ADP-ribose polymerase 1/2 (PARP1/2) inhibitor, could increase lncRNA [[PLK4]] expression in HepG2 cells. Importantly, we showed that talazoparib-induced lncRNA [[PLK4]] could function as a tumour suppressor gene by Yes-associated protein (YAP) inactivation and induction of cellular senescence to inhibit liver cancer cell viability and growth. In summary, our findings reveal the molecular mechanism of talazoparib-induced anti-tumor effect, and suggest a potential clinical use of talazoparib-targeted lncRNA [[PLK4]]/YAP-dependent cellular senescence for the treatment of HCC.

|keywords=* Yes-associated protein
* cellular senescence
* hepatocellular carcinoma
* polo-like kinase 4 associated lncRNA
* talazoparib
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7205816
}}
{{medline-entry
|title=Differential expression of AURKA/[[PLK4]] in quiescence and senescence of osteosarcoma U2OS cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32200684
|abstract=This study aimed to identify co-expressed differentially expressed genes (DEGs) in quiescence and senescence of osteosarcoma (OS) U2OS cells and investigate their biological functions. GSE94805 from Gene Expression Omnibus database was extracted, involving 12 samples of OS U2OS cells (4 quiescence, 4 senescence, and 4 control samples). After analysis of DEGs by limma package, VENN analysis was performed to identify co-expressed DEGs in quiescence and senescent. The Cytoscape software was used to construct an interactive network of co-expressed DEGs. Finally, box-plot was drawn for the co-expressed DEGs in sub-network. Besides, the relation literatures were selected in GenCLiP database for the co-expressed DEGs. Seven hundred and forty-three DEGs (255 up-regulated genes, 488 down-regulated genes) were obtained in quiescence and 2135 DEGs (1189 up-regulated genes, 946 down-regulated genes) in senescence. Through VENN analysis, 448 DEGs (131 up-regulated genes, 317 down-regulated genes) were co-expressed in quiescent and senescence. In the co-expressed DEGs network, 896 nodes (448 nodes in quiescent, 448 nodes in senescent) were obtained. Finally, 16 co-expressed DEGs were obtained in the sub-network analysis, in which Aurora kinase A (AURKA) and polo-like kinase ([[PLK4]]) had been reported in OS. AURKA and [[PLK4]] might be the key genes in quiescence and senescence of OS U2OS cells.

|keywords=* AURKA
* Osteosarcoma
* PLK4
* quiescence
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217361
}}
==PRDX3==

{{medline-entry
|title=Proteomic analyses reveal that ginsenoside Rg3([i]S[/i]) partially reverses cellular senescence in human dermal fibroblasts by inducing peroxiredoxin.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32148389
|abstract=The cellular senescence of primary cultured cells is an irreversible process characterized by growth arrest. Restoration of senescence by ginsenosides has not been explored so far. Rg3([i]S[/i]) treatment markedly decreased senescence-associated β-galactosidase activity and intracellular reactive oxygen species levels in senescent human dermal fibroblasts (HDFs). However, the underlying mechanism of this effect of Rg3([i]S[/i]) on the senescent HDFs remains unknown. We performed a label-free quantitative proteomics to identify the altered proteins in Rg3([i]S[/i])-treated senescent HDFs. Upregulated proteins induced by Rg3([i]S[/i]) were validated by real-time polymerase chain reaction and immunoblot analyses. Finally, 157 human proteins were identified, and variable peroxiredoxin (PRDX) isotypes were highly implicated by network analyses. Among them, the mitochondrial [[PRDX3]] was transcriptionally and translationally increased in response to Rg3([i]S[/i]) treatment in senescent HDFs in a time-dependent manner. Our proteomic approach provides insights into the partial reversing effect of Rg3 on senescent HDFs through induction of antioxidant enzymes, particularly [[PRDX3]].

|keywords=* Ginsenoside Rg3(S)
* Human dermal fibroblast
* Label-free quantitative proteomics
* Restoration
* Senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7033328
}}
==PSMD14==

{{medline-entry
|title=Upregulation of deubiquitinase [[PSMD14]] in lung adenocarcinoma (LUAD) and its prognostic significance.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32226511
|abstract=[[PSMD14]] is a 19S-proteasome-associated deubiquitinating enzyme that facilitates protein degradation by the 20S proteasome core particle. Although accumulating evidence indicates that [[PSMD14]] has emerged as a critical oncogenic factor by promoting tumor growth, the expression and function of [[PSMD14]] in non-small cell lung cancer (NSCLC) remain largely unknown. In this study, we assessed [[PSMD14]] expression and correlated it with clinical-pathological features and patient survival in NSCLC. We also determined the roles of [[PSMD14]] in the regulation of lung adenocarcinoma (LUAD) cell growth. The results showed that [[PSMD14]] expression was significantly upregulated in human NSCLC tissues compared with adjacent non-cancerous tissues. The [[PSMD14]] level was associated with tumor size, lymph node invasion, and TNM stage in LUAD patients. Importantly, high [[PSMD14]] expression was associated with poor overall survival (OS) and disease-free survival (DFS) in LUAD patients. Further, knockdown of [[PSMD14]] significantly inhibited cell growth and caused G1 arrest and cellular senescence by increasing p21 stability in LUAD cells. [[PSMD14]] knockdown also promoted cell apoptosis by increasing cleaved caspase-3 levels in H1299 cells. [[PSMD14]] may serve as a potential prognostic marker and therapeutic target for LUAD patients.

|keywords=* PMSD14
* apoptosis
* deubiquitinating enzyme
* lung adenocarcinoma
* prognosis
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7086243
}}
==PTH==

{{medline-entry
|title=Parathyroid hormone ameliorates temporomandibular joint osteoarthritic-like changes related to age.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32154622
|abstract=Ageing could be a contributing factor to the progression of temporomandibular joint osteoarthritis (TMJ OA), whereas its pathogenesis and potential therapeutic strategy have not been comprehensively investigated. We generated ageing mouse models (45-week and 60-week; 12-week mice as control) and intermittently injected 45-week mice with parathyroid hormone ([[PTH]](1-34)) or vehicle for 4 weeks. Cartilage and subchondral bone of TMJ were analysed by microCT, histological and immunostaining. Western blot, qRT-PCR, ChIP, ELISA and immunohistochemical analysis were utilized to examination the mechanism of [[PTH]](1-34)'s function. We showed apparent OA-like phenotypes in ageing mice. [[PTH]] treatment could ameliorate the degenerative changes and improve bone microarchitecture in the subchondral bone by activating bone remodelling. Moreover, [[PTH]] inhibited phosphorylation level of Smad3, which can combine with p16  gene promoter region, resulting in reduced senescent cells accumulation and increased cellular proliferation of marrow mesenchymal stem cells (MSCs). ELISA also showed relieved levels of specific senescent-associated secretory phenotype (SASP) in ageing mice after [[PTH]] treatment. In summary, [[PTH]] may reduce the accumulation of senescent cells in subchondral bone by inhibiting p16  and improve bone marrow microenvironment to active bone remodelling process, indicating [[PTH]] administration could be a potential preventative and therapeutic treatment for age-related TMJ OA.
|mesh-terms=* Aging
* Animals
* Calcium-Regulating Hormones and Agents
* Cells, Cultured
* Disease Models, Animal
* Male
* Mice
* Mice, Inbred C57BL
* Osteoarthritis
* Osteogenesis
* Parathyroid Hormone
* Temporomandibular Joint
|keywords=* cellular senescence
* cyclin-dependent kinase inhibitor P16INK4A
* marrow mesenchymal stem cells
* osteoarthritis
* temporomandibular joint disorders
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7162802
}}
==PTTG1==

{{medline-entry
|title=[Down-regulated [[PTTG1]] expression promotes the senescence of human prostate cancer LNCaP-AI].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32216239
|abstract=To investigate the effect of the down-regulated expression of pituitary tumor-transforming gene 1 ([[PTTG1]]) on the senescence of human castration-resistant prostate cancer LNCaP-AI cells. Human castration-resistant prostate cancer LNCaP-AI cells were induced in vitro and transfected with siRNA targeting [[PTTG1]] (the siRNA-[[PTTG1]] group), the reagent lip3000 only (the mock group) or siRNA negative control vector (the NC group). All the cells were cultured in fetal bovine serum (FBS) or charcoal-stripped bovine serum (CSS) and counted with the cell counting chamber. The senescence characteristics of the transfected LNCaP-AI cells were examined by senescence-associated β-galactosidase (SA-β-Gal) staining, and the expressions of the senescence-related β-galactosidase-1-like proteins (Glb1), the cyclin-dependent kinase inhibitors p-21CIP1 and p-27Kip1, and the chromatin-regulating heterochromatin protein 1γ (HP1γ) were detected by Western blot. The expression of [[PTTG1]] in the human prostate cancer LNCaP-AI cells was significantly reduced in the siRNA-[[PTTG1]] group compared with those in the mock and NC groups (0.21 ± 0.01 vs 0.56 ± 0.02 and 0.61 ± 0.02, P < 0.05). Culture with FBS markedly increased while that with CSS decreased the number of LNCaP-AI cells transfected with siRNA, but both FBS and CSS enhanced the proliferation of the LNCaP-AI cells in the mock and NC groups. SA-β-Gal staining revealed that reducing the expression of [[PTTG1]] induced a remarkably higher positive rate of the LNCaP-AI cells in the siRNA-[[PTTG1]] than in the mock and NC groups (［63.5 ± 2.35］% vs ［11.3 ± 1.24］% and ［12.4 ± 1.15］%, P < 0.05). The siRNA-[[PTTG1]] group, in comparison with the mock and NC groups, showed a significantly down-regulated expression of [[PTTG1]] (0.21 ± 0.01 vs 0.56 ± 0.02 and 0.61 ± 0.02, P < 0.05), but up-regulated expressions of p-21CIP1 (0.32 ± 0.03 vs 0.20 ± 0.02 and 0.21 ± 0.03, P < 0.05), p-27Kip1 (0.38 ± 0.02 vs 0.20 ± 0.03 and 0.22 ± 0.01, P < 0.05), Glb1 (0.24 ± 0.01 vs 0.13 ± 0.01 and 0.15 ± 0.01, P < 0.05), and HP1γ (0.41 ± 0.01 vs 0.26 ± 0.01 and 0.27 ± 0.02, P < 0.05) in the LNCaP-AI cells. Down-regulated expression of [[PTTG1]] induces senescence of human castration-resistant prostate cancer LNCaP-AI cells.
|mesh-terms=* Cell Line, Tumor
* Cell Proliferation
* Humans
* Male
* Prostatic Neoplasms, Castration-Resistant
* RNA, Small Interfering
* Securin
* beta-Galactosidase
|keywords=*  LNCaP-AI cell 

				
*  castration-resistant prostate cancer
*  cellular senescence
*  pituitary tumor-transforming gene-1
* prostate cancer

}}
==RELB==

{{medline-entry
|title=New control of the senescence barrier in breast cancer.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32158912
|abstract=Normal cells exposed to cancer-causing events respond by triggering cellular senescence, a stress response which halts cell proliferation and constitutes a protective anti-cancer barrier. We have uncovered a previously unknown signaling pathway implicating p21-activated kinase 4 (PAK4) in the control of senescence in breast cancer, via the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) subunit [[RELB]] and the CCAAT-enhancer-binding protein beta (C/EBPβ).

|keywords=* CEBPB
* Cellular senescence
* PAK4
* RELB
* p21-activated kinase
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7051141
}}
==REST==

{{medline-entry
|title=[Brain and Neuronal Aging: Aged Brain Controls via Gene Expression Fidelity and Master Regulatory Factors].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115559
|abstract=Providing plausible strategies for brain aging protection should be a critical concern for countries with large elderly populations including Japan. Age-related cognitive impairments and movement disorders, such as Alzheimer's and Parkinson's diseases, are caused by neurodegeneration that primarily initiates in the hippocampus and the midbrain substantia nigra, respectively. Neurons are postmitotic, and therefore, the accuracy of cellular metabolism should be crucial for maintaining neural functions throughout their life. Thus accuracy of protein synthesis is a critical concern in discussing mechanisms of aging. The essence of the so-called "error catastrophe theory" of aging was on the fidelity of ribosomal translation and/or aminoacylation of tRNA. There is evidence that reduced protein synthesis accuracy results in neurodegeneration. Similarly, reduced proteostasis via autophagy and proteasomes in aging is crucial for protein quality control and well documented as a risk for aging. In both neurodegeneration and protein quality controls, various proteins are involved in their regulation, but recent evidence suggests that repressor element-1 silencing transcription factor ([[REST]]) could be a master regulatory protein that is crucial for orchestrating the neural protecting events in human brain aging. [[REST]] is induced in the aged brain, and protects neurons against oxidative stress and protein toxicity. Interestingly, [[REST]] is identical with neuron-restrictive silencer factor (NRSF), the master regulator of neural development. Thus NRSF/[[REST]] play important roles in both neurogenesis and neurodegeneration. In this review, I summarize the interesting scientific crossover, and discuss the potential use of NRSF/[[REST]] as a pharmaceutical target for controlling aging, particularly in relation to brain aging.
|mesh-terms=* Aged
* Aged, 80 and over
* Aging
* Animals
* Brain
* Gene Expression
* Gene Expression Regulation, Developmental
* Humans
* Neurodegenerative Diseases
* Protein Biosynthesis
* Repressor Proteins
* Ribosomes
|keywords=* aging
* brain
* gene expression
* neurodegeneration
* ribosome
* translational fidelity
|full-text-url=https://sci-hub.do/10.1248/yakushi.19-00193-4
}}
==RET==

{{medline-entry
|title=Resistance exercise training promotes fiber type-specific myonuclear adaptations in older adults.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32134710
|abstract=Aging induces physiological decline in human skeletal muscle function and morphology, including type II fiber atrophy and an increase in type I fiber frequency. Resistance exercise training ([[RET]]) is an effective strategy to overcome muscle mass loss and improve strength, with a stronger effect on type II fibers. In the present study, we sought to determine the effect of a 12-wk progressive [[RET]] program on the fiber type-specific skeletal muscle hypertrophic response in older adults. Nineteen subjects [10 men and 9 women (71.1 ± 4.3 yr)] were studied before and after the 12-wk program. Immunohistochemical analysis was used to quantify myosin heavy chain (MyHC) isoform expression, cross-sectional area (CSA), satellite cell abundance, myonuclear content, and lipid droplet density. [[RET]] induced an increase in MyHC type II fiber frequency and a concomitant decrease in MyHC type I fiber frequency. Mean CSA increased significantly only in MyHC type II fibers (+23.3%, [i]P[/i] < 0.05), but myonuclear content increased only in MyHC type I fibers ([i]P[/i] < 0.05), with no change in MyHC type II fibers. Satellite cell content increased ~40% in both fiber types ([i]P[/i] > 0.05). [[RET]] induced adaptations to the capillary supply to satellite cells, with the distance between satellite cells and the nearest capillary increasing in type I fibers and decreasing in type II fibers. Both fiber types showed similar decrements in intramuscular lipid density with training ([i]P[/i] < 0.05). Our data provide intriguing evidence for a fiber type-specific response to [[RET]] in older adults and suggest flexibility in the myonuclear domain of type II fibers during a hypertrophic stimulus.  In older adults, progressive resistance exercise training ([[RET]]) increased skeletal muscle fiber volume and cross-sectional area independently of myonuclear accretion, leading to an expansion of the myonuclear domain. Fiber type-specific analyses illuminated differential adaptation; type II fibers underwent hypertrophy and exhibited myonuclear domain plasticity, whereas myonuclear accretion occurred in type I fibers in the absence of a robust hypertrophic response. [[RET]] also augmented satellite cell-capillary interaction and reduced intramyocellular lipid density to improve muscle quality.

|keywords=* aging
* hypertrophy
* myonuclear domain
* skeletal muscle
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191507
}}
==RHO==

{{medline-entry
|title=SARS-CoV-2 receptor ACE2 and TMPRSS2 are primarily expressed in bronchial transient secretory cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32246845
|abstract=The SARS-CoV-2 pandemic affecting the human respiratory system severely challenges public health and urgently demands for increasing our understanding of COVID-19 pathogenesis, especially host factors facilitating virus infection and replication. SARS-CoV-2 was reported to enter cells via binding to ACE2, followed by its priming by TMPRSS2. Here, we investigate ACE2 and TMPRSS2 expression levels and their distribution across cell types in lung tissue (twelve donors, 39,778 cells) and in cells derived from subsegmental bronchial branches (four donors, 17,521 cells) by single nuclei and single cell RNA sequencing, respectively. While TMPRSS2 is strongly expressed in both tissues, in the subsegmental bronchial branches ACE2 is predominantly expressed in a transient secretory cell type. Interestingly, these transiently differentiating cells show an enrichment for pathways related to [[RHO]] GTPase function and viral processes suggesting increased vulnerability for SARS-CoV-2 infection. Our data provide a rich resource for future investigations of COVID-19 infection and pathogenesis.
|mesh-terms=* Adult
* Aging
* Angiotensin-Converting Enzyme 2
* Bronchi
* COVID-19
* Cells, Cultured
* Chronic Disease
* Coronavirus Infections
* Epithelial Cells
* Female
* Gene Expression
* Gene Expression Profiling
* Germany
* Goblet Cells
* Humans
* Lung
* Male
* Middle Aged
* Pandemics
* Peptidyl-Dipeptidase A
* Pneumonia, Viral
* Reference Standards
* Sequence Analysis, RNA
* Serine Endopeptidases
* Sex Characteristics
* Single-Cell Analysis
* Smoking
* Tissue Banks
|keywords=* 
FURIN

* COVID-19
* Human Cell Atlas
* epithelial differentiation
* respiratory tract
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7232010
}}
==RPE==

{{medline-entry
|title=CSF1R blockade induces macrophage ablation and results in mouse choroidal vascular atrophy and [[RPE]] disorganization.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32234210
|abstract=The choroid, which provides vascular supply to the outer retina, demonstrates progressive degeneration in aging and age-related macular degeneration (AMD). However mechanisms that maintain or compromise choroidal homeostasis are obscure. We discovered that the ablation of choroidal macrophages via CSF1R blockade was associated with choroidal vascular atrophy and retinal pigment epithelial ([[RPE]]) changes including structural disruption, downregulation of visual cycle genes, and altered angiogenic factor expression. Suspending CSF1R blockade following ablation enabled spontaneous macrophage regeneration, which fully restored original macrophage distributions and morphologies. Macrophage regeneration was accompanied by arrested vascular degeneration and ameliorated pathological [[RPE]] alterations. These findings suggest that choroidal macrophages play a previously unappreciated trophic role in maintaining choroidal vasculature and [[RPE]] cells, implicating insufficiency in choroidal macrophage function as a factor in aging- and AMD-associated pathology. Modulating macrophage function may constitute a strategy for the therapeutic preservation of the choroid and [[RPE]] in age-related retinal disorders.

|keywords=* RPE disorganization
* aging
* choroid
* choroidal macrophage
* choroidal vasculature
* immunology
* inflammation
* mouse
* neuroscience
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156269
}}
{{medline-entry
|title=Extracellular microparticles exacerbate oxidative damage to retinal pigment epithelial cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32173468
|abstract=Oxidative stress-induced retinal pigment epithelial cell ([[RPE]]) dysfunction is a primary contributing factor to early dry age-related macular degeneration (AMD). Oxidative injury to the retina may promote extracellular vesicles (EVs) released from [[RPE]]. In this study, we investigated the effects of oxidative-induced [[RPE]] cell-derived microparticles (RMPs) on [[RPE]] cell functions. The oxidative stress induced more RMPs released from [[RPE]] cells in vitro and in vivo, and significant more RMPs were released from aged [[RPE]] cells than that from younger [[RPE]] cells. RMPs were taken up by [[RPE]] cells in a time-dependent manner; however, blockage of CD36 attenuated the uptake process. Furthermore, the decrease of [[RPE]] cell viability by RMPs treatment was associated with an increased expression of cyclin-dependent kinase inhibitors p15 and p21. RMPs enhanced senescence and interrupted phagocytic activity of [[RPE]] cells as well. The present study demonstrated that RMPs produce a strong effect of inducing [[RPE]] cell degeneration. This finding further supports the postulate that RMPs exacerbate oxidative stress damage to [[RPE]] cells, which may uncover a potentially relevant process in the genesis of dry AMD.

|keywords=* Extracellular vesicles
* Oxidative stress
* Phagocytosis
* RPE cell Dysfunction
* RPE cell-Derived microparticles (RMPs)
* Retinal pigment epithelial cell (RPE)
* Senescence
|full-text-url=https://sci-hub.do/10.1016/j.yexcr.2020.111957
}}
{{medline-entry
|title=Water-based continuous and interval training in older women: Cardiorespiratory and neuromuscular outcomes (WATER study).
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32145293
|abstract=The purpose of this study was to investigate the effects of two water-based aerobic programs on cardiorespiratory and neuromuscular outcomes in older women. Forty-one women (60 to 75 years old) volunteered to participate in the study. Participants were randomized into a water-based continuous (CTG; n = 21; 63.9 ± 2.5 years) or an interval (ITG; n = 20; 64.8 ± 3.6 years) aerobic training group. Both training programs were performed for 12 weeks (45-min sessions twice a week), with exercise intensity based on rating of perceived exertion (Borg's [[RPE]] 6-20 Scale). Pre and post training assessments of cardiorespiratory and neuromuscular outcomes were performed. Data analyses were conducted using Generalized Estimating Equations and Bonferroni post-hoc test (α = 0.05). After the intervention, the CTG and the ITG displayed similar improvements in time to exhaustion (8% vs. 11%), peak oxygen uptake (9% vs. 7%), maximal dynamic knee extension strength (5% vs. 6%), dynamic muscular endurance of knee extensors (10% vs. 11%), maximal vastus lateralis electromyographic signal amplitude (13% vs. 35%), as well as an increase in muscle thickness (5% vs. 6%) and decrease in muscle echo intensity (-2% vs. -3%) of the quadriceps femoris. In conclusion, older women benefited from water-based exercise training prescribed based on participants' [[RPE]], with both the interval and the continuous training programs resulting in similar increases in the cardiorespiratory and neuromuscular parameters.

|keywords=* Aerobic capacity
* Aerobic training
* Aging
* Aquatic exercise
* Interval exercise
* Muscle echo intensity
* Muscle strength
* Muscle thickness
|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110914
}}
==S100B==

{{medline-entry
|title=Aging protects rat cortical slices against to oxygen-glucose deprivation induced damage.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32064981
|abstract= In present study, we aimed to clarify effect of aging on the susceptibility of brain tissue to neurodegeneration induced by ischemia.  Damage induced by oxygen-glucose deprivation (OGD) followed by reoxygenation (REO) were compared in cortical slices prepared from young (3 months of age) and aged (22-24 months of age) male Sprague Dawley rats.  After incubation of the slices in an oxygen and glucose containing control condition, 2,3,5-triphenyl tetrazolium chloride (TTC) staining intensity was found significantly high in aged cortical slices. Although thirty minutes incubation of the slices in OGD medium followed by REO (OGD-REO) caused similar decline in TTC staining in young and aged cortical slices, staining intensity was still significantly higher in the slices prepared from aged animals. Thirty minutes of OGD-REO, on the other hand, also caused more increase in lactate dehydrogenase (LDH) leakage from young slices. While water contents of the slices were almost equal under control condition, it was significantly high in young cortical slices after OGD-REO incubations. In contrary to these findings, OGD and REO caused more increases in [[S100B]] output from aged rat cortical slices. [[S100B]] levels in brain regions including the cerebral cortex were also found higher in aged rats.  All these results indicate that, cortical slices prepared from aged male rats are significantly less responsive to [i]in vitro[/i] OGD-REO induced alterations. Since protein [[S100B]] outputs were almost doubled from aged cortical slices, a possible involvement of this enhanced [[S100B]] output seems to be likely.

|keywords=* Aging
* LDH
* S100B
* edema
* oxygen-glucose deprivation
|full-text-url=https://sci-hub.do/10.1080/00207454.2020.1730830
}}
==SAG==

{{medline-entry
|title=Neurogenesis in the inner ear: the zebrafish statoacoustic ganglion provides new neurons from a Neurod/Nestin-positive progenitor pool well into adulthood.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32165493
|abstract=The vertebrate inner ear employs sensory hair cells and neurons to mediate hearing and balance. In mammals, damaged hair cells and neurons are not regenerated. In contrast, hair cells in the inner ear of zebrafish are produced throughout life and regenerate after trauma. However, it is unknown whether new sensory neurons are also formed in the adult zebrafish statoacoustic ganglion ([[SAG]]), the sensory ganglion connecting the inner ear to the brain. Using transgenic lines and marker analysis, we identify distinct cell populations and anatomical landmarks in the juvenile and adult [[SAG]]. In particular, we analyze a Neurod/Nestin-positive progenitor pool that produces large amounts of new neurons at juvenile stages, which transitions to a quiescent state in the adult [[SAG]]. Moreover, BrdU pulse chase experiments reveal the existence of a proliferative but otherwise marker-negative cell population that replenishes the Neurod/Nestin-positive progenitor pool at adult stages. Taken together, our study represents the first comprehensive characterization of the adult zebrafish [[SAG]] showing that zebrafish, in sharp contrast to mammals, display continued neurogenesis in the [[SAG]] well beyond embryonic and larval stages.
|mesh-terms=* Adult Stem Cells
* Aging
* Animals
* Animals, Genetically Modified
* Basic Helix-Loop-Helix Transcription Factors
* Cell Differentiation
* Ear, Inner
* Embryo, Nonmammalian
* Ganglia, Sensory
* Gene Expression Regulation, Developmental
* Hair Cells, Auditory
* Larva
* Nerve Tissue Proteins
* Nestin
* Neural Stem Cells
* Neurogenesis
* Sensory Receptor Cells
* Stem Cell Niche
* Zebrafish
|keywords=* Inner ear
* Neuronal stem cells
* PNS
* Zebrafish
|full-text-url=https://sci-hub.do/10.1242/dev.176750
}}
==SCN2B==

{{medline-entry
|title=MicroRNA‑449a regulates the progression of brain aging by targeting [[SCN2B]] in SAMP8 mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32124967
|abstract=Our previous study demonstrated that the expression of sodium channel voltage‑gated beta 2 ([[SCN2B]]) increased with aging in senescence‑accelerated mouse prone 8 (SAMP8) mice, and was identified to be associated with a decline in learning and memory, while the underlying mechanism is unclear. In the present study, multiple differentially expressed miRNAs, which may be involved in the process of aging by regulating target genes, were identified in the prefrontal cortex and hippocampus of SAMP8 mice though miRNA microarray analysis. Using bioinformatics prediction, [[SCN2B]] was identified to be one of the potential target genes of miR‑449a, which was downregulated in the hippocampus. Previous studies demonstrated that miR‑449a is involved in the occurrence and progression of aging by regulating a variety of target genes. Therefore, it was hypothesized that miR‑449a may be involved in the process of brain aging by targeting [[SCN2B]]. To verify this hypothesis, the following experiments were conducted: A reverse transcription‑quantitative polymerase chain reaction assay revealed that the expression level of miR‑449a was significantly decreased in the prefrontal cortex and hippocampus of 12‑month old SAMP8 mice; a dual‑luciferase reporter assay verified that miR‑449a regulated [[SCN2B]] expression by binding to the 3'‑UTR 'seed region'; an anti‑Ago co‑immunoprecipitation combined with Affymetrix microarray analyses demonstrated that the target mRNA highly enriched with Ago‑miRNPs was confirmed to be [[SCN2B]]. Finally, overexpression of miR‑449a or inhibition of [[SCN2B]] promoted the extension of hippocampal neurons in vitro. The results of the present study suggested that miR‑449a was downregulated in the prefrontal cortex and hippocampus of SAMP8 mice and may regulate the process of brain aging by targeting [[SCN2B]].
|mesh-terms=* Aging
* Animals
* Brain
* Gene Expression Regulation
* Male
* Mice
* Mice, Transgenic
* MicroRNAs
* Voltage-Gated Sodium Channel beta-2 Subunit
|keywords=#f
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053848
}}
==SCO1==

{{medline-entry
|title=Real-Time PCR Analysis of Metabolism-Related Genes in a Long-Lived Model of C. elegans.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32219749
|abstract=In the nematode Caenorhabditis elegans, the mammalian tumor suppressor p53 ortholog CEP-1 (C. elegans p53-like protein) is associated not only with the stress response, germline apoptosis, and meiotic chromosome segregation but also with longevity through the modification of energy metabolism during aging. The mitochondrial respiration-related gene sco-1 in C. elegans is orthologous to the human [[SCO1]] gene and a target of p53/CEP-1. Using quantitative real-time polymerase chain reaction (PCR) analysis, we recently found that the expression levels of sco-1 gene were increased in wild-type C. elegans in an aging-related manner and decreased in long-lived cep-1 mutants. Here, we describe the relative quantitative strategy using a commercial real-time PCR system to detect more accurately differences in the levels of expressed genes between long-lived and wild-type C. elegans strains. To estimate the expression levels of target genes compared with wild-type using relative quantification, we used the expression levels of an endogenous control gene, such as a housekeeping gene. In addition, it is critical to normalize differences in the expression levels of the common housekeeping gene among the strains analyzed for an accurate comparison of the quantitative expression levels of target genes.

|keywords=* Caenorhabditis elegans
* Energy metabolism
* Longevity
* TaqMan real-time PCR
* p53/CEP-1
|full-text-url=https://sci-hub.do/10.1007/978-1-0716-0471-7_12
}}
==SFPQ==

{{medline-entry
|title=Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32267831
|abstract=Long noncoding RNAs (lncRNAs) play important roles in the development of vascular diseases. However, the effect of lncRNA NORAD on atherosclerosis remains unknown. This study aimed to investigate the effect NORAD on endothelial cell injury and atherosclerosis. Ox-LDL-treated human umbilical vein endothelial cells (HUVECs) and high-fat-diet (HFD)-fed ApoE  mice were used as [i]in vitro[/i] and [i]in vivo[/i] models. Results showed that NORAD-knockdown induced cell cycle arrest in G0/G1 phase, aggravated ox-LDL-induced cell viability reduction, cell apoptosis, and cell senescence along with the increased expression of Bax, P53, P21 and cleaved caspase-3 and the decreased expression of Bcl-2. The effect of NORAD on cell viability was further verified via NORAD-overexpression. NORAD- knockdown increased ox-LDL-induced reactive oxygen species, malondialdehyde, p-IKBα expression levels and NF-κB nuclear translocation. Proinflammatory molecules ICAM, VCAM, and IL-8 were also increased by NORAD- knockdown. Additionally, we identified the strong interaction of NORAD and IL-8 transcription repressor [[SFPQ]] in HUVECs. In ApoE  mice, NORAD-knockdown increased the lipid disorder and atherosclerotic lesions. The results have suggested that lncRNA NORAD attenuates endothelial cell senescence, endothelial cell apoptosis, and atherosclerosis via NF-κB and p53-p21 signaling pathways and IL-8, in which NORAD-mediated effect on IL-8 might through the direct interaction with [[SFPQ]].

|keywords=* IL-8
* NORAD
* cell apoptosis
* cell senescence
* ox-LDL
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185106
}}
==SGK1==

{{medline-entry
|title=Epigenetic Regulation of KL (Klotho) via H3K27me3 (Histone 3 Lysine [K] 27 Trimethylation) in Renal Tubule Cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32223380
|abstract=KL (klotho) levels decline with age, which is an important mechanistic driver of aging. [i]KL[/i] gene deficiency is associated with hypertension. The purpose of this study is to investigate the potential role of H3K27me3 (histone 3 lysine [K] 27 trimethylation) in the regulation of [i]KL[/i] gene expression and examine the related molecular pathways that may drive kidney cell aging. Kidneys were collected from 6-month-old WT (wild type; young WT), 30-month-old WT (aged WT), and 6- (young) and 20-month-old (aged) [i]KL[/i] mutant mice, respectively. We demonstrated that the H3K27me3 level was increased in kidneys of aged WT and KL mutant mice versus young WT mice. Elevation of H3K27me3 levels was likely due to downregulation of the H3K27 (histone H3 Lys 27)-specific demethylase JMJD3 (the Jumonji domain containing-3) in the aged kidneys. Inhibition of PRC2 (polycomb repressive complex C2; histone trimethyltransferase) decreased the H3K27me3 levels leading to an increase in the expression of KL in cultured primary renal tubule cells assessed by Western blot and [i]KL[/i] promoter activity assays. The chromatin immunoprecipitation qPCR assay revealed that H3K27me3 was physically associated with the [i]KL[/i] promoter region. Furthermore, aging impaired the [[SGK1]] (serum- and glucocorticoid-induced protein kinase 1)/FOXO3a (the forkhead box class O 3a) signaling leading to upregulation of p53 and p16 (aging markers) in the kidney of aged WT mice. KL may regulate the [[SGK1]]/FOXO3 signaling, which was decreased due to KL deficiency. Thus, aging-associated downregulation of [i]KL[/i] gene expression may be partly attributed to upregulation of H3K27me3 levels. Downregulation of KL may impair the [[SGK1]]/FOXO3 signaling contributing to kidney cell aging.

|keywords=* AKT
* EZH2
* aging
* mTOR
* p53
|full-text-url=https://sci-hub.do/10.1161/HYPERTENSIONAHA.120.14642
}}
==SI==

{{medline-entry
|title=Survival time after marked reduction in oral intake in terminally ill noncancer patients: A retrospective study.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32161695
|abstract=The prediction of short-term survival is important for noncancer patients and their families. Although a markedly reduced oral intake by cancer patients suggests a poor prognosis, the survival times of noncancer patients after its onset remain unclear. We herein investigated the time from a marked reduction in oral intake to death in noncancer patients as well as factors associated with their subsequent survival. We conducted a retrospective medical record review of noncancer patients who died in our hospital between April 2017 and April 2018. We recorded the day when oral intake markedly decreased and the date of death. We extracted data on age, gender, the Charlson Comorbidities Index, mean daily fluid volume, laboratory test results, and vital signs converted to the Shock Index ([[SI]]). We used Cox's proportional hazards models to assess relationships between these factors and survival times after the onset of a markedly reduced oral intake. We analyzed data from 44 noncancer patients. The median time from the onset of a markedly reduced oral intake to death was 16.5 days. Based on Cox's proportional hazards models, only [[SI]] ≧ 1.0 at the onset of a markedly reduced oral intake correlated with survival times (hazard ratio: 5.89, 95% confidence interval (CI): 1.71-20.1, [i]P[/i] = .005). Noncancer patients died a median of 16.5 days after the onset of a markedly reduced oral intake, and [[SI]] ≧1.0 correlated with subsequent survival times. These results will provide novel insights into the prognosis of noncancer patients at the end of life.

|keywords=* elderly
* geriatrics
* palliative medicine
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7060293
}}
{{medline-entry
|title=Adherence to Mediterranean diet moderates the association between multimorbidity and depressive symptoms in older adults.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109694
|abstract=Adherence to Mediterranean Diet (Med-Diet) has been associated with a lower incidence of chronic diseases and may be associated with lower risk for depression. The aim of the present study was to investigate (i) the association of adherence to Med-Diet with depressive symptoms and multimorbidity in a cohort of geriatric medical outpatients, and (ii) the role of Med-Diet in mediating the association between depressive symptoms and multimorbidity. A total of 143 geriatric patients (mean age: 73.1 ± 8.35) were included. Adherence to Med-Diet was evaluated using a validated 14-item questionnaire; depressive and cognitive symptoms were assessed through the 15-item Geriatric Depression Scale (GDS) and Mini Mental State Examination (MMSE) respectively; multimorbidity was evaluated using the Cumulative Illness Rating Scale for Geriatrics (CIRSG-[[SI]]). Significant associations were found between MDQ score, GDS and CIRSG-[[SI]] (MDQ score and GDS: r= -0.206, p = 0.014; MDQ score and CIRSG-[[SI]]: r= -0.247, p = 0.003; GDS and CIRSG-[[SI]]: r = 0.251; p = 0.003). These associations remained significant after adjusting for potential confounding factors. A mediational model analysis showed that the direct effect of CIRSG-[[SI]] on GDS was significant (b = 1.330; se = 0.59; p = 0.028) with this effect being counterbalanced by higher MDQ scores (indirect effect of CIRS-G on GDS through MDQ: b = 0.382; se = 0.19; p = 0.048). These findings (i) add to the accumulating evidence that Med-Diet may have a positive impact on mental health in the elderly, and (ii) suggest that Med-Diet may contribute, at least in part, to protect geriatric patients with multimorbidity from the development of depressive symptoms, ultimately promoting healthy aging.
|mesh-terms=* Aged
* Aged, 80 and over
* Cohort Studies
* Depression
* Diet, Mediterranean
* Healthy Aging
* Humans
* Multimorbidity
* Surveys and Questionnaires
|keywords=* Aging
* Depressive symptoms
* Mediterranean diet
* Mental health
* Multimorbidity
|full-text-url=https://sci-hub.do/10.1016/j.archger.2020.104022
}}
==SIRT1==

{{medline-entry
|title=Lymphocyte senescence in COPD is associated with decreased sirtuin 1 expression in steroid resistant pro-inflammatory lymphocytes.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32270742
|abstract=The class III NAD-dependent histone deacetylase (HDAC) sirtuin 1 ([[SIRT1]]) is an important regulator of senescence, aging, and inflammation. [[SIRT1]]de-acetylates chromatin histones, thereby silencing inflammatory gene transcription. We have reported increased steroid-resistant senescent pro-inflammatory CD28nullCD8+ T cells in patients with chronic obstructive pulmonary disease (COPD). We hypothesized that [[SIRT1]] is reduced in these cells in COPD, and that treatment with [[SIRT1]] activators (resveratrol, curcumin) and agents preventing NAD depletion (theophylline) would upregulate [[SIRT1]] and reduce pro-inflammatory cytokine expression in these steroid-resistant cells. Blood was collected from [i]n[/i] = 10 COPD and [i]n[/i] = 10 aged-matched controls. Expression of CD28, [[SIRT1]], and pro-inflammatory cytokines was determined in CD8+ and CD8- T and natural killer T (NKT)-like cells cultured in the presence of ±1 µM prednisolone, ±5 mg/L theophylline, ±1 µM curcumin, ±25 µM resveratrol, using flow cytometry and immunofluorescence. There was an increase in the percentage of CD28nullCD8+ T and NKT-like cells in COPD patients compared with controls. Decreased [[SIRT1]] expression was identified in CD28nullCD8+T and NKT-like cells compared with CD28+ counterparts from both patients and controls (e.g. CD28null 11 ± 3% [i]versus[/i] CD28+ 57 ± 9%). Loss of [[SIRT1]] was associated with increased production of IFNγ and TNFα, steroid resistance, and disease severity. [[SIRT1]] expression was upregulated in the presence of all drugs and was associated with a decrease in steroid resistance and IFNγ and TNFα production by CD28nullCD8+T and NKT-like cells. The presence of the [[SIRT1]] inhibitor, EX-527 negated [by 92 ± 12% (median ± SEM)] the effect of the [[SIRT1]] activator SRT720 on the percentage of CD8+ T cells producing IFNγ and TNFα. Steroid resistance in pro-inflammatory CD28nullCD8+ T and NKT-like cells is associated with decreased [[SIRT1]] expression. Treatment with prednisolone, in combination with theophylline, curcumin or resveratrol increases [[SIRT1]] expression, restores steroid sensitivity, and inhibits pro-inflammatory cytokine production from these cells and may reduce systemic inflammation in COPD. [i]The reviews of this paper are available via the supplemental material section.[/i]

|keywords=* CD28nullCD8+ T and NKT-like cells
* COPD
* IFNγ and TNFα
* SIRT1
* lymphocyte senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7153179
}}
{{medline-entry
|title=Therapeutic effects of hydro-alcoholic leaf extract of Withania somnifera on age-induced changes in daily rhythms of Sirt1, Nrf2 and Rev-erbα in the SCN of male Wistar rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32249404
|abstract=The temporal expression pattern of the circadian clock genes are known to be altered/attenuated with advance in age. Withania somnifera (WS) essentially consists of numerous active constituents including withanolides is known to have antioxidant, anti-inflammatory and adaptogenic properties. We have earlier demonstrated therapeutic effects of hydro-alcoholic leaf extract of WS on the age-induced alterations in the levels and daily rhythms of various clock genes such as rBmal1, rPer1, rPer2 and rCry1. We have now studied effects of hydro-alcoholic leaf extract of WS on the age-induced alterations in the levels and daily rhythms of expression of [[SIRT1]] (an NAD  dependent histone deacetylase and a modulator of clock) and NRF2 (a clock controlled gene and a master transcription factor regulating various endogenous antioxidant enzymes) in addition to rRev-erbα in SCN of adult [3 months (m)], middle-aged (12 m) and old-aged (24 m) male Wistar rats. The daily rhythms of rNrf2 expression showed 6 h phase delay in middle age and 12 h phase advance in old age. WS restored rSirt1 daily rhythms and phase in old age whereas it restored the phase of rNrf2 in the SCN of both middle and old aged animals. At protein level, [[SIRT1]] expression showed phase advances in 12 m and 24 m whereas NRF2 daily rhythms were abolished in both the age groups. WS restored the phase and daily rhythms of [[SIRT1]] as well as NRF2 in 12 m old rats. However, rRev-erbα expression was found insensitive to WS treatment in all the age groups studied. Pairwise correlation analysis demonstrated significant stoichiometric interactions among rSirt1, rNrf2 and rRev-erbα in 3 m which altered with aging significantly. WS treatment resulted in differential restorations of such interactions.

|keywords=* Aging
* Ashwagandha
* Circadian clock
* NRF2
* SCN
* SIRT1
|full-text-url=https://sci-hub.do/10.1007/s10522-020-09875-x
}}
{{medline-entry
|title=The Serum Concentration of Anti-Aging Proteins, Sirtuin1 and αKlotho in Patients with End-Stage Kidney Disease on Maintenance Hemodialysis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32214805
|abstract=Sirtuin1 ([[SIRT1]]) acts as an anti-aging protein due to anti-apoptotic, anti-oxidative and anti-inflammatory effect and is implicated in several diseases including diabetes or cardiovascular problems. [[SIRT1]] renal overexpression indicates oxidative stress. Similarly, αKlotho was primarily exposed as anti-aging factor. It is primary produced in kidney. It's deficiency is associated with progression of chronic kidney disease and heart disorders. The aim of the study was to assess the serum concentration of sirtuin1 and αKlotho in hemodialysis (HD) patients compared to healthy volunteers in regard to age, blood pressure control, residual kidney function (RKF), diabetes, cardiovascular disease, dialysis vintage and type of dialyzer. The serum level of [[SIRT1]] and αKlotho was evaluated using ELISA tests in 103 HD patients, median age 67 years and in 21 volunteers. Blood pressure, RRF, echocardiography and dialysis parameters were assessed. HD group was divided according to the presence/absence of RKF. The serum [[SIRT1]] level was higher (28.4 vs 2.71ng/mL, p<0.0001) and αKlotho was lower (433.9 vs 756.6pg/mL, p<0.0001) in HD then in control group. αKlotho was lower in those without RKF (387.2 vs 486.2pg/mL, p=0.028). [[SIRT1]] positively correlated with hemodialysis vintage. αKlotho negatively correlated with left ventricular posterior wall thickness. There was no significant relationship between [[SIRT1]] and αKlotho level and age, blood pressure control, type of dialyzer, Kt/V and diabetes. Multivariate analysis revealed association of [[SIRT1]] with ejection fraction (B -0.72; p=0.32). Elevated [[SIRT1]] and lower αKlotho concentration are associated with impaired kidney function. The decrease in levels of αKlotho may also indicate heart hypertrophy in hemodialysis patients. The role of anti-aging proteins, particularly [[SIRT1]] as biomarkers/predictors of oxidative stress, inflammation and cardiovascular diseases need further examination.
|mesh-terms=* Age Factors
* Aged
* Aging
* Biomarkers
* Blood Pressure
* Cardiovascular Diseases
* Case-Control Studies
* Diabetes Complications
* Echocardiography
* Female
* Glucuronidase
* Heart Ventricles
* Humans
* Kidney
* Kidney Failure, Chronic
* Male
* Middle Aged
* Renal Dialysis
* Sirtuin 1
* Stroke Volume
|keywords=* chronic kidney disease
* hemodialysis
* sirtuin1
* αKlotho
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7084123
}}
{{medline-entry
|title=Small extracellular vesicles deliver miR-21 and miR-217 as pro-senescence effectors to endothelial cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32158519
|abstract=The role of epigenetics in endothelial cell senescence is a cutting-edge topic in ageing research. However, little is known of the relative contribution to pro-senescence signal propagation provided by microRNAs shuttled by extracellular vesicles (EVs) released from senescent cells. Analysis of microRNA and DNA methylation profiles in non-senescent (control) and senescent (SEN) human umbilical vein endothelial cells (HUVECs), and microRNA profiling of their cognate small EVs (sEVs) and large EVs demonstrated that SEN cells released a significantly greater sEV number than control cells. sEVs were enriched in miR-21-5p and miR-217, which target DNMT1 and [[SIRT1]]. Treatment of control cells with SEN sEVs induced a miR-21/miR-217-related impairment of DNMT1-[[SIRT1]] expression, the reduction of proliferation markers, the acquisition of a senescent phenotype and a partial demethylation of the locus encoding for miR-21. MicroRNA profiling of sEVs from plasma of healthy subjects aged 40-100 years showed an inverse U-shaped age-related trend for miR-21-5p, consistent with senescence-associated biomarker profiles. Our findings suggest that miR-21-5p/miR-217 carried by SEN sEVs spread pro-senescence signals, affecting DNA methylation and cell replication.

|keywords=* Cellular senescence
* DNMT1
* SIRT1
* extracellular vesicles
* microRNAs
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7048230
}}
{{medline-entry
|title=Spatiotemporal gating of [[SIRT1]] functions by O-GlcNAcylation is essential for liver metabolic switching and prevents hyperglycemia.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32152092
|abstract=Inefficient physiological transitions are known to cause metabolic disorders. Therefore, investigating mechanisms that constitute molecular switches in a central metabolic organ like the liver becomes crucial. Specifically, upstream mechanisms that control temporal engagement of transcription factors, which are essential to mediate physiological fed-fast-refed transitions are less understood. [[SIRT1]], a NAD -dependent deacetylase, is pivotal in regulating hepatic gene expression and has emerged as a key therapeutic target. Despite this, if/how nutrient inputs regulate [[SIRT1]] interactions, stability, and therefore downstream functions are still unknown. Here, we establish nutrient-dependent O-GlcNAcylation of [[SIRT1]], within its N-terminal domain, as a crucial determinant of hepatic functions. Our findings demonstrate that during a fasted-to-refed transition, glycosylation of [[SIRT1]] modulates its interactions with various transcription factors and a nodal cytosolic kinase involved in insulin signaling. Moreover, sustained glycosylation in the fed state causes nuclear exclusion and cytosolic ubiquitin-mediated degradation of [[SIRT1]]. This mechanism exerts spatiotemporal control over [[SIRT1]] functions by constituting a previously unknown molecular relay. Of note, loss of [[SIRT1]] glycosylation discomposed these interactions resulting in aberrant gene expression, mitochondrial dysfunctions, and enhanced hepatic gluconeogenesis. Expression of nonglycosylatable [[SIRT1]] in the liver abrogated metabolic flexibility, resulting in systemic insulin resistance, hyperglycemia, and hepatic inflammation, highlighting the physiological costs associated with its overactivation. Conversely, our study also reveals that hyperglycosylation of [[SIRT1]] is associated with aging and high-fat-induced obesity. Thus, we establish that nutrient-dependent glycosylation of [[SIRT1]] is essential to gate its functions and maintain physiological fitness.
|mesh-terms=* Acetylglucosamine
* Aging
* Animals
* Fasting
* Gluconeogenesis
* Glycosylation
* HEK293 Cells
* Homeostasis
* Humans
* Hyperglycemia
* Insulin Resistance
* Liver
* Male
* Mice
* Mice, Inbred C57BL
* Obesity
* Phosphorylation
* Protein Processing, Post-Translational
* Sirtuin 1
* Spatio-Temporal Analysis
|keywords=* PGC1α
* fed–fast cycle
* gluconeogenesis
* insulin signaling
* ubiquitinylation
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7104039
}}
{{medline-entry
|title=Hydrogen Sulfide Inhibits Homocysteine-Induced Neuronal Senescence by Up-Regulation of [[SIRT1]].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32132865
|abstract=Homocysteine (Hcy) accelerates neuronal senescence and induces age-related neurodegenerative diseases. Silence signal regulating factor 1 ([[SIRT1]]) prolongs lifespan and takes neuroprotective effects. We have previously demonstrated that hydrogen sulfide (H S) prevents Hcy-induced apoptosis of neuronal cells and has neuroprotective effect. In the present work, we aimed to investigate whether H S protects HT22 cells against Hcy-induced neuronal senescence and whether [[SIRT1]] mediates this role of H S. We found that Hcy induced cellular senescence in HT22 cells, as determined by β-galactosidase staining, expressions of P16 , P21 , and trypan blue Staining, which are the markers of cellular senescence. However, sodium hydrosulfide (NaHS, the donor of H S) significantly reversed Hcy-induced cellular senescence. Interestingly, NaHS not only up-regulated the expression of [[SIRT1]] in HT22 cells but also reversed Hcy-downregulated the expression of [[SIRT1]] in HT22 cells. Furthermore, we found that pretreatment with Sirtinol (an inhibitor of [[SIRT1]]) markedly reversed the protection of NaHS against Hcy-induced HT22 cells senescence and apoptosis. Our findings illustrated that H S protects HT22 cells against Hcy-induced senescence by up-regulating [[SIRT1]].

|keywords=* SIRT1
* cell senescence
* homocysteine
* hydrogen sulfide
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053352
}}
{{medline-entry
|title=[[SIRT1]] and aging related signaling pathways.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32084459
|abstract=Aging is a biological phenomenon in which the structure and function of organisms declining with the increasing of age. It has become a major risk factor of human diseases, including diabetes, cancers, cardiovascular diseases and neurodegenerative diseases. Silencing information regulator 2 related enzyme 1(sirtuin1, [[SIRT1]]) is an NAD -dependent deacetylase, which has been reported to be involved in the regulation of cellular senescence and aging. The expression of [[SIRT1]] is diminished with aging in mice. By contrast, increased expression of [[SIRT1]] is sufficient to extend lifespan in yeast, caenorhabditis elegans and mice. In this review, the relationship between [[SIRT1]] and aging and various signaling networks associated with aging, including NF-κB, AMPK, mTOR, P53, PGC1α, and FoxOs will be discussed. Meanwhile, the potential therapeutic strategies of targeting [[SIRT1]] to anti-aging are also addressed.

|keywords=* Aging
* Deacetylate
* NAD(+)
* SIRT1
* Signaling pathways
|full-text-url=https://sci-hub.do/10.1016/j.mad.2020.111215
}}
{{medline-entry
|title=Tropisetron protects against brain aging via attenuating oxidative stress, apoptosis and inflammation: The role of [[SIRT1]] signaling.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32088214
|abstract=The aim of this study was to elucidate the signaling pathway involved in the anti-aging effect of tropisetron and to clarify whether it affects mitochondrial oxidative stress, apoptosis and inflammation in the aging mouse brain by upregulating Sirtuin 1 or silent information regulator 1 ([[SIRT1]]). Aging was induced by d-galactose (DG) at the dose of 200 mg/kg body weight/day subcutaneously injected to male mice for six weeks. Tropisetron was simultaneously administered intraperitoneally once a day at three various doses (1, 3 and 5 mg/kg body weight). Oxidative stress and mitochondrial dysfunction markers were evaluated. Nitric oxide (NO) and pro-inflammatory cytokines levels including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were studied. Besides, the expressions of apoptosis-associated genes (Bax and Bcl-2) and the aging-related gene ([[SIRT1]]) were determined by the real time polymerase chain reaction (RT-PCR). In addition, histopathological alterations were assessed. Tropisetron reversed the induction of oxidative damage, mitochondrial dysfunction and overproduction of inflammatory mediators induced by DG in the brain tissue. In addition, tropisetron suppressed DG-induced apoptosis and found to significantly elevate [[SIRT1]] gene expression. Besides, tropisetron could markedly alleviate DG-induced abnormal changes in the brain morphology. Tropisetron exhibited anti-aging effects in the context of DG-induced senescence in mouse brain through various pathways. Our results suggest that tropisetron may attenuate DG-induced brain aging via [[SIRT1]] signaling activation.
|mesh-terms=* Aging
* Animals
* Antioxidants
* Apoptosis
* Brain
* Drug Administration Schedule
* Galactose
* Gene Expression Regulation
* Inflammation
* Injections, Intraperitoneal
* Injections, Subcutaneous
* Interleukin-6
* Male
* Mice
* Mitochondria
* Neurons
* Nitric Oxide
* Oxidative Stress
* Proto-Oncogene Proteins c-bcl-2
* Reactive Oxygen Species
* Serotonin 5-HT3 Receptor Antagonists
* Sirtuin 1
* Tropisetron
* Tumor Necrosis Factor-alpha
* bcl-2-Associated X Protein
|keywords=* Aging
* Brain
* Neurotoxicity
* Sirtuin 1
* Tropisetron
* d-galactose
|full-text-url=https://sci-hub.do/10.1016/j.lfs.2020.117452
}}
==SIRT3==

{{medline-entry
|title=[i][[SIRT3]][/i] Transfection of Aged Human Bone Marrow-Derived Mesenchymal Stem Cells Improves Cell Therapy-Mediated Myocardial Repair.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32228121
|abstract=Sirtuin 3 ([[SIRT3]]) is a deacetylase important for antioxidant protection, cell longevity, and aging. We hypothesized that [[SIRT3]] improve oxidative resistance of aged cells and improve cell therapy in aged patients. [i]In vitro[/i], the proliferation and oxidative resistance of human mesenchymal stem cells (hMSCs) significantly declined with age. The expression and activity of antioxidant enzymes, including catalase (CAT) and manganese superoxide dismutase (MnSOD), increased after transfection of [i][[SIRT3]][/i] in hMSCs from older donors (O-hMSCs). The protein level of Forkhead box O3a (FOXO3a) in nucleus increased after [[SIRT3]] overexpression. The antioxidant capacity of O-hMSCs increased after [[SIRT3]] overexpression. 3-Amino-1,2,4-triazole (3-AT, CAT inhibitor) or diethyldithiocarbamate (DETC, SOD inhibitor) that was used to inhibit CAT or SOD activity significantly blocked the antioxidant function of [[SIRT3]]. When two inhibitors were used together, the antioxidant function of [[SIRT3]] almost disappeared. Following myocardial infarction and intramyocardial injections of O-hMSCs in rats [i]in vivo[/i], the survival rate of O-hMSCs increased by [i][[SIRT3]][/i] transfection. The cardiac function of rats was improved after [[SIRT3]]-overexpressed O-hMSC transplantation. The infarct size, collagen content, and expression levels of matrix metalloproteinase 2 (MMP2) and MMP9 decreased. Besides, the protein level of vascular endothelial growth factor A and vascular density increased after cell transplantation with [[SIRT3]]-modified O-hMSCs. These results indicate that damage resistance of hMSCs decline with age and [[SIRT3]] might protect O-hMSCs against oxidative damage by activating CAT and MnSOD through transferring FOXO3a into nucleus. Meanwhile, the therapeutic effect of aged hMSC transplantation can be improved by [[SIRT3]] overexpression.

|keywords=* O-hMSC transplantation
* SIRT3
* aging
* gene modification
* myocardial infarction
* myocardial repair
|full-text-url=https://sci-hub.do/10.1089/rej.2019.2260
}}
{{medline-entry
|title=17β-estradiol inhibits H O -induced senescence in HUVEC cells through upregulating [[SIRT3]] expression and promoting autophagy.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32172411
|abstract=17β-estradiol (17β-E ) has been implicated in inhibiting the senescence of vascular endothelial cells (VEC) and slowing down the process of atherosclerosis. However, the underlying molecular mechanisms are still unknown. In this study, we examined the roles of [[SIRT3]] in 17β-E -induced autophagy and 17β-E -mediated inhibition of hydrogen peroxide (H O )-induced senescence in Human umbilical vein endothelial cells (HUVEC). Cellular senescence was measured by immunoblot analysis with antibodies against phosphorylated Rb and senescence-associated β-galactosidase staining. Immunoblot analysis with antibodies against LC3 and p62 was performed to determine autophagy flux. Our findings show that 17β-E  activates [[SIRT3]] promoter and upregulates [[SIRT3]] gene expression in HUVEC cells. siRNA-mediated silencing of [[SIRT3]] gene expression inhibits 17β-E -induced processing of LC3-I to LC3-II and degradation of p62, two widely-used makers of autophagy. [[SIRT3]] knockdown also blocks 17β-E -induced inhibition of cellular senescence triggered by H O . Our data further reveal that [[SIRT3]] knockdown impairs 17β-E -induced co-localization of LC3 and VDAC1, a marker protein on mitochondria, when HUVEC cells were co-treated with H O . Together, our findings suggest that 17β-E  upregulates [[SIRT3]] gene expression by activating [[SIRT3]] promoter and then promotes autophagy, which in turn serves to remove dysfunctional mitochondria caused by H O  and consequently inhibit H O -induced senescence in HUVEC cells.

|keywords=* 17β-estradiol
* Autophagy
* SIRT3
* Senescence
|full-text-url=https://sci-hub.do/10.1007/s10522-020-09868-w
}}
{{medline-entry
|title=CR6 interacting factor 1 deficiency induces premature senescence via [[SIRT3]] inhibition in endothelial cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109515
|abstract=Vascular endothelial cell senescence is an important cause of cardiac-related diseases. Mitochondrial reactive oxygen species (mtROS) have been implicated in cellular senescence and multiple cardiovascular disorders. CR6 interacting factor 1 (CRIF1) deficiency has been shown to increase mtROS via the inhibition of mitochondrial oxidative phosphorylation; however, the mechanisms by which mtROS regulates vascular endothelial senescence have not been thoroughly explored. The goal of this study was to investigate the effects of CRIF1 deficiency on endothelial senescence and to elucidate the underlying mechanisms. CRIF1 deficiency was shown to increase the activity of senescence-associated β-galactosidase along with increased expression of phosphorylated p53, p21, and p16 proteins. Cell cycle arrested in the G0/G1 phase were identified in CRIF1-deficient cells using the flow cytometry. Furthermore, CRIF1 deficiency was also shown to increase cellular senescence by reducing the expression of Sirtuin 3 ([[SIRT3]]) via ubiquitin-mediated degradation of transcription factors PGC1α and NRF2. Downregulation of CRIF1 also attenuated the function of mitochondrial antioxidant enzymes including manganese superoxide dismutase (MnSOD), Foxo3a, nicotinamide-adenine dinucleotide phosphate, and glutathione via the suppression of [[SIRT3]]. Interestingly, overexpression of [[SIRT3]] in CRIF1-deficient endothelial cells not only reduced mtROS levels by elevating expression of the antioxidant enzyme MnSOD but also decreased the expression of cell senescence markers. Taken together, these results suggest that CRIF1 deficiency induces vascular endothelial cell senescence via ubiquitin-mediated degradation of the transcription coactivators PGC1α and NRF2, resulting in decreased expression of [[SIRT3]].

|keywords=* Antioxidant system
* Mitochondria
* Oxidative stress
* Senescence
* Vascular endothelial cell
|full-text-url=https://sci-hub.do/10.1016/j.freeradbiomed.2020.02.017
}}
==SOX9==

{{medline-entry
|title=Positive Effects of a Young Systemic Environment and High Growth Differentiation Factor 11 Levels on Chondrocyte Proliferation and Cartilage Matrix Synthesis in Old Mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32067417
|abstract=To investigate the effects of a young systemic environment and growth differentiation factor 11 (GDF-11) on aging cartilage. A heterochronic parabiosis model (2-month-old mouse and 12-month-old mouse [Y/O]), an isochronic parabiosis model (12-month-old mouse and 12-month-old mouse [O/O]), and 12-month-old mice alone (O) were evaluated. Knee joints and chondrocytes from old mice were examined by radiography, histology, cell proliferation assays, immunohistochemistry, Western blotting, and quantitative reverse transcriptase-polymerase chain reaction 16 weeks after parabiosis surgery. GDF-11 was injected into 12-month-old mouse joints daily for 16 weeks. Cartilage degeneration, cell proliferation, and osteoarthritis-related gene expression were evaluated. Osteoarthritis Research Society International scores in old mice were significantly lower in the Y/O group than in the O/O and O groups (both P < 0.05). The percentage of 5-ethynyl-2'-deoxyuridine-positive chondrocytes in old mice was significantly higher in the Y/O group than in the other groups (P < 0.05). Type II collagen (CII) and [[SOX9]] messenger RNA levels differed in cartilage from old mice in the Y/O group compared to the O/O and O groups (both P < 0.05). RUNX-2, CX, and matrix metalloproteinase 13 levels were significantly lower in cartilage from old mice in the Y/O group compared to the O/O and O groups (both P < 0.05). Similar results were obtained for protein expression levels and after GDF-11 treatment in vitro and in vivo. Phosphorylated Smad2/3 (pSmad2/3) levels were higher in the recombinant GDF-11-treated group than in the control group. A young systemic environment promotes chondrocyte proliferation and cartilage matrix synthesis in old mice. GDF-11, a "young factor," contributes to these effects through the up-regulation of pSmad2/3.
|mesh-terms=* Adolescent
* Aged
* Aging
* Animals
* Arthroplasty, Replacement, Knee
* Bone Morphogenetic Proteins
* Cartilage, Articular
* Cell Proliferation
* Chondrocytes
* Collagen Type II
* Collagen Type X
* Core Binding Factor Alpha 1 Subunit
* Extracellular Matrix
* Female
* Growth Differentiation Factors
* Humans
* In Vitro Techniques
* Knee Joint
* Male
* Matrix Metalloproteinase 13
* Mice
* Osteoarthritis, Knee
* Parabiosis
* Phosphorylation
* RNA, Messenger
* Reverse Transcriptase Polymerase Chain Reaction
* SOX9 Transcription Factor
* Smad2 Protein
* Smad3 Protein
* Stifle
* Young Adult
|keywords=#f
|full-text-url=https://sci-hub.do/10.1002/art.41230
}}
==SRD5A2==

{{medline-entry
|title=Extract of Plumbago zeylanica enhances the growth of hair follicle dermal papilla cells with down-regulation of 5α-reductase type II.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32125089
|abstract=Cellular senescence, a phenomenon of irreversible growth arrest of mammalian cells, is involved in various age-related phenomena in organisms. Hair follicle dermal papilla (DP) cells play important roles in the regulation of hair growth and loss. We examined the implication of cellular senescence of DP cells in androgenetic alopecia (AGA), the most common form of male hair loss, and searched for the compounds that have a beneficial effect on the prevention of AGA. Expression of the 5α-reductase type II ([[SRD5A2]]) gene, which plays a key role in the development of AGA, was examined by quantitative RT-PCR and Western blotting analysis in DP cells. Besides, DP cells were cultured with the extracts of herbs used in traditional Ayurvedic medicine to search for the compounds that have a beneficial effect on the growth of DP cells. We found that expression of the [[SRD5A2]] was up-regulated in senescent DP cells. We also found that the herbal extract of Plumbago zeylanica (root) enhanced the growth of DP cells and down-regulated the expression of [[SRD5A2]] in DP cells. Further, plumbagin, an ingredient of P zeylanica, would be responsible for the above effects of P zeylanica. These results suggested the possibility that senescent DP cells may have a role in the development of AGA through up-regulating [[SRD5A2]] expression, and the P zeylanica extract and plumbagin may suppress its development through enhancing the growth of DP cells and down-regulating [[SRD5A2]] expression in DP cells.

|keywords=* 
P zeylanica

* 5α-reductase
* dermal papilla
* hair
* plumbagin
* senescence
|full-text-url=https://sci-hub.do/10.1111/jocd.13355
}}
==SST==

{{medline-entry
|title=Examination on how emotion regulation mediates the relationship between future time perspective and well-being: a counter-evidence to the socioemotional selectivity theory.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32158369
|abstract=Previous studies have shown that older people maintain higher well-being than younger people despite their physical and cognitive functioning declining with age. This paradoxical phenomenon has been explained by the socioemotional selectivity theory ([[SST]]), in which a limited future time perspective (FTP) is an antecedent that leads to higher well-being through the use of adaptive emotion regulation. However, few empirical studies have examined the mediation process assumed in the [[SST]]. Moreover, it is unclear whether time left in life (TLL), which was originally referred to in the [[SST]] and is thought to be a different concept from FTP, relates to emotion regulation and well-being. Therefore, the current study investigated how emotion regulation mediates the relationship between FTP, TLL, and well-being by using a cross-sectional questionnaire that was responded to by 1393 Japanese adults (age range 20-89 years, [i]M[/i] = 54.23, SD = 19.01). The results of correlation and mediation analyses indicated that, in contrast to the assumption of the [[SST]], limited (expanded) FTP and TLL generally lead to lower (higher) well-being through the mediation of maladaptive (adaptive) emotion regulation. Although there are some methodological limitations, the findings imply that the relationship between FTP, TLL, and emotion regulation that is assumed in the [[SST]] should be reconsidered and that TLL should be thought of as a distinct variable from FTP.

|keywords=* Aging
* Emotion regulation
* Future time perspective
* Socioemotional selectivity theory
* Time left in life
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7040126
}}
==STAT3==

{{medline-entry
|title=Atorvastatin-induced senescence of hepatocellular carcinoma is mediated by downregulation of hTERT through the suppression of the IL-6/[[STAT3]] pathway.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32257389
|abstract=Hepatocellular carcinoma (HCC), a hepatic malignancy, has a poor prognosis and contributes to cancer-related death worldwide. Cellular senescence is an anticancer therapeutic strategy that causes irreversible cell cycle arrest and enables immune-mediated clearance of cancer cells. Atorvastatin, an HMG-CoA reductase inhibitor, has been shown to inhibit tumor growth and induce apoptosis or autophagy in malignant tumors. However, whether atorvastatin can induce HCC cell senescence and the mechanisms involved are poorly understood. The effects of atorvastatin-induced senescence were examined in both HCC cells and mouse xenograft models. The phenomenon and mechanism of senescence were examined by cell cycle analysis, senescence-associated β-galactosidase (SA-β-gal) staining and western blotting in HCC cells, and HCC tissues from mice were analyzed by immunohistochemical (IHC) staining. We demonstrated that atorvastatin induced cell growth inhibition and G0/G1 phase cell cycle arrest, leading to senescence in HCC cells. Atorvastatin-induced senescence was independent of p53, p14, and p16, and atorvastatin not only decreased the secretion of IL-6, a major senescence-associated secretory phenotype (SASP) factor, and the phosphorylation of [[STAT3]] but also inhibited the expression of hTERT, a catalytic subunit of telomerase. Supplementation with exogenous IL-6 reversed both atorvastatin-induced suppression of [[STAT3]] phosphorylation and hTERT expression and atorvastatin-induced senescence. Overexpression of constitutively activated [[STAT3]] rescued HCC cells from atorvastatin-induced hTERT suppression and senescence. Moreover, atorvastatin decreased tumor growth in mouse xenograft models. Consistent with these results, atorvastatin decreased the IL-6, p-[[STAT3]], and hTERT levels and increased β-gal expression in tumor sections. Taken together, these data indicate that atorvastatin can induce atypical cellular senescence in HCC cells to inhibit tumor growth, an effect mediated by downregulation of hTERT through suppression of the IL-6/[[STAT3]] pathway.

|keywords=* Cancer therapy
* Senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7105491
}}
==STS==

{{medline-entry
|title=The WRKY53 transcription factor enhances stilbene synthesis and disease resistance by interacting with MYB14 and MYB15 in Chinese wild grape.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32080737
|abstract=Resveratrol is notable not only for its functions in disease resistance in plants but also for its health benefits when it forms part of the human diet. Identification of new transcription factors helps to reveal the regulatory mechanisms of stilbene synthesis. Here, the WRKY53 transcription factor was isolated from the Chinese wild grape, Vitis quinquangularis. Vqwrky53 was expressed in a variety of tissues and responded to powdery mildew infection and to exogenous hormone application. VqWRKY53 was located in the nucleus and had transcriptional activation activity in yeast. A yeast two-hybrid assay and a bimolecular fluorescence complementation assay confirmed that VqWRKY53 interacted physically with VqMYB14 and VqMYB15, which have previously been reported to regulate stilbene synthesis. When Vqwrky53 was overexpressed in grape leaves, the expression of Vq[[STS]]32 and Vq[[STS]]41 and the content of stilbenes were increased. A yeast one-hybrid assay demonstrated that VqWRKY53 could bind directly to the promoters of [[STS]] genes. Overexpression of Vqwrky53 activated β-glucuronidase expression, driven by [[STS]] promoters, and co-expressing Vqwrky53 with VqMYB14 and VqMYB15 showed stronger regulatory functions. Heterologous overexpression of Vqwrky53 in Arabidopsis accelerated leaf senescence and disease resistance to PstDC3000.

|keywords=* Chinese wild grape (Vitis quinquangularis)
* WRKY transcription factor
* disease resistance
* leaf senescence
* stilbene
* transcriptional regulation
|full-text-url=https://sci-hub.do/10.1093/jxb/eraa097
}}
==SUCNR1==

{{medline-entry
|title=[The effect of Mexidol on cerebral mitochondriogenesis at a young age and during aging].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32105271
|abstract=To study the ability of mexidol to induce cerebral mitochondriogenesis in the brain of young and aging rats. Expression level of marker proteins of cerebral mitochondriogenesis was evaluated during treatment with mexidol (20, 40, 100 mg/kg; 20 days; intraperitoneally) in the cerebral cortex of young (3 month) and aging (6, 9, 12, and 15 month) outbred male rats, using the Western blot analysis. It has been shown for the first time that the course injections of mexidol in doses of 40 and 100 mg/kg is accompanied by dose-dependent induction of the succinate receptor [[SUCNR1]] and protein markers of mitochondrial biogenesis: transcription coactivator PGC-1α, transcription factors (NRF1, TFAM), catalytic subunits of respiratory enzymes (NDUV2, NDUV2,cytb, COX2) and ATP synthase (ATP5A) in the cerebral cortex of young and aging outbred male rats. Mexidol-dependent overexpression of subunits of mitochondrial enzymes and PGC-1α is observed only with the course of the drug. The results indicate the ability of mexidol to induce cerebral mitochondriogenesis and eliminate mitochondrial dysfunction in young and aging animals and, thus, exert an effect on one of the key pathogenetic links of the development of disorders in aging and neurodegenerative diseases.
|mesh-terms=* Age Factors
* Aging
* Animals
* Male
* Mitochondria
* Neurodegenerative Diseases
* Picolines
* Rats
* Receptors, G-Protein-Coupled
* Transcription Factors
|keywords=* Western blot analysis
* aging
* cerebral mitochondriogenesis
* mexidol
* mitochondrial dysfunction
* rats
* respiratory enzyme subunits
* succinate receptor
* transcriptional coactivator PGC-1α
|full-text-url=https://sci-hub.do/10.17116/jnevro202012001162
}}
==TEC==

{{medline-entry
|title=Gender Disparity Impacts on Thymus Aging and LHRH Receptor Antagonist-Induced Thymic Reconstitution Following Chemotherapeutic Damage.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32194555
|abstract=One of the main consequences of thymus aging is the decrease in naïve T cell output. This condition accelerates at the onset of puberty, and presents as a major clinical complication for cancer patients who require cytoablative therapy. Specifically, the extensive use of chemotherapeutics, such as cyclophosphamide, in such treatments damage thymic structure and eliminate the existing naïve T cell repertoire. The resulting immunodeficiency can lead to increased incidence of opportunistic infections, tumor growth relapse and/or autoimmune diseases, particularly in older patients. Thus, strategies aimed at rejuvenating the aged thymus following chemotherapeutic damage are required. Previous studies have revealed that sex hormone deprivation in male mice is capable of regenerating the thymic microenvironment following chemotherapy treatment, however, further investigation is crucial to identify gender-based differences, and the molecular mechanisms involved during thymus regeneration. Through phenotypic analyzes, we identified gender-specific alterations in thymocytes and thymic epithelial cell ([[TEC]]) subsets from the onset of puberty. By middle-age, females presented with a higher number of thymocytes in comparison to males, yet a decrease in their Aire  medullary [[TEC]]/thymocyte ratio was observed. This reduction could be associated with an increased risk of autoimmune disease in middle-aged women. Given the concurrent increase in female Aire  c[[TEC]]/thymocyte ratio, we proposed that there may be an impediment in Aire  m[[TEC]]  differentiation, and Aire  c[[TEC]]  as its upstream precursor. The regenerative effects of LHRH receptor antagonist, degarelix, on [[TEC]] subsets was also less pronounced in middle-aged females compared to males, possibly due to slower progression of thymic involution in the former, which presented with greater [[TEC]]  proportions. Furthermore, following cyclophosphamide treatment, degarelix enhanced thymocyte and mature [[TEC]] subset recovery, with faster recovery kinetics observed in females. These events were found to involve both reactivation and proliferation of thymic epithelial progenitor cells. Taken together, the findings from this study portray a relationship between gender disparity and thymus aging, and highlight the potential benefits of LHRH receptor antagonist treatment for thymic regeneration. Further research is required, however, to determine how gender may impact on the mechanisms underpinning these events.

|keywords=* aging
* chemotherapy
* gender
* luteinizing hormone-releasing hormone
* regeneration
* sex hormone deprivation
* thymic epithelial cell
* thymus
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7062683
}}
==TEF==

{{medline-entry
|title=Expression of human HSP27 in yeast extends replicative lifespan and uncovers a hormetic response.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32189112
|abstract=Human HSP27 is a small heat shock protein that modulates the ability of cells to respond to heat shock and oxidative stress, and also functions as a chaperone independent of ATP, participating in the proteasomal degradation of proteins. The expression of HSP27 is associated with survival in mammalian cells. In cancer cells, it confers resistance to chemotherapy; in neurons, HSP27 has a positive effect on neuronal viability in models of Alzheimer's and Parkinson's diseases. To better understand the mechanism by which HSP27 expression contributes to cell survival, we expressed human HSP27 in the budding yeast Saccharomyces cerevisiae under control of different mutant [[TEF]] promoters, that conferred nine levels of graded basal expression, and showed that replicative lifespan and proteasomal activity increase as well as the resistance to oxidative and thermal stresses. The profile of these phenotypes display a dose-response effect characteristic of hormesis, an adaptive phenomenon that is observed when cells are exposed to increasing amounts of stress or toxic substances. The hormetic response correlates with changes in expression levels of HSP27 and also with its oligomeric states when correlated to survival assays. Our results indicate that fine tuning of HSP27 concentration could be used as a strategy for cancer therapy, and also for improving neuronal survival in neurodegenerative diseases.

|keywords=* Aging
* Cancer
* HSP27
* Hormesis
* Neurodegeneratve diseases
* Proteasome
|full-text-url=https://sci-hub.do/10.1007/s10522-020-09869-9
}}
==TERT==

{{medline-entry
|title=Unravelling Cellular Mechanisms of Stem Cell Senescence: An Aid from Natural Bioactive Molecules.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32244882
|abstract=Cellular senescence plays a role in the onset of age-related pathologies and in the loss of tissue homeostasis. Natural compounds of food or plants exert an important antioxidant activity, counteracting the formation of harmful free radicals. In the presence of an intense stressing event, cells activate specific responses to counteract senescence or cell death. In the present paper, we aimed at evaluating the levels of expression of specific markers of senescence, in order to demonstrate that extracts from [i]Myrtus Communis L[/i]. can prevent premature senescence in ADSCs exposed to oxidative stress. Cells were cultured in the presence of [i]Myrtus[/i] extracts for 12-24 and 48 h and then incubated with H O  to induce senescence. We then evaluated the expression of senescence-related markers p16, p19, p21, p53, [[TERT]], c-Myc, and the senescence-associated β-Galactoidase activity. Our results showed that pre-treatment with [i]Myrtus[/i] extracts protects cells from premature senescence, by regulating the cell cycle, and inducing the expression of [[TERT]] and c-Myc. These findings suggest a potential application of these natural compounds in the prevention and treatment of various diseases, counteracting premature senescence and preserving tissue functions.

|keywords=* cellular mechanisms
* gene expression
* nutraceuticals
* oxidative stress
* senescence
* stem cells
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7150900
}}
{{medline-entry
|title=Expression of telomerase reverse transcriptase positively correlates with duration of lithium treatment in bipolar disorder.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32114208
|abstract=Bipolar disorder (BD) may be associated with accelerated cellular aging. However, previous studies on telomere length (TL), an important biomarker of cellular aging, have yielded mixed results in BD. We aimed to evaluate the hypothesis that BD is associated with telomere shortening and whether this is counteracted by long-term lithium treatment. We also sought to determine whether long-term lithium treatment is associated with increased expression of telomerase reverse transcriptase ([[TERT]]), the catalytic subunit of telomerase. We determined TL and [[TERT]] expression in 100 BD I patients and 100 healthy controls. We also genotyped three single nucleotide polymorphisms associated with TL. [[TERT]] expression was significantly increased in BD I patients currently on lithium treatment. [[TERT]] expression was also significantly positively correlated with duration of lithium treatment in patients treated for 24 months or more. However, we did not find any significant effect of lithium treatment on TL. Neither did we find significant differences in TL between BD patients and controls. We suggest that long-term lithium treatment is associated with an increase in the expression of [[TERT]]. We hypothesize that an increase in [[TERT]] expression may contribute to lithium's mood stabilizing and neuroprotective properties by improving mitochondrial function and decreasing oxidative stress.
|mesh-terms=* Adult
* Aging
* Antimanic Agents
* Bipolar Disorder
* Cellular Senescence
* Female
* Humans
* Lithium
* Lithium Compounds
* Male
* Middle Aged
* Mitochondria
* Oxidative Stress
* Polymorphism, Single Nucleotide
* Real-Time Polymerase Chain Reaction
* Telomerase
* Telomere
* Telomere Homeostasis
* Telomere Shortening
|keywords=* Affective disorder
* Aging
* Mitochondria
* Oxidative stress
* TERT
* Telomere
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7334059
}}
==TF==

{{medline-entry
|title=Expression of Transferrin and Albumin in the Sperm-Storage Tubules of Japanese Quail and their Possible Involvement in Long-Term Sperm Storage.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32174770
|abstract=Because of the presence of sperm storage tubules (SSTs) in the utero-vaginal junction (UVJ) in the oviduct, once ejaculated sperm enter the female reproductive tract, they can survive for a prolonged period in domestic birds; however, the specific mechanisms involved in sperm maintenance within the SST remain to be elucidated. In this study, we showed that transferrin ([[TF]]) and albumin (ALB) are expressed in SSTs. When UVJ extracts were subjected to size-exclusion column chromatography, we obtained fractions that extend sperm longevity [i]in vitro[/i]. LC-MS/MS analysis of the two major proteins in the fractions identified these proteins as [[TF]] and ALB. Immunohistochemical analysis using specific antisera against [[TF]] and ALB indicated that both proteins were localized not only in the SSTs, but also in the surface epithelium of the UVJ. When the ejaculated sperm were incubated with either purified [[TF]] or ALB, sperm viability increased after 24 h. These results indicated that oviductal [[TF]] and ALB are involved in the process of sperm storage in SSTs and may open a new approach for technological improvement to prolong sperm longevity [i]in vitro[/i].

|keywords=* Japanese quail
* albumin
* sperm longevity
* sperm storage tubules
* transferrin
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7063080
}}
==TG==

{{medline-entry
|title=Awareness of major cardiovascular risk factors and its relationship with markers of vascular aging: Data from the Brisighella Heart Study.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32249143
|abstract=General population awareness about cardiovascular risk factors is usually low. The aim of the present study was to evaluate the vascular aging of subjects aware and not aware to be hypertensive, hypercholesterolemic, hypertriglyceridemic or diabetics in a general population sample. We interviewed 1652 subjects without atherosclerotic cardiovascular diseases (M: 46.6%, F: 53.4%) about their awareness of hypertension, hypercholesterolemia, hypertriglyceridemia or type 2 diabetes. Then we compared the augmentation index and pulse wave velocity of subjects aware and not aware of the investigated cardiovascular risk factors. 1049 participants declared not to be hypertensive, while 32 were not sure. Among them, respectively, 23.5% and 50% were hypertensive. Subjects not aware of their hypertension had significantly higher aortic blood pressure than aware ones (p < 0.001). 841 participants declared not to be hypercholesterolemic, while 60 were not sure. Among them, respectively, 18.1% and 40% were hypercholesterolemic. Subjects not aware of their hypercholesterolemia had significantly higher augmentation index than the aware ones (p < 0.05). 1226 participants declared not to be hypertriglyceridemic, while 200 were not sure. Among them, respectively, 19.2% and 44% were hypertriglyceridemic. Subjects not aware of their hypertriglyceridemia had significantly higher [[TG]] levels aware ones (p < 0.05), although this seemed to not related to increased arterial stiffness. 1472 participants declared not to be diabetic, while 20 were not sure. Among them, respectively, 2.0% and 25.0% were diabetics. Subjects not aware of their diabetes had significantly higher augmentation index than the aware ones (p < 0.05). In conclusion, the lack of awareness of hypertension and hypercholesterolemia is relatively frequent in the general population and is associated to significantly higher arterial stiffness.
|mesh-terms=* Adolescent
* Adult
* Age Factors
* Aged
* Aged, 80 and over
* Aging
* Biomarkers
* Blood Glucose
* Blood Pressure
* Cardiovascular Diseases
* Cholesterol
* Cross-Sectional Studies
* Diabetes Mellitus
* Female
* Humans
* Hypercholesterolemia
* Hypertension
* Hypertriglyceridemia
* Italy
* Male
* Middle Aged
* Risk Assessment
* Risk Factors
* Triglycerides
* Vascular Stiffness
* Young Adult
|keywords=* Arterial aging
* Awareness
* Epidemiology
* Pulse wave velocity
* Risk factors
|full-text-url=https://sci-hub.do/10.1016/j.numecd.2020.03.005
}}
{{medline-entry
|title=Characterisation of the dynamic nature of lipids throughout the lifespan of genetically identical female and male Daphnia magna.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32221338
|abstract=Lipids play a significant role in regulation of health and disease. To enhance our understanding of the role of lipids in regulation of lifespan and healthspan additional studies are required. Here, UHPLC-MS/MS lipidomics was used to measure dynamic changes in lipid composition as a function of age and gender in genetically identical male and female Daphnia magna with different average lifespans. We demonstrate statistically significant age-related changes in triglycerides ([[TG]]), diglycerides (DG), phosphatidylcholine, phosphatidylethanolamine, ceramide and sphingomyelin lipid groups, for example, in males, 17.04% of [[TG]] lipid species decline with age whilst 37.86% increase in relative intensity with age. In females, 23.16% decrease and 25.31% increase in relative intensity with age. Most interestingly, the rate and direction of change can differ between genetically identical female and male Daphnia magna, which could be the cause and/or the consequence of the different average lifespans between the two genetically identical genders. This study provides a benchmark dataset to understand how lipids alter as a function of age in genetically identical female and male species with different average lifespan and ageing rate.
|mesh-terms=* Aging
* Animals
* Daphnia
* Diglycerides
* Female
* Lipid Metabolism
* Longevity
* Male
* Phosphatidylcholines
* Sphingomyelins
* Triglycerides
|keywords=#f
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7101400
}}
==TH==

{{medline-entry
|title=Quantitative proteomic profiling of the rat substantia nigra places glial fibrillary acidic protein at the hub of proteins dysregulated during aging: Implications for idiopathic Parkinson's disease.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32270889
|abstract=There is a strong correlation between aging and onset of idiopathic Parkinson's disease, but little is known about whether cellular changes occur during normal aging that may explain this association. Here, proteomic and bioinformatic analysis was conducted on the substantia nigra (SN) of rats at four stages of life to identify and quantify protein changes throughout aging. This analysis revealed that proteins associated with cell adhesion, protein aggregation and oxidation-reduction are dysregulated as early as middle age in rats. Glial fibrillary acidic protein (GFAP) was identified as a network hub connecting the greatest number of proteins altered during aging. Furthermore, the isoform of GFAP expressed in the SN varied throughout life. However, the expression levels of the rate-limiting enzyme for dopamine production, tyrosine hydroxylase ([[TH]]), were maintained even in the oldest animals, despite a reduction in the number of dopamine neurons in the SN pars compact(SNc) as aging progressed. This age-related increase in [[TH]] expression per neuron would likely to increase the vulnerability of neurons, since increased dopamine production would be an additional source of oxidative stress. This, in turn, would place a high demand on support systems from local astrocytes, which themselves show protein changes that could affect their functionality. Taken together, this study highlights key processes that are altered with age in the rat SN, each of which converges upon GFAP. These findings offer insight into the relationship between aging and increased challenges to neuronal viability, and indicate an important role for glial cells in the aging process.

|keywords=* RRID:AB_11145309
* RRID:AB_2109791
* RRID:AB_228307
* RRID:AB_228341
* RRID:AB_2336820
* RRID:AB_2631098
* RRID:AB_390204
* RRID:MGI:5651135
* RRID:SCR_001881
* RRID:SCR_002798
* RRID:SCR_003070
* RRID:SCR_004946
* RRID:SCR_005223
* aging
* dopaminergic neuron
* glial fibrillary acidic protein
* proteome
* proteomics
* substantia nigra
|full-text-url=https://sci-hub.do/10.1002/jnr.24622
}}
==TNC==

{{medline-entry
|title=Tenascin-C expression controls the maturation of articular cartilage in mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32066496
|abstract=Expression of the de-adhesive extracellular matrix protein tenascin-C ([[TNC]]) is associated with the early postnatal development of articular cartilage which is both load-dependent and associated with chondrocyte differentiation. We assessed morphological changes in the articular cartilage of [[TNC]] deficient mice at postnatal ages of 1, 4 and 8 weeks compared to age-matched wildtype mice. Cartilage integrity was assessed based on hematoxylin and eosin stained-sections from the tibial bone using a modified Mankin score. Chondrocyte density and cartilage thickness were assessed morphometrically. [[TNC]] expression was localized based on immunostaining. At 8 weeks of age, the formed tangential/transitional zone of the articular cartilage was 27% thicker and the density of chondrocytes in the articular cartilage was 55% lower in wildtype than the [[TNC]]-deficient mice. [[TNC]] protein expression was associated with chondrocytes. No relevant changes were found in mice at 1 and 4 weeks of age. The findings indicate a role of tenascin-C in the post-natal maturation of the extracellular matrix in articular cartilage. This might be a compensatory mechanism to strengthen resilience against mechanical stress.
|mesh-terms=* Aging
* Animals
* Cartilage, Articular
* Cell Count
* Genotype
* Mice
* Tenascin
|keywords=* Adhesion
* Articular cartilage
* Cartilage defect
* Cell density
* Knock-out mouse
* Load
* Tenascin C
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7027060
}}
==TNF==

{{medline-entry
|title=Synergistic Antitumor Efficacy of Magnetohyperthermia and Poly(lactic-co-glycolic acid)-Encapsulated Selol in Ehrlich Breast Adenocarcinoma Treatment in Elderly Swiss Mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32252879
|abstract=Nanobiotechnology strategies for cancer treatments are currently being tested with increasing interest, except in elderly groups. It is well established that breast cancer incidence increases with age and that traditional therapies usually generate severe adverse effects, especially for elderly groups. To investigate if the benefits of nanotechnology could be extended to treating cancer in this group, citrate-coated maghemite nanoparticles (NpCit) were used for magnetohyperthermia (MHT) in combination with the administration of PLGA-Selol nanocapsule (NcSel), a formulation with antioxidant and antitumor activity. The combined therapies significantly inhibited breast Ehrlich tumor growth and prevented metastases to the lymph nodes, liver and lungs until 45 days after tumor induction, a better result than the group undergoing conventional drug treatment. The levels of [[TNF]]-α, associated with poor prognosis in Ehrlich tumor, were also normalized. Therefore, the results evidenced the potential use of these therapies for future clinical trials in elderly breast cancer patients.
|mesh-terms=* Adenocarcinoma
* Aging
* Animals
* Cell Line, Tumor
* Glycols
* Humans
* Mice
* Nanoparticles
* Polylactic Acid-Polyglycolic Acid Copolymer
* Selenium Compounds
|keywords=#f
|full-text-url=https://sci-hub.do/10.1166/jbn.2020.2890
}}
{{medline-entry
|title=Pinitol suppresses [[TNF]]-α-induced chondrocyte senescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32200264
|abstract=Osteoarthritis (OA) is a highly prevalent joint disorder that is tightly correlated with age. As the body ages, cell replication and function decline until homeostasis can no longer be maintained. This process involves cellular senescence as well as replicative senescence. Telomere length, cell cycle arrest, expression of p16 and p53, and the release of senescence-associated β-galactosidase (SA-β-Gal) are all markers of cell senescence. In OA joints, chondrocytes undergo cellular senescence prematurely, thereby ceasing to synthesize and maintain cartilage tissue. Upregulation of proinflammatory cytokines, such as tumor necrosis factor-α ([[TNF]]-α), and oxidative stress induced by overproduction of reactive oxygen species (ROS) are key events in the pathogenesis of OA. In the present study, we investigated the effects of pinitol, a naturally occurring compound, on the effects of [[TNF]]-α on chondrocyte senescence and cell cycle arrest. We found that pinitol has a favorable safety profile in terms of cell viability. Pinitol significantly inhibited cellular senescence and cell cycle arrest in the G0/G1 phase induced by [[TNF]]-α. We also found that pinitol could inhibit [[TNF]]-α-induced increased telomerase activity and expression of p16 and p53. Importantly, we found that the effects of pinitol may be mediated through rescue of Nrf2 signaling, which is recognized as a key protective factor in OA. This finding was verified through a Nrf2 silencing experiment using Nrf2 siRNA. Together, our findings reveal the potential of pinitol as a safe therapeutic option for the prevention of OA-associated chondrocyte senescence and oxidative stress.

|keywords=* Cellular senescence
* Nrf2
* Osteoarthritis
* Pinitol
* TNF-α
|full-text-url=https://sci-hub.do/10.1016/j.cyto.2020.155047
}}
{{medline-entry
|title=[Aging of skin fibroblasts: genetic and epigenetic factors.]
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32160428
|abstract=Gerontocosmetology is the rapid developing knowledge area that has a very large applied meaning. Herewith a lot of information about skin aging and geroprotectors for skin rejuvenation hasn't a scientific background. Thus, understanding the fundamental mechanisms of skin aging becomes the actual task of molecular gerontology. Skin fibroblasts are the polyfunctional cell population that synthesize a number of biologically active substances and participate in maintaining of extracellular matrix homeostasis, skin hydratation and endocrine and immune function. In the review genetic (accumulation of nuclear and mitochondrial DNA mistakes) and epigenetic factors of skin fibroblasts aging are described. Role of AP-1, NF-κB, c-jun, CCN1, TGF-β, [[TNF]]-α, MMP-1, MMP-3, MMP-8, MMP-9 and glycation in skin fibroblasts aging are discussed. There are some data about decreasing of skin fibroblasts ability to migration and synthesis of paxillins and aquaporin-3 (AQP3) during aging. Role of hormonal regulation in skin fibroblasts aging are described. Geroprotective action of melatonin to skin fibroblasts are showed. Reviewed molecular-cellular aspects of skin fibroblasts aging can be take into consideration for scientific background of using of cosmetic products for retarding of skin aging rate.
|mesh-terms=* Cells, Cultured
* Epigenesis, Genetic
* Fibroblasts
* Humans
* Skin Aging
|keywords=* aging
* melatonin
* signal molecules
* skin fibroblasts

}}
{{medline-entry
|title=Functional and traditional training improve muscle power and reduce proinflammatory cytokines in older women: A randomized controlled trial.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32151735
|abstract=Aging is a natural process that, even in the nonattendance of complex diseases, is associated with a numerous behavioral change that attributes reduced muscle mass, power, strength and function. In addition, aging linked to low-grade inflammatory status, characterized by increased plasma concentrations of inflammatory cytokines such as [[TNF]]-α and IL-6. Physical exercise is the main non-pharmacological strategy for improving the physical fitness of the aged individuals. However, it is still controversial whether exercise can reduce aging-mediated inflammation. To analyze the effects of functional (FT) and traditional (TT) training practice on muscle power and inflammatory profile in physically active older women. The study has been performed for twenty-six weeks in which twenty-four weeks utilized for training sessions and two weeks for physical and biochemical assessments. Forty-three older women (age FT: 64.25 ± 4.70, range: 60-75; TT: 64.90 ± 3.03, range: 60-71; Control: 65.91 ± 5.79, range: 60-75) were randomly divided into three groups: Functional (FT; n = 16); Traditional (TT; n = 16) training groups; and Control Group (CG; n = 11) respectively. Muscle power tests were performed by push (Bench press) and squatting (Squat) actions. The jumping ability was performed through Counter Movement Jump (CMJ). In addition, isometric strength were assessed by Hand Grip Test. Plasma cytokine concentration was measured using flow cytometry. Functional and traditional training sessions subjected to aged women demonstrated a significant enhancement in their physical activity and muscle power. The trained individuals from above two groups showed significant improvements in all analyzed parameters excluding hand-grip. Functional and traditional training exercise reduced the plasma concentrations of [[TNF]]-α (FT: p = 0.0001; TT: p = 0.0410) and whereas FT group has reduced IL-6 (p = 0.0072), but did not affect the alterations of pre and post measurements of IL-2 (FT: p = 0.0651; TT: p = 0.2146) and IL-10 values (FT: p = 0.2658; TT: p = 0.3116). There was no significant difference in any of the test parameters between FT and TT groups. The functional and traditional training practices showed equivalent beneficial outcomes by increasing muscle power and reducing systemic markers associated with inflammation.

|keywords=* Aging
* Cytokines.
* Dynapenia
* Inflamm-aging
|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110920
}}
{{medline-entry
|title=Associations of [[TNF]]-α -308 G>A and [[TNF]]-β 252 A>G with Physical Function and BNP-Rugao Longevity and Ageing Study.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115620
|abstract=To explore the associations of [[TNF]]-α -308 G>A (rs1800629) and [[TNF]]-β 252 A>G (rs909253) with physical function and plasma B-type natriuretic peptide (BNP). Data of 1747 community-dwelling elders from the ageing arm of the Rugao Longevity and Ageing Study was used. Physical function was measured by handgrip strength, Timed Up and Go (TUG) test and 5-meter walking test (5MWT). AA genotype of the [[TNF]]-α -308 G>A was associated with higher mean time of TUG test and 5MWT (multivariable adjusted β=5.75 and 5.70, respectively, p<0.05), compared with GG genotype. For the [[TNF]]-β 252 A>G polymorphism, GG genotype was associated with higher mean time of TUG test and 5MWT (multivariable adjusted β=1.55 and 0.83, respectively, p<0.05) and lower handgrip strength (multivariable adjusted β=-0.69, p<0.05), compared with AA genotype. Further, GG was associated with greater odds of low handgrip strength (OR=1.47, 95% CI=1.06-2.04), low speed of TUG test (OR=1.87, 95% CI=1.20-2.01) and elevated BNP (OR=1.30, 95% CI=1.08-1.84). GG also interacted with elevated BNP to be associated with greater odds of low handgrip strength and 5MWT. [[TNF]]-β 252 A>G was associated with physical function measurements, plasma BNP level, and odds of elevated BNP in an elderly population. [[TNF]]-β 252 A>G also interacted with elevated BNP to be associated with greater odds of physical function measurements.
|mesh-terms=* Aged
* Aged, 80 and over
* Aging
* Female
* Humans
* Longevity
* Male
* Natriuretic Peptide, Brain
* Tumor Necrosis Factor-alpha
|keywords=* Physical function
* TNF-α -308 G>A polymorphism
* TNF-β 252 A>G polymorphism
* plasma BNP
* population study.
|full-text-url=https://sci-hub.do/10.1007/s12603-020-1336-1
}}
{{medline-entry
|title=3D TECA hydrogel reduces cellular senescence and enhances fibroblasts migration in wound healing.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32104405
|abstract=This study was designed to investigate the effect of 3D TECA hydrogel on the inflammatory-induced senescence marker, and to assess the influence of the gel on the periodontal ligament fibroblasts (PDLFs) migration in wound healing [i]in vitro[/i]. PDLFs were cultured with 20 ng/ml [[TNF]]-α to induce inflammation in the presence and absence of 50 µM 3D TECA gel for 14 d. The gel effect on the senescence maker secretory associated-β-galactosidase (SA-β-gal) activity was measured by a histochemical staining. Chromatin condensation and DNA synthesis of the cells were assessed by 4',6-diamidino-2-phenylindole and 5-ethynyl-2'-deoxyuridine fluorescent staining respectively. For evaluating fibroblasts migration, scratch wound healing assay and Pro-Plus Imaging software were used. The activity of senescence marker, SA-β-gal, was positive in the samples with [[TNF]]-α-induced inflammation. SA-β-gal percentage is suppressed (>65%, [i]P[/i] < 0.05) in the treated cells with TECA gel as compared to the non-treated cells. Chromatin foci were obvious in the non-treated samples. DNA synthesis was markedly recognized by the fluorescent staining in the treated compared to non-treated cultures. Scratch wound test indicated that the cells migration rate was significantly higher (14.9 µm /h, [i]P[/i] < 0.05) in the treated versus (11 µm /h) for control PDLFs. The new formula of 3D TECA suppresses the inflammatory-mediated cellular senescence and enhanced fibroblasts proliferation and migration. Therefore, 3D TECA may be used as an adjunct to accelerate repair and healing of periodontal tissues.

|keywords=* 3D TECA
* Cellular senescence
* Fibroblast migration
* SA-β-gal
* TNF-α
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7032142
}}
{{medline-entry
|title=Regulatory Effect of Anwulignan on the Immune Function Through Its Antioxidation and Anti-Apoptosis in D-Galactose-Induced Aging Mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32099340
|abstract=Aging is a spontaneous and inevitable phenomenon of biology, which can lead to the gradual deterioration of tissues and organs. One of the age-related deterioration processes is immunosenescence, which leads to changes in the function of immune systems, including immune cells and associated cytokines. A proper modulation of immune responses can improve the age-related immunosenescence process and then reach healthy aging. [i]Schisandra sphenanthera[/i], a traditional Chinese medicine, has been used as both a medicine and a nutritional supplement for thousands of years. Anwulignan, a monomer compound of [i]Schisandra sphenanthera[/i] lignans, has been reported to possess an immunomodulatory effect. Therefore, this study was designed to further explore whether Anwulignan could also modulate the immune functions in aging model mice and the underlying mechanism. D-galactose (D-gal) is often used as an inducer of immunosenescence in animals. In this study, a mice model was created by subcutaneous D-gal (220 mg kg ) for successive 42 days. Then, the blood and spleen tissue samples were taken for the analysis and observation of cytokine levels, immunoglobulin levels, leukocyte numbers, and the phagocytic activity of macrophages, as well as the histological changes, the proliferation ability of lymphocytes, and the biochemical parameters in the spleen tissue. Anwulignan significantly increased the serum levels of IL-2, IL-4, IFN-γ, lgG, lgM, and lgA, decreased the content of [[TNF]]-α and IL-6 in the aging mice, and increased the blood leukocyte number, the phagocytic activity, the lymphocyte proliferation, and the spleen index in vitro. Anwulignan also significantly increased the activities of SOD and GSH-Px, decreased the contents of MDA and 8-OHdG in the spleen tissue, up-regulated the expressions of Nrf2, HO-1, and Bcl2, down-regulated the expressions of Keap1, Caspase-3, and Bax in the spleen cells, and reduced the apoptosis of spleen lymphocytes. Anwulignan can restore the immune function that is declined in D-gal-induced aging mice partly related to its antioxidant capacity by activating the Nrf2/ARE pathway and downstream enzymes, as well as its anti-apoptotic effect by regulating Caspase-3 and the ratio of Bcl2 to Bax in the spleen.
|mesh-terms=* Animals
* Antioxidants
* Apoptosis
* Cytokines
* Immunologic Factors
* Immunosenescence
* Male
* Medicine, Chinese Traditional
* Mice
* Models, Animal
* NF-E2-Related Factor 2
* Oxidative Stress
* Phytochemicals
* Schisandra
* Spleen
|keywords=* Anwulignan
* anti-apoptosis
* antioxidation
* immunosenescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996228
}}
{{medline-entry
|title=Pretreatment Frailty Is Independently Associated With Increased Risk of Infections After Immunosuppression in Patients With Inflammatory Bowel Diseases.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32105728
|abstract=Infections are an important adverse effect of immunosuppression for treatment of inflammatory bowel diseases (IBDs). However, risk of infection cannot be sufficiently determined based on patients' ages or comorbidities. Frailty has been associated with outcomes of patients with other inflammatory diseases. We aimed to determine the association between frailty and risk of infections after immunosuppression for IBD. We performed a cohort study of 11,001 patients with IBD, using a validated frailty definition based on International Classification of Disease codes to identify patients who were frail vs fit in the 2 years before initiation of an anti-tumor necrosis factor ([[TNF]]) or immunomodulator therapy, from 1996 through 2010. Our primary outcome was an infection in the first year after treatment. We constructed multivariable logistic regression models, adjusting for clinically pertinent confounders (age, comorbidities, steroid use, and combination therapy) to determine the association between frailty and posttreatment infections. There were 1299 patients treated with an anti-[[TNF]] agent and 2676 patients treated with an immunomodulator. In this cohort, 5% of patients who received anti-[[TNF]] therapy and 7% of patients who received an immunomodulator were frail in the 2 years before immunosuppression. Frail patients were older and had more comorbidities. Higher proportions of frail patients developed infections after treatment (19% after [[TNF]] and 17% after immunomodulators) compared with fit patients (9% after [[TNF]] and 7% after immunomodulators; P < .01 for frail vs fit in both groups). Frail patients had an increased risk of infection after we adjusted for age, comorbidities, and concomitant medications (anti-[[TNF]] adjusted odds ratio, 2.05 [95% confidence interval, 1.07-3.93] and immunomodulator adjusted odds ratio, 1.81 [95% confidence interval, 1.22-2.70]). Frailty was associated with infections after immunosuppression in patients with IBD after we adjust for age and comorbidities. Systematic assessment and strategies to improve frailty might reduce infection risk in patients with IBD.

|keywords=* Aging
* Immunosuppression
* Side Effect
* Thiopurine
|full-text-url=https://sci-hub.do/10.1053/j.gastro.2020.02.032
}}
==TP53==

{{medline-entry
|title=Mutational spectrum and dynamics of clonal hematopoiesis in anemia of older individuals.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32243522
|abstract=Anemia is a major and currently poorly understood clinical manifestation of hematopoietic aging. Upon aging, hematopoietic clones harboring acquired leukemia-associated mutations expand and become detectable, now referred to as clonal hematopoiesis (CH). To investigate the relationship between CH and anemia of the elderly, we explored the landscape and dynamics of CH in older individuals with anemia. From the prospective, population-based Lifelines cohort (n = 167 729), we selected all individuals at least 60 years old who have anemia according to World Health Organization criteria (n = 676) and 1:1 matched control participants. Peripheral blood of 1298 individuals was analyzed for acquired mutations at a variant allele frequency (VAF) of 1% or higher in 27 driver genes. To track clonal evolution over time, we included all available follow-up samples (n = 943). CH was more frequently detected in individuals with anemia (46.6%) compared with control individuals (39.1%; P = .007). Although no differences were observed regarding commonly detected DTA mutations (DNMT3A, TET2, ASXL1) in individuals with anemia compared with control individuals, other mutations were enriched in the anemia cohort, including [[TP53]] and SF3B1. Unlike individuals with nutrient deficiency (P = .84), individuals with anemia of chronic inflammation and unexplained anemia revealed a higher prevalence of CH (P = .035 and P = .017, respectively) compared with their matched control individuals. Follow-up analyses revealed that clones may expand and decline, generally showing only a subtle increase in VAF (mean, 0.56%) over the course of 44 months, irrespective of the presence of anemia. Specific mutations were associated with different growth rates and propensities to acquire an additional hit. In contrast to smaller clones (<5% VAF), which did not affect overall survival, larger clones were associated with increased risk for death.
|mesh-terms=* Age Factors
* Aged
* Aging
* Anemia
* Female
* Hematopoiesis
* Humans
* Kaplan-Meier Estimate
* Male
* Middle Aged
* Mutation
* Prospective Studies
|keywords=#f
|full-text-url=https://sci-hub.do/10.1182/blood.2019004362
}}
==TRAF3==

{{medline-entry
|title=[[TRAF3]], a Target of MicroRNA-363-3p, Suppresses Senescence and Regulates the Balance Between Osteoblastic and Adipocytic Differentiation of Rat Bone Marrow-Derived Mesenchymal Stem Cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32111144
|abstract=Bone marrow-derived mesenchymal stem cells (BMSCs) have the potential to differentiate into osteoblasts or adipocytes, and an imbalance between adipogenesis and osteogenesis causes age-related bone loss. In this study, we determined the influence of tumor necrosis factor receptor-associated factor 3 ([[TRAF3]]) on senescence and osteoblastic and adipocytic differentiation of rat BMSCs. [[TRAF3]] expression increased during osteogenic differentiation but decreased during adipocytic differentiation of rat BMSCs, and compared with day 0 cultures, on day 14, the differences were significant. Overexpression of [[TRAF3]] significantly promoted BMSC osteogenic differentiation and suppressed adipogenic differentiation and senescence. Furthermore, [i]Traf3[/i] was determined to be a target gene of miR-363-3p in BMSCs, and [[TRAF3]] expression in BMSCs was reduced by miR-363-3p overexpression. This overexpression attenuated the effects of [[TRAF3]] on BMSC adipogenic differentiation, osteogenic differentiation, and senescence. Taken together, these results uncovered the mechanism by which [[TRAF3]] promotes BMSC osteogenic differentiation and suppresses adipogenic differentiation and senescence, indicating that the miR-363-3p-[[TRAF3]] axis might be a novel therapeutic target for BMSC-based bone tissue engineering in osteoporosis.

|keywords=* TRAF3
* adipogenic differentiation
* bone marrow-derived mesenchymal stem cells
* miR-363-3p
* osteogenic differentiation
* senescence
|full-text-url=https://sci-hub.do/10.1089/scd.2019.0276
}}
==TRIM21==

{{medline-entry
|title=[[TRIM21]] overexpression promotes tumor progression by regulating cell proliferation, cell migration and cell senescence in human glioma.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32064156
|abstract=Molecular biomarkers combined with histopathological examination are of critical importance in the diagnosis and treatment of gliomas. Although recent studies have shown that many tripartite motif-containing (TRIM) family proteins could regulate the cell cycle, cell proliferation, and differentiation in cancers, the precise role of [[TRIM21]] has been unknown in glioma. In this study, we analyzed [[TRIM21]], which was upregulated in gliomas and identified its role in tumor proliferation, migration and drug resistance. By using immunohistochemical analysis, we found that the expression level of [[TRIM21]] was upregulated in glioma specimens and the higher expression level of [[TRIM21]] was associated with poorer clinical outcomes in glioma patients. Moreover, we demonstrated that [[TRIM21]] could act as a regulator of the proliferation, cell cycle, and migration of glioma cells by gain- and loss-of function assays in vitro. In vivo, [[TRIM21]] could also modulate glioma progression in murine intracranial xenografts. Furthermore, we found that [[TRIM21]] suppressed cellular senescence via the p53-p21 pathway, and increased drug resistance in glioma cells by RNA-seq analysis, SA-[i]β[/i]-Gal activity assay, and Cell Counting Kit-8 (CCK-8) assay. These results indicated that [[TRIM21]] is a novel regulator in the diagnosis, prognosis, and therapy of gliomas.

|keywords=* Glioma
* TRIM21
* cell senescence
* drug resistance
* p53-p21 pathway
* prognosis
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7017742
}}
==TST==

{{medline-entry
|title=Adaptations in mechanical muscle function, muscle morphology, and aerobic power to high-intensity endurance training combined with either traditional or power strength training in older adults: a randomized clinical trial.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32239311
|abstract=There is a lack of information on the effects of power training (PT) as an alternative to traditional strength training ([[TST]]) during concurrent training (CT) in older individuals. This study aimed to verify the neuromuscular adaptations that occurred following 16-week interventions with two CT models in older men: high-intensity interval training (HIIT) combined with either [[TST]] or PT. Thirty-five older men (65.8 ± 3.9 years) were randomly assigned into one of two training groups CTS: [[TST]] + HIIT (n = 18) or CTP: PT + HIIT (n = 17). CTS performed resistance training at intensities ranging from 65 to 80% of 1 RM at slow controlled speed, whereas CTP trained at intensities ranging from 40 to 60% of 1 RM at maximal intentional speed. Lower body one-repetition maximum (1 RM), isometric rate of force development (RFD), countermovement jump (CMJ) muscle power output, quadriceps femoris muscles thickness (QF MT), and peak oxygen uptake (VO ) were assessed before training and after 8 and 16 weeks of CT. Groups improved similarly in all primary outcomes (P < 0.05), with mean increases ranging: 1 RM (from 39.4 to 75.8%); RFD (from 9.9 to 64.8%); and CMJ muscle power (from 1.8 to 5.2%). Significant increases (P < 0.05) were observed in all secondary outcomes (QF MT, specific tension and VO ) with no differences between groups. CT models were effective for improving maximal and explosive force (1 RM, RFD, and CMJ power), QF MT, and VO . Moreover, despite that using lower loading intensities, PT induced similar adaptations to those of [[TST]].

|keywords=* Aging
* Concurrent training
* Explosive force
* Functional capacity
* HIIT
|full-text-url=https://sci-hub.do/10.1007/s00421-020-04355-z
}}
==U2AF1==

{{medline-entry
|title=Isobaric tags for relative and absolute quantitation (iTRAQ)-based proteomic analysis of mRNA splicing relevant proteins in aging HSPCs.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32141009
|abstract=HSPC (hematopoietic stem/progenitor cell) aging was closely associated with the organism aging, senile diseases and hematopoietic related diseases. Therefore, study on HSPC aging is of great significance to further elucidate the mechanisms of aging and to treat hematopoietic disease resulting from HSPC aging. Little attention had been paid to mRNA splicing as a mechanism underlying HSPC senescence. We used our lab's patented in vitro aging model of HSPCs to analyze mRNA splicing relevant protein alterations with iTRAQ-based proteomic analysis. We found that not only the notable mRNA splicing genes such as SR, hnRNP, WBP11, Sf3b1, Ptbp1 and [[U2AF1]] but also the scarcely reported mRNA splicing relevant genes such as Rbmxl1, Dhx16, Pcbp2, Pabpc1 were significantly down-regulated. We further verified their gene expressions by qRT-PCR. In addition, we reported the effect of Spliceostatin A (SSA), which inhibits mRNA splicing in vivo and in vitro, on HSPC aging. It was concluded that mRNA splicing emerged as an important factor for the vulnerability of HSPC aging. This study improved our understanding of the role of mRNA splicing in the HSPC aging process.

|keywords=* Aging
* DEPs
* HSPC
* iTRAQ
* mRNA splicing
|full-text-url=https://sci-hub.do/10.1007/s40520-020-01509-z
}}
==UCP1==

{{medline-entry
|title=Lack of [[UCP1]] stimulates fatty liver but mediates [[UCP1]]-independent action of beige fat to improve hyperlipidemia in Apoe knockout mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32179129
|abstract=Brown adipose tissue (BAT) plays a critical role in lipid metabolism and may protect from hyperlipidemia; however, its beneficial effect appears to depend on the ambient temperature of the environment. In this study, we investigated the effects of uncoupling protein 1 ([[UCP1]]) deficiency on lipid metabolism, including the pathophysiology of hyperlipidemia, in apolipoprotein E knockout (APOE-KO) mice at a normal (23 °C) and thermoneutral (30 °C) temperature. Unexpectedly, [[UCP1]] deficiency caused improvements in hyperlipidemia, atherosclerosis, and glucose metabolism, regardless of an increase in hepatic lipid deposition, in Ucp1/Apoe double-knockout (DKO) mice fed a high-fat diet at 23 °C, with BAT hyperplasia and robust browning of inguinal white adipose tissue (IWAT) observed. Proteomics and gene expression analyses revealed significant increases in many proteins involved in energy metabolism and strong upregulation of brown/beige adipocyte-related genes and fatty acid metabolism-related genes in browned IWAT, suggesting an induction of beige fat formation and stimulation of lipid metabolism in DKO mice at 23 °C. Conversely, mRNA levels of fatty acid oxidation-related genes decreased in the liver of DKO mice. The favorable phenotypic changes were lost at 30 °C, with BAT whitening and disappearance of IWAT browning, while fatty liver further deteriorated in DKO mice compared with that in APOE-KO mice. Finally, longevity analysis revealed a significant lifespan extension of DKO mice compared with that of APOE-KO mice at 23 °C. Irrespective of the fundamental role of [[UCP1]] thermogenesis, our results highlight the importance of beige fat for the improvement of hyperlipidemia and longevity under the atherogenic status at normal room temperature.

|keywords=* Apoe knockout mice
* Beige fat
* Gene expression
* Hyperlipidemia
* Longevity
* Uncoupling protein 1
|full-text-url=https://sci-hub.do/10.1016/j.bbadis.2020.165762
}}
==VDAC1==

{{medline-entry
|title=Changes in the expression of oxidative phosphorylation complexes in the aging intestinal mucosa.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32173460
|abstract=Mitochondria produce cellular energy via oxidative phosphorylation (OXPHOS), mediated by respiratory chain complexes I to IV and ATP synthase (complex V). Mitochondrial respiratory complexes have been shown to decline with age in several tissues. As the intestinal epithelium is a tissue with a high energy demand, the aim of the present study was to establish whether the expression profile of OXPHOS subunits in the intestinal mucosa changes during the aging process. Biopsies of intestinal mucosa with no evidence of endoscopic or histomorphologic abnormalities, taken from 55 patients (mean age 42 years, age range 4-82 years; 62% female), were divided into four age groups (4-19, 20-39, 40-59, ≥60 years). Sections from different intestinal segments (terminal ileum, ascending colon, and sigmoid colon/rectum) were stained immunohistochemically (IHC) for subunits of OXPHOS complexes I-V and the voltage-dependent anion-selective channel 1 protein ([[VDAC1]], porin), a marker of mitochondrial mass. Scores for IHC staining were determined by multiplication of the staining intensity and the percentage of positive cells. In addition, the numbers of intestinal crypts staining positive, partly positive, and negative were assessed. The average protein expression levels of OXPHOS subunits increased continuously from childhood onward, peaked in persons aged 20 to 59 years, and declined thereafter. This was seen for complexes II to V in the terminal ileum, complexes I to V in the ascending colon, and complexes I to IV in the sigmoid colon/rectum. Across all age groups, no effect of age on expression of the porin subunit [[VDAC1]] was detected. The number of complex I- and IV-negative crypts in different intestinal segments increased with age. The protein expression levels of OXPHOS complexes increases from childhood onward and declines in elderly individuals, while the numbers of crypts with partial or complete loss of expression of complexes I and IV increase continuously with age. These data suggest that the continued reductions in the levels of mitochondrial OXPHOS complexes in crypts might be compensated in adulthood, but that, ultimately, reduced expression levels occur in persons aged 60 years and older. These findings raise two important questions: first, can the process of aging could be delayed through (pharmacological) intervention of mitochondrial pathways, and second, pathophysiologically, are these findings associated with disorders of the intestinal mucosa, e.g. inflammation?

|keywords=* Aging
* Colonic crypt
* Expression
* Intestine
* Mitochondria
* OXPHOS
|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110924
}}
==WNT3A==

{{medline-entry
|title=Chronic WNT/β-catenin signaling induces cellular senescence in lung epithelial cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109549
|abstract=The rapid expansion of the elderly population has led to the recent epidemic of age-related diseases, including increased incidence and mortality of chronic lung diseases, such as Idiopathic Pulmonary Fibrosis (IPF). Cellular senescence is a major hallmark of aging and has a higher occurrence in IPF. The lung epithelium represents a major site of tissue injury, cellular senescence and aberrant activity of developmental pathways such as the WNT/β-catenin pathway in IPF. The potential impact of WNT/β-catenin signaling on alveolar epithelial senescence in general as well as in IPF, however, remains elusive. Here, we characterized alveolar epithelial cells of aged mice and assessed the contribution of chronic WNT/β-catenin signaling on alveolar epithelial type (AT) II cell senescence. Whole lungs from old (16-24 months) versus young (3 months) mice had relatively less epithelial (EpCAM ) but more inflammatory (CD45 ) cells, as assessed by flow cytometry. Compared to young ATII cells, old ATII cells showed decreased expression of the ATII cell marker Surfactant Protein C along with increased expression of the ATI cell marker Hopx, accompanied by increased WNT/β-catenin activity. Notably, when placed in an organoid assay, old ATII cells exhibited decreased progenitor cell potential. Chronic canonical WNT/β-catenin activation for up to 7 days in primary ATII cells as well as alveolar epithelial cell lines induced a robust cellular senescence, whereas the non-canonical ligand WNT5A was not able to induce cellular senescence. Moreover, chronic [[WNT3A]] treatment of precision-cut lung slices (PCLS) further confirmed ATII cell senescence. Simultaneously, chronic but not acute WNT/β-catenin activation induced a profibrotic state with increased expression of the impaired ATII cell marker Keratin 8. These results suggest that chronic WNT/β-catenin activity in the IPF lung contributes to increased ATII cell senescence and reprogramming. In the fibrotic environment, WNT/β-catenin signaling thus might lead to further progenitor cell dysfunction and impaired lung repair.

|keywords=* ATII cells
* Aging
* Cellular senescence
* IPF
* WNT signaling
|full-text-url=https://sci-hub.do/10.1016/j.cellsig.2020.109588
}}
==XDH==

{{medline-entry
|title=Enhancing xanthine dehydrogenase activity is an effective way to delay leaf senescence and increase rice yield.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32162142
|abstract=Xanthine dehydrogenase ([[XDH]]) is an important enzyme in purine metabolism. It is involved in regulation of the normal growth and non-biological stress-induced ageing processes in plants. The present study investigated [[XDH]]'s role in regulating rice leaf senescence. We measured physical characteristics, chlorophyll content and fluorescence parameters, active oxygen metabolism, and purine metabolism in wild-type Kitaake rice (Oryza sativa L.), an Os[[XDH]] over-expression transgenic line (OE9), and an Os[[XDH]] RNA interference line (Ri3) during different growth stages. The expression patterns of the Os[[XDH]] gene confirmed that [[XDH]] was involved in the regulation of normal and abiotic stress-induced ageing processes in rice. There was no significant difference between the phenotypes of transgenic lines and wild type at the seedling stage, but differences were observed at the full heading and maturation stages. The OE9 plants were taller, with higher chlorophyll content, and their photosystems had stronger light energy absorption, transmission, dissipation, and distribution capacity, which ultimately improved the seed setting rate and 1000-seed weight. The opposite effect was found in the Ri3 plants. The OE9 line had a strong ability to remove reactive oxygen species, with increased accumulation of allantoin and alantoate. Experimental spraying of allantoin on leaves showed that it could alleviate chlorophyll degradation and decrease the content of H O  and malonaldehyde (MDA) in rice leaves after the full heading stage. The urate oxidase gene (UO) expression levels in the interference line were significantly lower than those in the over-expression line and wild-type lines. The allantoinase (ALN) and allantoate amidinohydrolase (AAH) genes had significantly higher expression in the Ri3 plants than the in OE9 or wild-type plants, with OE9 plants showing the lowest levels. The senescence-related genes ACD1, WRKY23, WRKY53, SGR, XERO1, and GH27 in Ri3 plants had the highest expression levels, followed by those in the wild-type plants, with OE9 plants showing the lowest levels. These results suggest that enhanced activity of [[XDH]] can regulate the synthesis of urea-related substances, improve plant antioxidant capacity, effectively delay the ageing process in rice leaves, and increase rice yield.

|keywords=* Allantoin
* Reactive oxygen species
* Rice (Oryza sativa L.)
* Senescence
* Xanthine dehydrogenase
* Yield
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7065298
}}
==ZEB2==

{{medline-entry
|title=miR-200b regulates cellular senescence and inflammatory responses by targeting [[ZEB2]] in pulmonary emphysema.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32070140
|abstract=Smoking is an important factor in the pathogenesis of chronic obstructive pulmonary disease (COPD), which is commonly characterised by cellular senescence and inflammation. Recently, miR-200b has emerged as an important target to cure lung disease; however, the function of miR-200b in reducing cellular senescence and inflammatory responses has not been reported. In this study, we found that miR-200b was downregulated in the lungs of COPD model mice, and its expression is correlated with cellular senescence and inflammatory responses. We hypothesised that miR-200b may be a potential novel therapy for treating COPD. We performed senescence-Associated-β-galactosidase (SA-β-GAL) staining, western blot, qRT-PCR and ELISA; our data suggested that miR-200b is an anti-aging factor in the lungs that is involved in inflammatory responses. We also confirmed that [[ZEB2]] (Zinc finger E-box binding homeobox 2) is a target gene of miR-200b using luciferase reporter assay. In addition, we verified the function of [[ZEB2]] in cellular senescence and inflammatory responses through transfection experiments. Moreover, we found that the protective effects of miR-200b are inhibited when cells overexpress the [[ZEB2]] protein. In conclusion, our results suggest that miR-200b may attenuate cellular senescence and inflammatory responses by targeting [[ZEB2]] in pulmonary emphysema.
|mesh-terms=* Animals
* Cell Line
* Cellular Senescence
* Disease Models, Animal
* Gene Expression
* Gene Expression Regulation
* Inflammation
* Lung
* Mice
* MicroRNAs
* Pulmonary Emphysema
* Zinc Finger E-box Binding Homeobox 2
|keywords=* ZEB2
* cellular senescence
* inflammation
* miR-200b
* pulmonary emphysema
|full-text-url=https://sci-hub.do/10.1080/21691401.2020.1725029
}}
@@ Строка 1: / Строка 1: @@
 __NOTOC__
-==A2M==
-{{medline-entry
-|title=Age-Dependent Variation in Glycosylation Features of Alpha-2-Macroglobulin.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31489526
-|mesh-terms=* Adult
-* Aging
-* Electrophoresis, Gel, Two-Dimensional
-* Glycosylation
-* Humans
-* Infant, Newborn
-* Polysaccharides
-* Pregnancy-Associated alpha 2-Macroglobulins
-* Protein Isoforms
-* Umbilical Cord
-|keywords=* Alpha-2-macroglobulin
-* Glycosylation
-* Newborn
-* Plasma
-|full-text-url=https://sci-hub.do/10.1007/s12013-019-00883-4
-}}
-==AACS==
-{{medline-entry
-|title=Sex differences in subjective age-associated changes in sleep: a prospective elderly cohort study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33170149
-|keywords=* aging
-* longitudinal studies
-* normative
-* self-report
-* sex characteristics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7695390
-}}
 ==ABCG2==
-{{medline-entry
-|title=Contribution of senescence in human endometrial stromal cells during proliferative phase to embryo receptivity†.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32285109
-|keywords=* cellular senescence
-* embryo receptivity
-* endometrial stem cell
-* human endometrial stromal cell
-* infertility
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7313258
-}}
 {{medline-entry
 |title=[[ABCG2]] rs2231142 variant in hyperuricemia is modified by SLC2A9 and SLC22A12 polymorphisms and cardiovascular risk factors in an elderly community-dwelling population.
 |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32183743
+|abstract=The [[ABCG2]] rs2231142 single nucleotide polymorphism (SNP) is one of the most significant genetic variants associated with hyperuricemia (HUA) in Asian populations. However, the risk of [[ABCG2]] rs2231142 variants for HUA could interact with other important HUA risk variants and cardiovascular factors. This study investigated the effects of the combined association among [[ABCG2]] rs2231142 and multiple HUA genetic variants or cardiovascular risk factors on HUA risk and serum uric acid (sUA) levels in an elderly Chinese population. A total of 1206 participants over 65 years old were enrolled in this study. Physical and laboratory examinations were performed for all participants. The [[ABCG2]] rs2231142, SLC2A9 rs3733591, and SLC22A12 rs893006 SNPs were assayed using a standardized protocol. Logistic regression analysis and liner regression were adjusted respectively to account for the association between [[ABCG2]] rs2231142 and other genetic variants, as well as between cardiovascular risk factors and HUA risk and sUA levels. The prevalence of HUA was 14.71% in the elderly community-dwelling population. The [[ABCG2]] rs2231142 risk T allele was associated with HUA risk (odds ratio (OR) = 1.63, 95% confidence interval (CI): 1.27-2.11; p = 1.65 × 10 ) and with increased sUA levels (Beta = 0.16, p = 6.75 × 10 ) in the whole study population. Linear regression analysis showed that the mean sUA level increased linearly with the number of risk alleles of the three candidate genetic variants (Beta = 0.18, p = 1.94 × 10 ) The joint effect of the [[ABCG2]] rs2231142 T allele and cardiovascular risk factors (obesity, hypertension and dyslipidemia) was also associated with increased HUA risk and sUA levels. Each copy of the risk T allele was significantly associated with enhanced HUA risk in patients with hypertriglyceridemia (OR = 2.52, 95% CI: 1.33-4.60; p = 0.003) compared to controls. Our findings reinforce the importance of the [[ABCG2]] rs2231143 variant as a crucial genetic locus for HUA in Chinese populations and demonstrated the combined effects of multiple genetic risk variants and cardiovascular risk exposures on HUA risk and increased sUA level.
 |mesh-terms=* ATP Binding Cassette Transporter, Subfamily G, Member 2
 * Aged
@@ Строка 91: / Строка 43: @@
 |title=European LeukemiaNet 2020 recommendations for treating chronic myeloid leukemia.
 |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32127639
+|abstract=The therapeutic landscape of chronic myeloid leukemia (CML) has profoundly changed over the past 7 years. Most patients with chronic phase (CP) now have a normal life expectancy. Another goal is achieving a stable deep molecular response (DMR) and discontinuing medication for treatment-free remission (TFR). The European LeukemiaNet convened an expert panel to critically evaluate and update the evidence to achieve these goals since its previous recommendations. First-line treatment is a tyrosine kinase inhibitor (TKI; imatinib brand or generic, dasatinib, nilotinib, and bosutinib are available first-line). Generic imatinib is the cost-effective initial treatment in CP. Various contraindications and side-effects of all TKIs should be considered. Patient risk status at diagnosis should be assessed with the new EUTOS long-term survival (ELTS)-score. Monitoring of response should be done by quantitative polymerase chain reaction whenever possible. A change of treatment is recommended when intolerance cannot be ameliorated or when molecular milestones are not reached. Greater than 10% BCR-[[ABL1]] at 3 months indicates treatment failure when confirmed. Allogeneic transplantation continues to be a therapeutic option particularly for advanced phase CML. TKI treatment should be withheld during pregnancy. Treatment discontinuation may be considered in patients with durable DMR with the goal of achieving TFR.
 |mesh-terms=* Aniline Compounds
 * Antineoplastic Agents
@@ Строка 111: / Строка 63: @@
 * Quinolines
 * Survival Analysis
+|keywords=#f
 |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7214240
 }}
-==ABO==
+==ACE==
 {{medline-entry
-|title=Allelic distribution of [i][[ABO]][/i] gene in Chinese centenarians.
+|title=Angiotensin-Converting Enzyme ([[ACE]]) genetic variation and longevity in Peruvian older people: a cross-sectional study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33103040
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32281429
+|abstract= Some studies have suggested that the insertion(I)/deletion(D) polymorphism of the Angiotensin-Converting Enzyme ([[ACE]]) gene may be associated with human longevity, especially in centenarians. However, this association is still controversial. Besides, there have been no studies in Peruvians.  To describe the age distribution of the [[ACE]] polymorphism in a convenience sample of Peruvian older people.  This was a cross-sectional study in 104 Geriatric Day Hospital patients in Lima, Perú. The [[ACE]] polymorphism was determined in all patients. For the purpose of association with age, the sample was divided into four categories: young (< 65), youngest-old (65-74), middle-old (75-84) and oldest-old (85 or more).  The distribution of genotype frequencies was consistent with a population in Hardy-Weinberg equilibrium ([i]p[/i] = 0.62). The number (%) of D/D, I/D and I/I genotypes in the young was 2 (14.3%), 3 (21.4%) and 9 (64.3%), respectively; in youngest-old: 4 (11.4%), 15 (42.9%) and 16 (45.7%); in middle-old: 6 (12.2%), 20 (40.8%) and 23 (46.9%); and in oldest-old: 0 (0.0%), 4 (66.7%) and 2 (33.3%). A chi-square analysis showed no significant differences in genotype distribution between age groups ([i]p[/i] = 0.647).  No significant age differences were found in the distribution of the [[ACE]] polymorphism in this sample. Further studies with greater statistical power are recommended.
+|mesh-terms=* Aged
-|keywords=* ABO gene
+* Aged, 80 and over
-* centenarian
+* Cross-Sectional Studies
-* longevity
-* single nucleotide polymorphisms
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7574633
-}}
-{{medline-entry
-|title=Genetically Determined [[ABO]] Blood Group and its Associations With Health and Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31969017
-|mesh-terms=* ABO Blood-Group System
-* Adult
-* Age Factors
-* Aged
-* Cardiovascular Diseases
 * Female
-* Gene Frequency
+* Genetic Variation
-* Genetic Predisposition to Disease
-* Health Status
-* Healthy Aging
 * Humans
-* Incidence
+* Longevity
 * Male
 * Middle Aged
-* Phenotype
+* Peptidyl-Dipeptidase A
-* Polymorphism, Single Nucleotide
+* Peru
-* Prevalence
+* Polymorphism, Genetic
-* Risk Assessment
+|keywords=* ACE gene
-* Risk Factors
+* Longevity
-* United Kingdom
+* Perú
-|keywords=* ABO
+* ageing
-* aging
+|full-text-url=https://sci-hub.do/10.1080/03014460.2020.1748227
-* blood
-* genetics
-* hypertension
-* phenotype
-|full-text-url=https://sci-hub.do/10.1161/ATVBAHA.119.313658
 }}
-==ABR==
 {{medline-entry
-|title=[Hidden hearing loss and early identification].
+|title=COVID-19 and chronological aging: senolytics and other anti-aging drugs for the treatment or prevention of corona virus infection?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32791650
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32229706
+|abstract=COVID-19, also known as SARS-CoV-2, is a new emerging zoonotic corona virus of the SARS (Severe Acute Respiratory Syndrome) and the MERS (Middle East Respiratory Syndrome) family. COVID-19 originated in China and spread world-wide, resulting in the pandemic of 2020. For some reason, COVID-19 shows a considerably higher mortality rate in patients with advanced chronological age. This begs the question as to whether there is a functional association between COVID-19 infection and the process of chronological aging. Two host receptors have been proposed for COVID-19. One is CD26 and the other is [[ACE]]-2 (angiotensin-converting enzyme 2). Interestingly, both CD26 and the angiotensin system show associations with senescence. Similarly, two proposed therapeutics for the treatment of COVID-19 infection are Azithromycin and Quercetin, both drugs with significant senolytic activity. Also, Chloroquine-related compounds inhibit the induction of the well-known senescence marker, Beta-galactosidase. Other anti-aging drugs should also be considered, such as Rapamycin and Doxycycline, as they behave as inhibitors of protein synthesis, blocking both SASP and viral replication. Therefore, we wish to speculate that the fight against COVID-19 disease should involve testing the hypothesis that senolytics and other anti-aging drugs may have a prominent role in preventing the transmission of the virus, as well as aid in its treatment. Thus, we propose that new clinical trials may be warranted, as several senolytic and anti-aging therapeutics are existing FDA-approved drugs, with excellent safety profiles, and would be readily available for drug repurposing efforts. As Azithromycin and Doxycycline are both commonly used antibiotics that inhibit viral replication and IL-6 production, we may want to consider this general class of antibiotics that functionally inhibits cellular protein synthesis as a side-effect, for the treatment and prevention of COVID-19 disease.
-|mesh-terms=* Acoustic Stimulation
+|mesh-terms=* Age Factors
-* Audiometry, Pure-Tone
+* Aged
-* Auditory Threshold
+* Aged, 80 and over
-* Evoked Potentials, Auditory, Brain Stem
+* Aging
-* Hearing Loss, Noise-Induced
+* Angiotensin-Converting Enzyme 2
-* Humans
+* Antiviral Agents
-* Noise
+* Azithromycin
-|keywords=* aging
+* Betacoronavirus
-* drug damage
+* COVID-19
-* hidden hearing loss
+* Coronavirus Infections
-* noise exposure
+* Dipeptidyl Peptidase 4
-|full-text-url=https://sci-hub.do/10.13201/j.issn.2096-7993.2020.07.023
+* Humans
-}}
+* Hydroxychloroquine
-{{medline-entry
+* Pandemics
-|title=Aging But Not Age-Related Hearing Loss Dominates the Decrease of Parvalbumin Immunoreactivity in the Primary Auditory Cortex of Mice.
+* Peptidyl-Dipeptidase A
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32327469
+* Pneumonia, Viral
+* Quercetin
+* Receptors, Virus
-|keywords=* age-related hearing loss
+* SARS-CoV-2
+|keywords=* Azithromycin
+* COVID-19
+* Doxycycline
+* Hydroxy-chloroquine
+* Quercetin
+* Rapamycin
 * aging
-* mouse primary auditoy cortex
+* antibiotic
-* parvalbumin
+* corona virus
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7210488
+* drug repurposing
+* prevention
+* senescence
+* senolytic drug therapy
+* viral replication
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7202514
 }}
+==ACR==
 {{medline-entry
-|title=Hearing loss through apoptosis of the spiral ganglion neurons in apolipoprotein E knockout mice fed with a western diet.
+|title=Progenitor cell niche senescence reflects pathology of the parotid salivary gland in primary Sjögren's syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31948760
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32159757
+|abstract=Salivary gland (SG) progenitor cells (SGPCs) maintain SG homeostasis. We have previously shown that in primary Sjögren's syndrome (pSS), SGPCs are likely to be senescent, and may underpin SG dysfunction. This study assessed the extent of senescence of cells in a SGPC niche in pSS patients' SGs, and its correlation with functional and clinical parameters. The expression of p16 and p21 as markers of senescence in both total SG epithelium and a SGPC niche (basal striated duct cells, BSD) was examined in SGs of pSS (n = 35), incomplete pSS (n = 13) (patients with some signs of pSS, but not fulfilling all classification criteria) and non-SS sicca control (n = 21) patients. This was correlated with functional and clinical parameters. pSS patient SGs contained significantly more p16+ cells both in the epithelium in general (P <0.01) and in the BSD layer (P <0.001), than non-SS SGs. Significant correlations were found in pSS patients between p16+ BSD cells and secretion of unstimulated whole saliva, stimulated whole saliva, stimulated parotid saliva, CD45+ infiltrate, ultrasound total score and [[ACR]]-EULAR classification score, but not with EULAR Sjögren's syndrome disease activity index (ESSDAI) and EULAR Sjögren's Syndrome Patient Reported Index (ESSPRI) scores. Correlations with total epithelium p16+ cells were weaker. Incomplete pSS patients also had increased numbers of p16+ epithelial and BSD cells. Based on protein and mRNA expression, p21+ appears not to play a significant role in the SG in pSS. These findings suggest SGPC senescence may be an early feature of primary Sjögren's syndrome and may contribute to defective SG function in pSS but not to systemic disease activity.
-|mesh-terms=* Aging
+|keywords=* p16
-* Animals
+* primary Sjögren’s syndrome
-* Apolipoproteins E
+* salivary gland
-* Apoptosis
+* salivary gland progenitor cells
-* Diet, Western
+* senescence
-* Disease Models, Animal
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7516109
-* Hearing Loss
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Neurons
-* Spiral Ganglion
-|keywords=* Apoptosis
-* Atherosclerosis
-* Hearing loss
-* Reactive oxygen specie
-* Spiral ganglion neurons
-|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2019.12.100
 }}
-{{medline-entry
+==ADAM10==
-|title=Effects of enriched endogenous omega-3 fatty acids on age-related hearing loss in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31771637
-|mesh-terms=* Aging
-* Animals
-* Body Weight
-* Caenorhabditis elegans Proteins
-* Cochlea
-* Evoked Potentials, Auditory, Brain Stem
-* Fatty Acid Desaturases
-* Fatty Acids, Omega-3
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Mice, Transgenic
-* Neurons
-* Presbycusis
-* Spiral Ganglion
-|keywords=* Age-related hearing loss
-* C57BL/6 mouse
-* Cochlea
-* Omega-3 (n-3) fatty acids
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6878677
-}}
 {{medline-entry
-|title=Hearing impairment and associated morphological changes in pituitary adenylate cyclase activating polypeptide (PACAP)-deficient mice.
+|title=NKG2D Ligand Shedding in Response to Stress: Role of [[ADAM10]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31601840
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32269567
+|abstract=NKG2D is an activating receptor expressed by NK cells and some subsets of T cells and represents a major recognition receptor for detection and elimination of cancer cells. The ligands of NKG2D are stress-induced self-proteins that can be secreted as soluble molecules by protease-mediated cleavage. The release of NKG2D ligands in the extracellular milieu is considered a mode of finely controlling their surface expression levels and represents a relevant immune evasion mechanism employed by cancer cells to elude NKG2D-mediated immune surveillance. A disintegrin and metalloproteinase 10 ([[ADAM10]]), a catalytically active member of the ADAM family of proteases, is involved in the cleavage of some NKG2D ligands in various types of cancer cells either in steady state conditions and in response to an ample variety of stress stimuli. Appealing immunotherapeutic strategies devoted to promoting NK cell-mediated recognition and elimination of cancer cells are based on the upregulation of NK cell activating ligands. In particular, activation of DNA damage response (DDR) and the induction of cellular senescence by chemotherapeutic agents are associated with increased expression of NKG2D ligands on cancer cell surface. Herein, we will review advances on the protease-mediated cleavage of NKG2D ligands in response to chemotherapy-induced stress focusing on: (i) the role played by [[ADAM10]] in this process and (ii) the implications of NKG2D ligand shedding in the course of cancer therapy and in senescent cells.
-|mesh-terms=* Aging
+|keywords=* ADAM10
-* Animals
+* NKG2D
-* Cochlea
+* NKG2D ligands
-* Evoked Potentials, Auditory, Brain Stem
+* cancer
-* Genotype
+* chemotherapy
-* Hearing
+* senescence
-* Hearing Loss
+* shedding
-* Inflammation
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7109295
-* Male
+}}
-* Mice
+==AFM==
-* Mice, Knockout
-* Models, Animal
+{{medline-entry
-* Neovascularization, Pathologic
+|title=The Effect of Waste Engine Oil and Waste Polyethylene on UV Aging Resistance of Asphalt.
-* Neurons
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32155867
-* Pituitary Adenylate Cyclase-Activating Polypeptide
+|abstract=Waste engine oil (WEO) and waste polyethylene (WPE) are two common wastes, which are easy to pollute the environment. As the primary material in road construction, natural asphalt is a non-renewable energy source and asphalt is vulnerable to ultraviolet (UV) radiation during the service life. It results in degradation of asphalt pavement performance. In this paper, 22 wt % to 82 wt % of WEO and WPE were used to modify asphalts and the UV aging simulation experiment was carried out. The physical parameters of asphalts before the UV aging experiment show that the asphalt containing 42 wt % WPE and 62 wt % WEO mixture (42 wt % WPE + 62 wt % WEO) has similar physical properties with that of the matrix asphalt. Besides, gel permeation chromatography (GPC) verifies that the molecular weight distribution of the asphalt containing 42 wt % WPE + 62 wt % WEO is close to that of the matrix asphalt. The storage stability test shows that 42 wt % WPE + 62 wt % WEO has good compatibility with the matrix asphalt. The functional groups and micro-morphology of asphalts before and after the UV aging experiment were investigated by Fourier transform infrared spectroscopy (FTIR) and atomic force microscopy ([[AFM]]). FTIR results display that 42 wt % WPE + 62 wt % WEO can effectively reduce the formation of carbonyl and sulfoxide functional groups. [[AFM]] shows that 42 wt % WPE + 62 wt % WEO can also retard the formation of a "bee-like" structure in asphalt after the UV aging experiment. Based on the above results, it can be concluded that WEO and WPE mixture can replace part of asphalt and improve the UV aging resistance of asphalt.
-* Proteome
-* Proto-Oncogene Proteins c-fos
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6787024
+|keywords=* Fourier transform infrared spectroscopy
+* atomic force microscopy
+* gel permeation chromatography
+* ultraviolet aging
+* waste engine oil
+* waste polyethylene
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7182932
 }}
 {{medline-entry
-|title=Global nurse/midwife workforce and reproductive health through social ecology lens.
+|title=Mechanical properties measured by atomic force microscopy define health biomarkers in ageing C. elegans.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31402489
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32098962
+|abstract=Genetic and environmental factors are key drivers regulating organismal lifespan but how these impact healthspan is less well understood. Techniques capturing biomechanical properties of tissues on a nano-scale level are providing new insights into disease mechanisms. Here, we apply Atomic Force Microscopy ([[AFM]]) to quantitatively measure the change in biomechanical properties associated with ageing Caenorhabditis elegans in addition to capturing high-resolution topographical images of cuticle senescence. We show that distinct dietary restriction regimes and genetic pathways that increase lifespan lead to radically different healthspan outcomes. Hence, our data support the view that prolonged lifespan does not always coincide with extended healthspan. Importantly, we identify the insulin signalling pathway in C. elegans and interventions altering bacterial physiology as increasing both lifespan and healthspan. Overall, [[AFM]] provides a highly sensitive technique to measure organismal biomechanical fitness and delivers an approach to screen for health-improving conditions, an essential step towards healthy ageing.
-|mesh-terms=* Adolescent
+|mesh-terms=* Aging
-* Cross-Sectional Studies
+* Animal Feed
-* Employment
+* Animals
-* Female
+* Bacillus subtilis
-* Global Health
+* Biomarkers
-* Health Education
+* Caenorhabditis elegans
-* Humans
+* Caenorhabditis elegans Proteins
-* Income
+* Comamonas
-* Life Expectancy
+* Escherichia coli
-* Male
+* Forkhead Transcription Factors
-* Midwifery
+* Hot Temperature
-* Pregnancy
+* Insulin
-* Reproductive Health
+* Microbiota
-* Social Environment
+* Microscopy, Atomic Force
-* Socioeconomic Factors
+* Mutation
-* Workforce
+* Receptor, Insulin
-|keywords=* global health
+* Signal Transduction
-* nurse/midwife workforce
+* Ultraviolet Rays
-* reproductive health
+|keywords=#f
-* social ecology
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7042263
-|full-text-url=https://sci-hub.do/10.1111/phn.12648
 }}
-==ACD==
+==ALOX12==
 {{medline-entry
-|title=Genetics of cognitive trajectory in Brazilians: 15 years of follow-up from the Bambuí-Epigen Cohort Study of Aging.
+|title=Arachidonate 12-lipoxygenase and 12-hydroxyeicosatetraenoic acid contribute to stromal aging-induced progression of pancreatic cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31792241
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32265301
+|abstract=The incidence of pancreatic cancer increases with age, suggesting that chronological aging is a significant risk factor for this disease. Fibroblasts are the major nonmalignant cell type in the stroma of human pancreatic ductal adenocarcinoma (PDAC). In this study, we investigated whether the chronological aging of normal human fibroblasts (NHFs), a previously underappreciated area in pancreatic cancer research, influences the progression and therapeutic outcomes of PDAC. Results from experiments with murine xenografts and 2D and 3D co-cultures of NHFs and PDAC cells revealed that older NHFs stimulate proliferation of and confer resistance to radiation therapy of PDAC. MS-based metabolite analysis indicated that older NHFs have significantly increased arachidonic acid 12-lipoxygenase ([[ALOX12]]) expression and elevated levels of its mitogenic metabolite, 12-([i]S[/i])-hydroxy-5,8,10,14-eicosatetraenoic acid (12-([i]S[/i])-HETE) compared with their younger counterparts. In co-cultures with older rather than with younger NHFs, PDAC cells exhibited increases in mitogen-activated protein kinase signaling and cellular metabolism, as well as a lower oxidation state that correlated with their enhanced proliferation and resistance to radiation therapy. Expression of [[ALOX12]] was found to be significantly lower in PDAC cell lines and tumor biopsies, suggesting that PDAC cells rely on a stromal supply of mitogens for their proliferative needs. Pharmacological (hydroxytyrosol) and molecular (siRNA) interventions of [[ALOX12]] in older NHFs suppressed their ability to stimulate proliferation of PDAC cells. We conclude that chronological aging of NHFs contributes to PDAC progression and that [[ALOX12]] and 12-([i]S[/i])-HETE may be potential stromal targets for interventions that seek to halt progression and improve therapy outcomes.
-|mesh-terms=* Age Factors
+|keywords=* aging
-* Aged
+* arachidonic acid (AA) (ARA)
-* Aging
+* cancer biology
-* Brazil
+* cell proliferation
-* Cognition
+* fibroblast
-* Cognitive Dysfunction
+* pancreatic cancer
-* Cohort Studies
+* stromal cell
-* Female
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7242692
-* Follow-Up Studies
-* Genetic Predisposition to Disease
-* Genome-Wide Association Study
-* Humans
-* Male
-* Middle Aged
-* Polymorphism, Single Nucleotide
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6889148
 }}
-==ACE==
+==AMH==
 {{medline-entry
-|title=Elite swimmers possess shorter telomeres than recreationally active controls.
+|title=Modeling Variation in the Reproductive Lifespan of Female Adolescent and Young Adult Cancer Survivors Using [[AMH]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33068677
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32270202
+|abstract=Many female survivors of adolescent and young adult cancers (AYA survivors) have shortened reproductive lifespans. However, the timing and duration of ovarian function after cancer treatment are largely unknown. To model the trajectory of ovarian function over two decades following cancer treatment and evaluate how trajectories vary by treatment gonadotoxicity and age. In a prospective cohort, AYA survivors aged 18-39 at variable times since cancer treatment completion provided dried blood spots (DBS) every 6 months for up to 18 months. Anti-Müllerian hormone ([[AMH]]) levels were measured using the Ansh DBS [[AMH]] enzyme-linked immunosorbent assay. The mean [[AMH]] trajectory was modeled for the entire cohort and separately by treatment gonadotoxicity and age using functional principal components analysis. 763 participants, mean (standard deviation) enrollment age 33.3 (4.7) and age at cancer diagnosis 25.9 (5.7) years, contributed 1905 DBS samples. The most common cancers were breast (26.9%), lymphoma (24.8%), and thyroid (18.0%). [[AMH]] trajectories differed among survivors by treatment gonadotoxicity (low, moderate, or high) (P < 0.001). Following low or moderately gonadotoxic treatments, [[AMH]] levels increased over 2-3 years and plateaued over 10-15 years before declining. In contrast, following highly gonadotoxic treatment, [[AMH]] levels were lower overall and declined shortly after peak at 2-3 years. Younger age at treatment was associated with higher trajectories, but a protective effect of younger age was not observed in survivors exposed to highly gonadotoxic treatments (Pinteraction < 0.001). In this large AYA survivor cohort, timing and duration of ovarian function strongly depended on treatment gonadotoxicity and age at treatment. The findings provide novel, more precise information to guide reproductive decision-making.
+|keywords=* AMH
-|keywords=* Aging
+* adolescent and young adult cancer
-* Athlete
+* functional principal components analysis
-* Exercise
+* ovarian reserve
-* Genetics
+* reproductive lifespan
-|full-text-url=https://sci-hub.do/10.1016/j.gene.2020.145242
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7329316
 }}
 {{medline-entry
-|title=Coronavirus Disease-2019 Conundrum: RAS Blockade and Geriatric-Associated Neuropsychiatric Disorders.
+|title=Improving Prediction of Age at Menopause Using Multiple Anti-Müllerian Hormone Measurements: the Tehran Lipid-Glucose Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32850927
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109280
+|abstract=Several statistical models were introduced for the prediction of age at menopause using a single measurement of anti-müllerian hormone ([[AMH]]); however, individual prediction is challenging and needs to be improved. The objective of this study was to determine whether multiple [[AMH]] measurements can improve the prediction of age at menopause. All eligible reproductive-age women (n = 959) were selected from the Tehran Lipid and Glucose Study. The serum concentration of [[AMH]] was measured at the time of recruitment and twice after that at an average of 6-year intervals. An accelerated failure-time model with Weibull distribution was used to predict age at menopause, using a single [[AMH]] value vs a model that included the annual [[AMH]] decline rate. The adequacy of these models was assessed using C statistics. The median follow-up period was 14 years, and 529 women reached menopause. Adding the annual decline rate to the model that included single [[AMH]] improved the model's discrimination adequacy from 70% (95% CI: 67% to 71%) to 78% (95% CI: 75% to 80%) in terms of C statistics. The median of differences between actual and predicted age at menopause for the first model was -0.48 years and decreased to -0.21 in the model that included the decline rate. The predicted age at menopause for women with the same amount of age-specific [[AMH]] but an annual [[AMH]] decline rate of 95 percentiles was about one decade lower than in those with a decline rate of 5 percentiles. Prediction of age at menopause could be improved by multiple [[AMH]] measurements; it will be useful in identifying women at risk of early menopause.
+|keywords=* Tehran Lipid and Glucose Study (TLGS)
-|keywords=* ACE2
+* anti-müllerian hormone (AMH)
-* ACEIs
+* menopause
-* ARBs
+* reproductive aging
-* COVID-19
+|full-text-url=https://sci-hub.do/10.1210/clinem/dgaa083
-* RAS
-* SARS-CoV-2
-* geriatrics
-* neuropsychiatric disorders
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431869
 }}
-{{medline-entry
+==AMT==
-|title=Pregnancy Protects Hyperandrogenemic Female Rats From Postmenopausal Hypertension.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32755410
-|keywords=* aging
-* endothelin
-* menopause
-* nitric oxide
-* renin-angiotensin system
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7429272
-}}
 {{medline-entry
-|title=Heart failure is associated with accelerated age related metabolic bone disease.
+|title=A multi-method comparison of autobiographical memory impairments amongst younger and older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32498656
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32162531
+|abstract= Research indicates that, compared to younger adults, older adults have difficulty recalling memories of specific past events (those lasting less than 24 h) and this difficulty is associated with depression. These studies are largely confined to a single measure of specific memory recall and there are conflicting findings when alternative measures are used. This investigation provides the first comparison of memory specificity between younger and older adults using several different measures.  Older ([i]n[/i] = 105) and younger ([i]n[/i] = 88) adults completed the Autobiographical Memory Test ([[AMT]]), Autobiographical Memory Interview (AMI) and Sentence Completion for Events from the Past Test (SCEPT) and the number of specific memories was quantified for each measure. Participants also completed the Beck Depression Inventory Version II (BDI-II).  Compared to younger adults, older adults recalled fewer specific memories in the [[AMT]] and more specific memories in the AMI. This latter effect was particularly pronounced for memories related to childhood. There was no group difference in responses in the SCEPT. There was no evidence of an association between memory specificity and depression for any of the measures.  Older adults have difficulty retrieving specific memories after cuing by nouns and adjectives, as in the [[AMT]], but they have enhanced recall of specific memories after cuing by life periods, as in the AMI, and this is particularly true of memories related to childhood. Individual differences in memory specificity are not related to depression symptoms in healthy samples.
+|keywords=* Depression
-|keywords=* Heart failure
+* aging
-* comorbidities
+* episodic memory
-* geriatrics
+* overgeneral
-* metabolic bone disease
+* specificity
-* osteoporosis
+|full-text-url=https://sci-hub.do/10.1080/13607863.2020.1729338
-|full-text-url=https://sci-hub.do/10.1080/00015385.2020.1771885
 }}
-{{medline-entry
+==APOE==
-|title=Management of heart failure: an Italian national survey on fellows/specialists in geriatrics.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32383033
-|mesh-terms=* Aged
-* Geriatrics
-* Heart Failure
-* Humans
-* Italy
-* Specialization
-* Stroke Volume
-* Surveys and Questionnaires
-|keywords=* Aged, 65 years or over
-* Care survey
-* Health
-* Heart failure
-|full-text-url=https://sci-hub.do/10.1007/s40520-020-01577-1
-}}
 {{medline-entry
-|title=Angiotensin-Converting Enzyme ([[ACE]]) genetic variation and longevity in Peruvian older people: a cross-sectional study.
+|title=Alzheimer's Risk Factors Age, [[APOE]] Genotype, and Sex Drive Distinct Molecular Pathways.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32281429
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32199103
+|abstract=Evidence suggests interplay among the three major risk factors for Alzheimer's disease (AD): age, [[APOE]] genotype, and sex. Here, we present comprehensive datasets and analyses of brain transcriptomes and blood metabolomes from human apoE2-, apoE3-, and apoE4-targeted replacement mice across young, middle, and old ages with both sexes. We found that age had the greatest impact on brain transcriptomes highlighted by an immune module led by Trem2 and Tyrobp, whereas [[APOE]]4 was associated with upregulation of multiple Serpina3 genes. Importantly, these networks and gene expression changes were mostly conserved in human brains. Finally, we observed a significant interaction between age, [[APOE]] genotype, and sex on unfolded protein response pathway. In the periphery, [[APOE]]2 drove distinct blood metabolome profile highlighted by the upregulation of lipid metabolites. Our work identifies unique and interactive molecular pathways underlying AD risk factors providing valuable resources for discovery and validation research in model systems and humans.
-|mesh-terms=* Aged
+|mesh-terms=* Adaptor Proteins, Signal Transducing
-* Aged, 80 and over
+* Age Factors
-* Cross-Sectional Studies
+* Aging
+* Alzheimer Disease
+* Animals
+* Apolipoprotein E2
+* Apolipoprotein E3
+* Apolipoprotein E4
+* Apolipoproteins E
+* Brain
 * Female
-* Genetic Variation
+* Gene Expression
+* Gene Expression Profiling
+* Gene Regulatory Networks
+* Genotype
 * Humans
-* Longevity
 * Male
-* Middle Aged
+* Membrane Glycoproteins
-* Peptidyl-Dipeptidase A
+* Membrane Proteins
-* Peru
+* Metabolome
-* Polymorphism, Genetic
+* Mice
-|keywords=* ACE gene
+* Mice, Transgenic
-* Longevity
+* Protective Factors
-* Perú
+* Receptors, Immunologic
-* ageing
+* Risk Factors
-|full-text-url=https://sci-hub.do/10.1080/03014460.2020.1748227
+* Serpins
+* Sex Factors
+* Unfolded Protein Response
+|keywords=* APOE
+* Alzheimer’s disease
+* Serpina3
+* age
+* extracellular vesicles
+* inflammation
+* lipid metabolism
+* metabolomics
+* sex
+* transcriptomics
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388065
 }}
 {{medline-entry
-|title=COVID-19 and chronological aging: senolytics and other anti-aging drugs for the treatment or prevention of corona virus infection?
+|title=Less agreeable, better preserved? A PET amyloid and MRI study in a community-based cohort.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32229706
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32169357
+|abstract=The relationship between personality profiles and brain integrity in old age is still a matter of debate. We examined the association between Big Five factor and facet scores and MRI brain volume changes on a 54-month follow-up in 65 elderly controls with 3 neurocognitive assessments (baseline, 18 months, and 54 months), structural brain MRI (baseline and 54 months), brain amyloid PET during follow-up, and [[APOE]] genotyping. Personality was assessed with the Neuroticism Extraversion Openness Personality Inventory-Revised. Regression models were used to identify predictors of volume loss including time, age, sex, personality, amyloid load, presence of [[APOE]] ε4 allele, and cognitive evolution. Lower agreeableness factor scores (and 4 of its facets) were associated with lower volume loss in the hippocampus, entorhinal cortex, amygdala, mesial temporal lobe, and precuneus bilaterally. Higher openness factor scores (and 2 of its facets) were also associated with lower volume loss in the left hippocampus. Our findings persisted when adjusting for confounders in multivariable models. These data suggest that the combination of low agreeableness and high openness is an independent predictor of better preservation of brain volume in areas vulnerable to neurodegeneration.
-|mesh-terms=* Age Factors
+|mesh-terms=* Aged
-* Aged
 * Aged, 80 and over
-* Aging
+* Amyloidogenic Proteins
-* Angiotensin-Converting Enzyme 2
+* Apolipoproteins E
-* Antiviral Agents
+* Brain
-* Azithromycin
+* Cognition
-* Betacoronavirus
+* Cohort Studies
-* COVID-19
+* Female
-* Coronavirus Infections
+* Follow-Up Studies
-* Dipeptidyl Peptidase 4
 * Humans
-* Hydroxychloroquine
+* Magnetic Resonance Imaging
-* Pandemics
+* Male
-* Peptidyl-Dipeptidase A
+* Neuroimaging
-* Pneumonia, Viral
+* Organ Size
-* Quercetin
+* Personality
-* Receptors, Virus
+* Positron-Emission Tomography
-* SARS-CoV-2
+|keywords=* Amyloid load
-|keywords=* Azithromycin
+* Cognitive aging
-* COVID-19
+* Cohort studies
-* Doxycycline
+* Personality
-* Hydroxy-chloroquine
+* Structural MRI
-* Quercetin
+|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.02.004
-* Rapamycin
-* aging
-* antibiotic
-* corona virus
-* drug repurposing
-* prevention
-* senescence
-* senolytic drug therapy
-* viral replication
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7202514
 }}
 {{medline-entry
-|title=[i]A[/i]ngiotensin Converting Enzyme Inhibitors [i]C[/i]ombined with [i]E[/i]xercise for Hypertensive [i]S[/i]eniors (The [[ACE]]S Trial): Study Protocol of a Randomized Controlled Trial.
+|title=Physical Activity as Moderator of the Association Between [[APOE]] and Cognitive Decline in Older Adults: Results from Three Longitudinal Cohort Studies.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32039215
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32110803
+|abstract=Previous studies have suggested that the association between [[APOE]] ɛ 4 and dementia is moderated by physical activity (PA), but the results remain inconclusive and longitudinal data on cognitive decline are missing. In this study, we examine whether there is a gene-environment interaction between [[APOE]] and PA on cognitive decline in older adults using 9-year follow-up data of three cohort studies. We followed 7,176 participants from three longitudinal cohort studies: Longitudinal Aging Study Amsterdam (LASA), InCHIANTI, and Rotterdam Study for 9 years. PA was assessed with self-reported questionnaires and was categorized in low, moderate, and high PA. Cognitive function was assessed with the Mini-Mental State Examination (MMSE) and cognitive decline was defined as a decrease of three points or more on the MMSE during 3 years follow-up. We fitted logistic regression models using generalized estimating equations adjusting for age, sex, education, depressive symptoms, and number of chronic disease. Interaction between [[APOE]] and PA was tested on multiplicative and additive scale. Cohorts were similar in most aspects but InCHIANTI participants were on average older and had lower education. [[APOE]] ɛ 4 carriers had higher odds of cognitive decline (odds ratio [OR] = 1.46, 95% confidence interval [CI]: 1.29-1.64) while PA was not significantly associated with cognitive decline overall (moderate PA: OR = 0.87, 0.67-1.13; high PA: OR = 0.71, 0.36-1.40). There was no evidence for an interaction effect between PA and [[APOE]] ɛ 4 in cognitive decline in older adults ([[APOE]] × moderate PA: p = .83; [[APOE]] × high PA: p = .90). Previous claims of a gene-environment interaction between [[APOE]] ɛ 4 and PA in cognitive decline are not supported by our results.
+|keywords=* Gene–environment interaction
-|keywords=* aging
+* InCHIANTI
-* antihypertensive
+* Longitudinal Aging Study Amsterdam
-* exercise
+* Rotterdam Study
-* functional status
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7518558
-* hypertension
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6988302
 }}
 {{medline-entry
-|title=Vascular age.
+|title=Longitudinal Maintenance of Cognitive Health in Centenarians in the 100-plus Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32013519
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32101309
+|abstract=Some individuals who reach ages beyond 100 years in good cognitive health may be resilient against risk factors associated with cognitive decline. Exploring the processes underlying resilience may contribute to the development of therapeutic strategies that help to maintain cognitive health while aging. To identify individuals who escape cognitive decline until extreme ages and to investigate the prevalence of associated risk factors. The 100-plus Study is a prospective observational cohort study of community-based Dutch centenarians enrolled between 2013 and 2019 who were visited annually until death or until participation was no longer possible. The centenarians self-reported their cognitive health, as confirmed by a proxy. Of the 1023 centenarians approached for study inclusion, 340 fulfilled the study criteria and were included in analyses. Data analysis was performed from April 2019 to December 2019. Cognition was assessed using the Mini-Mental State Examination (MMSE). To identify centenarians who escape cognitive decline, this study investigated the association of baseline cognition with survivorship and cognitive trajectories for at least 2 years of follow-up using linear mixed models, adjusted for sex, age, and education. This study investigated the prevalence of apolipoprotein E ([[APOE]]) genotypes and cardiovascular disease as risk factors associated with cognitive decline. At baseline, the median age of 340 centenarians was 100.5 years (range, 100.0-108.2 years); 245 participants (72.1%) were female. The maximum survival estimate plateaued at 82% per year (95% CI, 77% to 87%) across centenarians who scored 26 to 30 points on the baseline MMSE (hazard ratio, 0.56; 95% CI, 0.42 to 0.75; P < .001), suggesting that an MMSE score of 26 or higher is representative of both cognitive and physical health. Among the 79 centenarians who were followed up for 2 years or longer, those with baseline MMSE score less than 26 experienced a decline in MMSE score of 1.68 points per year (95% CI, -2.45 to -0.92 points per year; P = .02), whereas centenarians with MMSE scores of 26 or higher at baseline experienced a decline of 0.71 point per year (95% CI, -1.08 to -0.35 points per year). For 73% of the centenarians with baseline MMSE scores of 26 or higher, no cognitive changes were observed, which often extended to ensuing years or until death. It is estimated that this group is representative of less than 10% of Dutch centenarians. In this group, 18.6% carried at least 1 [[APOE]]-ε4 allele, compared with 5.6% of the centenarians with lower and/or declining cognitive performance. Most centenarians who scored 26 or higher on the MMSE at baseline maintained high levels of cognitive performance for at least 2 years, in some cases despite the presence of risk factors associated with cognitive decline. Investigation of this group might reveal the processes underlying resilience against risk factors associated with cognitive decline.
-|mesh-terms=* Adolescent
+|mesh-terms=* Aged, 80 and over
-* Adult
-* Aged
 * Aging
-* Angiotensin-Converting Enzyme Inhibitors
+* Apolipoprotein E4
-* Atherosclerosis
+* Cognition
-* Child
+* Female
-* Elasticity
 * Humans
-* Middle Aged
+* Longitudinal Studies
-* Perindopril
+* Male
-* Pulse Wave Analysis
+* Mental Status and Dementia Tests
-* Vascular Stiffness
+* Prospective Studies
-* Young Adult
+|keywords=#f
-|keywords=* ACE inhibitors
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7137688
-* CT angiography
-* atorvastatin
-* dyslipidemia
-* hypertension
-* intima media thickness (IMT)
-* perindopril
-* pulse wave velocity (PWV)
-* statins
-* vascular age
 }}
-==ACE2==
+==APP==
 {{medline-entry
-|title=How Does SARS-CoV-2 Affect the Central Nervous System? A Working Hypothesis.
+|title=Transcriptomic profiling of microglia and astrocytes throughout aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33304284
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32238175
+|abstract=Activation of microglia and astrocytes, a prominent hallmark of both aging and Alzheimer's disease (AD), has been suggested to contribute to aging and AD progression, but the underlying cellular and molecular mechanisms are largely unknown. We performed RNA-seq analyses on microglia and astrocytes freshly isolated from wild-type and [[APP]]-PS1 (AD) mouse brains at five time points to elucidate their age-related gene-expression profiles. Our results showed that from 4 months onward, a set of age-related genes in microglia and astrocytes exhibited consistent upregulation or downregulation (termed "age-up"/"age-down" genes) relative to their expression at the young-adult stage (2 months). And most age-up genes were more highly expressed in AD mice at the same time points. Bioinformatic analyses revealed that the age-up genes in microglia were associated with the inflammatory response, whereas these genes in astrocytes included widely recognized AD risk genes, genes associated with synaptic transmission or elimination, and peptidase-inhibitor genes. Overall, our RNA-seq data provide a valuable resource for future investigations into the roles of microglia and astrocytes in aging- and amyloid-β-induced AD pathologies.
+|keywords=* Aging
+* Alzheimer’s disease (AD)
+* Astrocyte
+* Microglia
+* RNA-seq
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7115095
+}}
+{{medline-entry
+|title=Platelets in Amyloidogenic Mice Are Activated and Invade the Brain.
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32194368
+|abstract=Alzheimer's disease (AD) is a neurodegenerative disease with a complex and not fully understood pathogenesis. Besides brain-intrinsic hallmarks such as abnormal deposition of harmful proteins, i.e., amyloid beta in plaques and hyperphosphorylated Tau in neurofibrillary tangles, blood-derived elements, in particular, platelets have been discussed to be involved in AD pathogenesis. The underlying mechanisms, however, are rather unexplored. Here, we investigate a potential role of platelets in an AD transgenic animal model with severe amyloid plaque formation, the [[APP]]-PS1 transgenic mice, and analyzed the presence, spatial location and activation status of platelets within the brain. In [[APP]]-PS1 mice, a higher number of platelets were located within the brain parenchyma, i.e., outside the cerebral blood vessels compared to WT controls. Such platelets were activated according to the expression of the platelet activation marker CD62P and to morphological hallmarks such as membrane protrusions. In the brain, platelets were in close contact exclusively with astrocytes suggesting an interaction between these two cell types. In the bloodstream, although the percentage of activated platelets did not differ between transgenic and age-matched control animals, [[APP]]-PS1 blood-derived platelets showed remarkable ultrastructural peculiarities in platelet-specific organelles such as the open canalicular system (OCS). This work urges for further investigations on platelets and their yet unknown functional roles in the brain, which might go beyond AD pathogenesis and be relevant for various age-related neurodegenerative diseases.
-|keywords=* ACE2
+|keywords=* Alzheimer’s disease
-* Alzheimer disease
+* aging
-* Ang(1-7)/Mas
+* astrocytes
-* COVID-19
+* platelets
-* RAAS
+* vascular pathology
-* SARS-CoV
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7063083
-* brain aging
-* neurodegenerative and psychiatric disorders abstract
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7701095
 }}
+==ATF6==
 {{medline-entry
-|title=Bioinformatic characterization of angiotensin-converting enzyme 2, the entry receptor for SARS-CoV-2.
+|title=ER stress activates immunosuppressive network: implications for aging and Alzheimer's disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33112891
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32279085
+|abstract=The endoplasmic reticulum (ER) contains stress sensors which recognize the accumulation of unfolded proteins within the lumen of ER, and subsequently these transducers stimulate the unfolded protein response (UPR). The ER sensors include the IRE1, PERK, and [[ATF6]] transducers which activate the UPR in an attempt to restore the quality of protein folding and thus maintain cellular homeostasis. If there is excessive stress, UPR signaling generates alarmins, e.g., chemokines and cytokines, which activate not only tissue-resident immune cells but also recruit myeloid and lymphoid cells into the affected tissues. ER stress is a crucial inducer of inflammation in many pathological conditions. A chronic low-grade inflammation and cellular senescence have been associated with the aging process and many age-related diseases, such as Alzheimer's disease. Currently, it is known that immune cells can exhibit great plasticity, i.e., they are able to display both pro-inflammatory and anti-inflammatory phenotypes in a context-dependent manner. The microenvironment encountered in chronic inflammatory conditions triggers a compensatory immunosuppression which defends tissues from excessive inflammation. Recent studies have revealed that chronic ER stress augments the suppressive phenotypes of immune cells, e.g., in tumors and other inflammatory disorders. The activation of immunosuppressive network, including myeloid-derived suppressor cells (MDSC) and regulatory T cells (Treg), has been involved in the aging process and Alzheimer's disease. We will examine in detail whether the ER stress-related changes found in aging tissues and Alzheimer's disease are associated with the activation of immunosuppressive network, as has been observed in tumors and many chronic inflammatory diseases.
-|mesh-terms=* Aging
+|keywords=* Ageing
-* Angiotensin-Converting Enzyme 2
+* Immunometabolism
-* Betacoronavirus
+* Immunosenescence
-* Binding Sites
+* Immunosuppression
-* COVID-19
+* Inflammaging
-* Carrier Proteins
+* Neurodegeneration
-* Computational Biology
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7220864
-* Coronavirus Infections
+}}
-* Female
+==ATG3==
-* Gene Expression Regulation, Enzymologic
-* Gene Ontology
-* Humans
-* Interferons
-* Lung
-* Male
-* Metalloproteases
-* Neovascularization, Physiologic
-* Organ Specificity
-* Pandemics
-* Peptidyl-Dipeptidase A
-* Pneumonia, Viral
-* Promoter Regions, Genetic
-* RNA, Messenger
-* Receptors, Virus
-* Renin-Angiotensin System
-* SARS-CoV-2
-* Sex Characteristics
-* Single-Cell Analysis
-* Transcription Factors
-* Transcription Initiation Site
-* Virus Attachment
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7592753
-}}
 {{medline-entry
-|title=A mouse-adapted model of SARS-CoV-2 to test COVID-19 countermeasures.
+|title=Estrogen Signaling Induces Mitochondrial Dysfunction-Associated Autophagy and Senescence in Breast Cancer Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32854108
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32244623
+|abstract=Previous work has shown that although estrogen (E2) disrupts cellular iron metabolism and induces oxidative stress in breast and ovarian cancer cells, it fails to induce apoptosis. However, E2 treatment was reported to enhance the apoptotic effects of doxorubicin in cancer cells. This suggests that E2 can precipitate anti-growth effects that render cancer cells more susceptible to chemotherapy. To investigate such anti-growth non-apoptotic, effects of E2 in cancer cells, MDA-MB-231 and MCF-7 cells were evaluated for the expression of key autophagy and senescence markers and for mitochondrial damage following E2 treatment. Treated cells experienced mitochondrial membrane depolarization along with increased expression of LC3-I/II, Pink1 and LAMP2, increased LC3-II accumulation and increased lysosomal and mitochondrial accumulation and flattening. E2-treated MCF-7 cells also showed reduced P53 and pRb780 expression and increased Rb and P21 expression. Increased expression of the autophagy markers [[ATG3]] and Beclin1 along with increased levels of β-galactosidase activity and IL-6 production were evident in E2-treated MCF-7 cells. These findings suggest that E2 precipitates a form of mitochondrial damage that leads to cell senescence and autophagy in breast cancer cells.
-|mesh-terms=* Aging
+|keywords=* Estrogen
-* Angiotensin-Converting Enzyme 2
+* MCF-7
-* Animals
+* MDA-MB-231
-* Betacoronavirus
+* autophagy
-* COVID-19
+* mitochondria
-* COVID-19 Vaccines
+* senescence
-* Coronavirus Infections
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7235898
-* Disease Models, Animal
+}}
-* Female
+==ATM==
-* Forkhead Transcription Factors
-* Humans
-* Interferon-alpha
-* Interferons
-* Interleukins
-* Male
-* Mice
-* Mice, Inbred BALB C
-* Mice, Transgenic
-* Models, Molecular
-* Pandemics
-* Peptidyl-Dipeptidase A
-* Pneumonia, Viral
-* Receptors, Virus
-* SARS-CoV-2
-* Viral Vaccines
-|full-text-url=https://sci-hub.do/10.1038/s41586-020-2708-8
-}}
 {{medline-entry
-|title=COVID-19 and Senotherapeutics: Any Role for the Naturally-occurring Dipeptide Carnosine?
+|title=[[ATM]] is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32765939
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32201398
+|abstract=NF-κB is a transcription factor activated in response to inflammatory, genotoxic and oxidative stress and important for driving senescence and aging. Ataxia-telangiectasia mutated ([[ATM]]) kinase, a core component of DNA damage response signaling, activates NF-κB in response to genotoxic and oxidative stress via post-translational modifications. Here we demonstrate that [[ATM]] is activated in senescent cells in culture and murine tissues from [i]Ercc1[/i]-deficient mouse models of accelerated aging, as well as naturally aged mice. Genetic and pharmacologic inhibition of [[ATM]] reduced activation of NF-κB and markers of senescence and the senescence-associated secretory phenotype (SASP) in senescent [i]Ercc1 [/i] MEFs. [i]Ercc1 [/i] mice heterozygous for [i]Atm[/i] have reduced NF-κB activity and cellular senescence, improved function of muscle-derived stem/progenetor cells (MDSPCs) and extended healthspan with reduced age-related pathology especially age-related bone and intervertebral disc pathologies. In addition, treatment of [i]Ercc1[/i]  mice with the [[ATM]] inhibitor KU-55933 suppressed markers of senescence and SASP. Taken together, these results demonstrate that the [[ATM]] kinase is a major mediator of DNA damage-induced, NF-κB-mediated cellular senescence, stem cell dysfunction and aging and thus represents a therapeutic target to slow the progression of aging.
+|keywords=* ATM
-|keywords=* acetyl-carnosine
+* DNA damage response
+* NF-κB
 * aging
-* carnosine
+* cellular senescence
-* inflammation
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7138542
-* lungs
-* olfaction
-* virus
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7390525
 }}
 {{medline-entry
-|title=The dual impact of [[ACE2]] in COVID-19 and ironical actions in geriatrics and pediatrics with possible therapeutic solutions.
+|title=[[ATM]] suppresses leaf senescence triggered by DNA double-strand break through epigenetic control of senescence-associated genes in Arabidopsis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32653522
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32163596
+|abstract=All living organisms are unavoidably exposed to various endogenous and environmental stresses that trigger potentially fatal DNA damage, including double-strand breaks (DSBs). Although a growing body of evidence indicates that DNA damage is one of the prime drivers of aging in animals, little is known regarding the importance of DNA damage and its repair on lifespan control in plants. We found that the level of DSBs increases but DNA repair efficiency decreases as Arabidopsis leaves age. Generation of DSBs by inducible expression of I-PpoI leads to premature senescence phenotypes. We examined the senescence phenotypes in the loss-of-function mutants for 13 key components of the DNA repair pathway and found that deficiency in ATAXIA TELANGIECTASIA MUTATED ([[ATM]]), the chief transducer of the DSB signal, results in premature senescence in Arabidopsis. [[ATM]] represses DSB-induced expression of senescence-associated genes, including the genes encoding the WRKY and NAC transcription factors, central components of the leaf senescence process, via modulation of histone lysine methylation. Our work highlights the significance of [[ATM]] in the control of leaf senescence and has significant implications for the conservation of aging mechanisms in animals and plants.
+|keywords=*
+Arabidopsis thaliana
-|mesh-terms=* Age Factors
+* ATM
-* Aged
+* DNA repair
-* Aged, 80 and over
+* double-strand breaks
-* Angiotensin-Converting Enzyme 2
+* histone methylation
-* Anti-Inflammatory Agents
+* leaf senescence
-* Betacoronavirus
+|full-text-url=https://sci-hub.do/10.1111/nph.16535
-* COVID-19
-* Child
-* Child, Preschool
-* Coronavirus
-* Coronavirus Infections
-* Female
-* Geriatrics
-* Humans
-* Infant
-* Infant, Newborn
-* Male
-* Pandemics
-* Pediatrics
-* Peptidyl-Dipeptidase A
-* Pneumonia, Viral
-* Protein Binding
-* Receptors, Virus
-* Renin-Angiotensin System
-* SARS-CoV-2
-* Severe Acute Respiratory Syndrome
-* Virus Internalization
-|keywords=* ACE2
-* Angiotensin 2
-* Angiotensin-(1–7)
-* Corona virus
-* Glycoprotein spikes
-* RAAS system
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7347488
 }}
 {{medline-entry
-|title=The possible pathophysiology mechanism of cytokine storm in elderly adults with COVID-19 infection: the contribution of "inflame-aging".
+|title=Glioblastoma Cells Do Not Affect Axitinib-Dependent Senescence of HUVECs in a Transwell Coculture Model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32529477
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32098270
+|abstract=Axitinib is an orally available inhibitor of tyrosine kinases, with high specificity for vascular endothelial growth factor receptors (VEGFRs) 1, 2, and 3. It is approved for the treatment of advanced renal cell carcinoma and is in phase II clinical trials for recurrent glioblastoma (GBM). GBM is a brain tumor peculiar in its ability to induce neoangiogenesis. Since both GBM tumor cells and endothelial cells of tumor vasculature express VEGFRs, Axitinib exerts its inhibitory action on both tumor and endothelial cells. We and others previously demonstrated that Axitinib triggers cellular senescence. In particular, Axitinib-dependent senescence of HUVECs (human umbilical vein endothelial cells) is accompanied by intracellular reactive oxygen species(ROS) increase and early ataxia telangiectasia mutated([[ATM]]) activation. Here we wondered if the presence of glioblastoma tumor cells could affect the HUVEC senescence upon Axitinib exposure. To address this issue, we cocultured HUVECs together with GBM tumor cells in transwell plates. HUVEC senescence did not result in being affected by GBM cells, neither in terms of β galactosidase activity nor of proliferation index or [[ATM]] phosphorylation. Conversely, Axitinib modulation of HUVEC gene expression was altered by cocultured GBM cells. These data demonstrate that the GBM secretome modifies HUVECs' transcriptomic profile upon Axitinib exposure, but does not prevent drug-induced senescence.
-|mesh-terms=* Adipocytes
+|mesh-terms=* Ataxia Telangiectasia Mutated Proteins
-* Age Factors
+* Axitinib
-* Aged
+* Cell Line, Tumor
-* Aging
-* Angiotensin II Type 2 Receptor Blockers
-* Autophagy
-* Betacoronavirus
-* COVID-19
 * Cellular Senescence
-* Coronavirus Infections
+* Coculture Techniques
-* Cytokine Release Syndrome
+* Gene Expression Profiling
-* Cytokines
+* Glioblastoma
+* Human Umbilical Vein Endothelial Cells
 * Humans
-* Immune System
+* Phosphorylation
-* Inflammation
+|keywords=* Axitinib
-* Pandemics
+* endothelial cells
-* Pneumonia, Viral
+* glioblastoma
-* Reactive Oxygen Species
+* senescence
-* Receptor, Angiotensin, Type 2
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7073100
-* SARS-CoV-2
-* Vitamin D
-* Vitamin D Deficiency
-|keywords=* ACE2 receptor
-* Autophagy
-* COVID-19
-* Cytokine storm
-* Senescent cell
-* Vitamin D
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7289226
 }}
+==ATR==
 {{medline-entry
-|title=Decoding SARS-CoV-2 hijacking of host mitochondria in COVID-19 pathogenesis.
+|title=Supraphysiological protection from replication stress does not extend mammalian lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32510973
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32253367
+|abstract=Replication Stress (RS) is a type of DNA damage generated at the replication fork, characterized by single-stranded DNA (ssDNA) accumulation, and which can be caused by a variety of factors. Previous studies have reported elevated RS levels in aged cells. In addition, mouse models with a deficient RS response show accelerated aging. However, the relevance of endogenous or physiological RS, compared to other sources of genomic instability, for the normal onset of aging is unknown. We have performed long term survival studies of transgenic mice with extra copies of the [i]Chk1[/i] and/or [i]Rrm2[/i] genes, which we previously showed extend the lifespan of a progeroid [[ATR]]-hypomorphic model suffering from high levels of RS. In contrast to their effect in the context of progeria, the lifespan of [i]Chk1, Rrm2[/i] and [i]Chk1/Rrm2[/i] transgenic mice was similar to WT littermates in physiological settings. Most mice studied died due to tumors -mainly lymphomas- irrespective of their genetic background. Interestingly, a higher but not statistically significant percentage of transgenic mice developed tumors compared to WT mice. Our results indicate that supraphysiological protection from RS does not extend lifespan, indicating that RS may not be a relevant source of genomic instability on the onset of normal aging.
-|mesh-terms=* Adaptive Immunity
+|keywords=* DNA damage
-* Angiotensin-Converting Enzyme 2
-* Animals
-* Betacoronavirus
-* COVID-19
-* Coronavirus Infections
-* DNA, Mitochondrial
-* Gene Expression Regulation, Viral
-* Host Microbial Interactions
-* Humans
-* Immunity, Innate
-* Mitochondria
-* Pandemics
-* Peptidyl-Dipeptidase A
-* Pneumonia, Viral
-* RNA, Viral
-* SARS-CoV-2
-* Virus Replication
-|keywords=* COVID-19
-* SARS-CoV
 * aging
-* coronavirus
+* cancer
-* mitochondria
+* mouse models
-* mitochondrial DNA
+* replication stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7381712
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185120
 }}
 {{medline-entry
-|title=A Mouse Model of SARS-CoV-2 Infection and Pathogenesis.
+|title=Assessing the Retest Reliability of Prefrontal EEG Markers of Brain Rhythm Slowing in the Eyes-Closed Resting State.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32485164
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32253926
+|abstract=[i]Objective[/i]. We examined whether prefrontal lobe EEG markers of slower brain rhythms, which are correlated with functional brain aging, can reliably reflect those of other brain lobes, as measured by a multichannel device. [i]Methods[/i]. EEG measurements were taken of 112 healthy individuals aged 20 to 69 years in the eyes-closed resting state. A 5-minute measurement was taken at 8 regions (Fp1, Fp2, F3, F4, T3, T4, O1, O2). Indices (median frequency [MDF], peak frequency [PF]) that quantitatively reflect the characteristics of EEG slowing, and traditional commonly used spectral indices (absolute powers as delta, theta, alpha, beta, and relative power as alpha-to-theta ratio [[[ATR]]]), were extracted from the EEG signals. For these indices, the differences between the prefrontal lobe and other areas were analyzed and the test-retest reproducibility was investigated. [i]Results[/i]. The EEG slowing indicators showed high conformity over all brain lobes and stable reproducibility. On the other hand, the typical EEG spectral indicators delta, theta, alpha, beta, and [[ATR]] differed between brain regions. [i]Conclusion[/i]. It was found that EEG slowing markers, which were used for assessing the aging or degeneration of brain functions, could be reliably extracted from a prefrontal EEG alone. [i]Significance[/i]. These findings suggest that EEG prefrontal markers may reflect markers of other brain regions when a multi-channel device is used. Thus, this method may constitute a low-cost, wearable, wireless, easily accessible, and noninvasive tool for neurological assessment that could be used in the early detection of cognitive decline and in the prevention of dementia.
+|keywords=* EEG
+* EEG slowing
+* brain aging
+* dominant frequency
+* prefrontal
+|full-text-url=https://sci-hub.do/10.1177/1550059420914832
+}}
+==BAZ2B==
+{{medline-entry
+|title=Two conserved epigenetic regulators prevent healthy ageing.
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32103178
+|abstract=It has long been assumed that lifespan and healthspan correlate strongly, yet the two can be clearly dissociated . Although there has been a global increase in human life expectancy, increasing longevity is rarely accompanied by an extended healthspan . Thus, understanding the origin of healthy behaviours in old people remains an important and challenging task. Here we report a conserved epigenetic mechanism underlying healthy ageing. Through genome-wide RNA-interference-based screening of genes that regulate behavioural deterioration in ageing Caenorhabditis elegans, we identify 59 genes as potential modulators of the rate of age-related behavioural deterioration. Among these modulators, we found that a neuronal epigenetic reader, BAZ-2, and a neuronal histone 3 lysine 9 methyltransferase, SET-6, accelerate behavioural deterioration in C. elegans by reducing mitochondrial function, repressing the expression of nuclear-encoded mitochondrial proteins. This mechanism is conserved in cultured mouse neurons and human cells. Examination of human databases  shows that expression of the human orthologues of these C. elegans regulators, [[BAZ2B]] and EHMT1, in the frontal cortex increases with age and correlates positively with the progression of Alzheimer's disease. Furthermore, ablation of Baz2b, the mouse orthologue of BAZ-2, attenuates age-dependent body-weight gain and prevents cognitive decline in ageing mice. Thus our genome-wide RNA-interference screen in C. elegans has unravelled conserved epigenetic negative regulators of ageing, suggesting possible ways to achieve healthy ageing.
 |mesh-terms=* Aging
-* Angiotensin-Converting Enzyme 2
 * Animals
-* Betacoronavirus
+* Caenorhabditis elegans
-* Brain
+* Caenorhabditis elegans Proteins
-* COVID-19
+* Cognition
-* CRISPR-Cas Systems
+* Cognitive Dysfunction
-* Coronavirus Infections
+* Epigenesis, Genetic
-* Cytokines
+* Healthy Aging
-* Disease Models, Animal
+* Histone-Lysine N-Methyltransferase
-* Gene Knock-In Techniques
+* Histones
-* Lung
-* Lung Diseases, Interstitial
-* Mice, Inbred C57BL
-* Nose
-* Pandemics
-* Peptidyl-Dipeptidase A
-* Pneumonia, Viral
-* RNA, Viral
-* SARS-CoV-2
-* Stomach
-* Trachea
-* Viral Load
-* Virus Replication
-|keywords=* SARS-CoV-2
-* angiotensin-converting enzyme II
-* hACE2-KI/NIFDC
-* mouse model
-* pathogenesis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7250783
-}}
-{{medline-entry
-|title=COVID-19-associated cardiovascular morbidity in older adults: a position paper from the Italian Society of Cardiovascular Researches.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32430627
-|mesh-terms=* Age Factors
-* Aged
-* Betacoronavirus
-* COVID-19
-* Cardiovascular Diseases
-* Coronavirus Infections
-* Female
 * Humans
-* Italy
+* Longevity
+* Lysine
 * Male
-* Middle Aged
+* Memory
-* Pandemics
+* Methylation
-* Pneumonia, Viral
+* Mice
-* Risk Factors
+* Mitochondria
-* SARS-CoV-2
+* Neurons
-|keywords=* Acute myocardial injury
+* Proteins
-* Aging
+* RNA Interference
-* COVID-19
+* Spatial Learning
-* Cardiovascular system
+* Transcription Factors, General
-* Frailty
+|keywords=#f
-* SARS-CoV-2
+|full-text-url=https://sci-hub.do/10.1038/s41586-020-2037-y
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7237344
 }}
+==BDNF==
 {{medline-entry
-|title=Gut microbiota and Covid-19- possible link and implications.
+|title=Spermidine and spermine delay brain aging by inducing autophagy in SAMP8 mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32430279
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32268299
+|abstract=The natural polyamine spermidine and spermine have been reported to ameliorate aging and aging-induced dementia. However, the mechanism is still confused. An aging model, the senescence accelerated mouse-8 (SAMP8), was used in this study. Novel object recognition and the open field test results showed that oral administration of spermidine, spermine and rapamycin increased discrimination index, modified number, inner squares distance and times. Spermidine and spermine increased the activity of SOD, and decreased the level of MDA in the aging brain. Spermidine and spermine phosphorylate AMPK and regulate autophagy proteins (LC3, Beclin 1 and p62). Spermidine and spermine balanced mitochondrial and maintain energy for neuron, with the regulation of MFN1, MFN2, DRP1, COX IV and ATP. In addition, western blot results (Bcl-2, Bax and Caspase-3, NLRP3, IL-18, IL-1β) showed that spermidine and spermine prevented apoptosis and inflammation, and elevate the expression of neurotrophic factors, including NGF, PSD95and PSD93 and [[BDNF]] in neurons of SAMP8 mice. These results indicated that the effect of spermidine and spermine on anti-aging is related with improving autophagy and mitochondrial function.
-|mesh-terms=* Aging
+|keywords=* aging
-* Betacoronavirus
+* autophagy
-* COVID-19
+* mitochondrial dysfunction
-* Coronavirus Infections
+* polyamine
-* Diet
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185103
-* Dysbiosis
-* Gastrointestinal Microbiome
-* Gastrointestinal Tract
-* Homeostasis
-* Humans
-* Immunity
-* Lung
-* Pandemics
-* Pneumonia, Viral
-* SARS-CoV-2
-|keywords=* Covid-19
-* Diet
-* Dysbiosis
-* Gut microbiome
-* Immunity
-* Lung microbiota
-* SARS-CoV-2
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217790
 }}
 {{medline-entry
-|title=Inflamm-aging: Why older men are the most susceptible to SARS-CoV-2 complicated outcomes.
+|title=Microglia senescence occurs in both substantia nigra and ventral tegmental area.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32389499
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32275335
+|abstract=During aging humans lose midbrain dopamine neurons, but not all dopamine regions exhibit vulnerability to neurodegeneration. Microglia maintain tissue homeostasis and neuronal support, but microglia become senescent and likely lose some of their functional abilities. Since aging is the greatest risk factor for Parkinson's disease, we hypothesized that aging-related changes in microglia and neurons occur in the vulnerable substantia nigra pars compacta (SNc) but not the ventral tegmental area (VTA). We conducted stereological analyses to enumerate microglia and dopaminergic neurons in the SNc and VTA of 1-, 6-, 9-, 18-, and 24-month-old C57BL/J6 mice using sections double-stained with tyrosine hydroxylase (TH) and Iba1. Both brain regions show an increase in microglia with aging, whereas numbers of TH+ cells show no significant change after 9 months of age in SNc and 6 months in VTA. Morphometric analyses reveal reduced microglial complexity and projection area while cell body size increases with aging. Contact sites between microglia and dopaminergic neurons in both regions increase with aging, suggesting increased microglial support/surveillance of dopamine neurons. To assess neurotrophin expression in dopaminergic neurons, [[BDNF]] and TH mRNA were quantified. Results show that the ratio of [[BDNF]] to TH decreases in the SNc, but not the VTA. Gait analysis indicates subtle, aging-dependent changes in gait indices. In conclusion, increases in microglial cell number, ratio of microglia to dopamine neurons, and contact sites suggest that innate biological mechanisms compensate for the aging-dependent decline in microglia morphological complexity (senescence) to ensure continued neuronal support in the SNc and VTA.
-|mesh-terms=* Aged
+|keywords=* Parkinson's disease
-* Aged, 80 and over
+* aging-dependent neurodegeneration
-* Aging
+* dopamine neurons
-* Angiotensin-Converting Enzyme 2
+* microglia complexity
-* Antibodies, Monoclonal, Humanized
+* stereological analyses
-* Betacoronavirus
+* tyrosine hydroxylase; microglia senescence
-* COVID-19
+|full-text-url=https://sci-hub.do/10.1002/glia.23834
-* Comorbidity
+}}
-* Coronavirus Infections
+{{medline-entry
+|title=Towards an understanding of the physical activity-[[BDNF]]-cognition triumvirate: A review of associations and dosage.
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32171785
+|abstract=Physical activity has received substantial research attention due to its beneficial impact on cognition in ageing, particularly via the action of brain-derived neurotrophic factor ([[BDNF]]). It is well established that physical activity can elevate circulating levels of [[BDNF]], and that [[BDNF]] has neurotrophic, neuroprotective and cognitively beneficial properties. Yet, practical implementation of this knowledge is limited by a lack of clarity on context and dose-effect. Against a shifting backdrop of gradually diminishing physical and cognitive capacity in normal ageing, the type, intensity, and duration of physical activity required to elicit elevations in [[BDNF]], and more importantly, the magnitude of [[BDNF]] elevation required for detectable neuroprotection remains poorly characterised. The purpose of this review is to provide an overview of the association between physical activity, [[BDNF]], and cognition, with a focus on clarifying the magnitude of these effects in the context of normative ageing. We discuss the implications of the available evidence for the design of physical activity interventions intended to promote healthy cognitive ageing.
+|mesh-terms=* Aging
+* Brain-Derived Neurotrophic Factor
+* Cognition
+* Exercise
+* Healthy Aging
+* Humans
+|keywords=* Ageing
+* BDNF
+* Brain
+* Physical activity
+|full-text-url=https://sci-hub.do/10.1016/j.arr.2020.101044
+}}
+==BMP2==
+{{medline-entry
+|title=Interleukin-1β-Induced Senescence Promotes Osteoblastic Transition of Vascular Smooth Muscle Cells.
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32126555
+|abstract=Interleukin (IL)-1β, as a key biomarker and mediator of vascular calcification in patients with end-stage renal disease (ESRD), may be involved in the process of premature senescence of vascular smooth muscle cells (VSMCs). This work sought to investigate whether IL-1β-induced premature senescence contributes to the process of osteoblastic transition and vascular calcification in VSMCs. Eighty-eight patients with ESRD (aged 25-81 years), 11 healthy individuals, and 15 cases of lesion-free distal radial arteries from dialysis ESRD patients with angiostomy were collected in this study. Immunohistochemical analysis was performed to detect expression of IL-1β, p21, and bone morphogenetic protein-2 ([[BMP2]]) in the distal radial arteries. Primary human VSMCs from healthy neonatal umbilical cords were incubated with test agents for 1-3 days. Intracellular levels of reactive oxygen species (ROS) and senescence-associated-β-galactosidase (SA-β-gal) staining were used to detect senescent cells. Alizarin red staining and the calcium content of the cell layer were used to detect mineral deposition in VSMCs. Coincident with positive staining of IL-1β, p21, and [[BMP2]] in the lesion-free distal radial arteries, 66.67% patients showed mineral deposition. Serum IL-1β was 0.24 ± 0.57, 1.20 ± 2.95, and 9.41 ± 40.52 pg/mL in 11 healthy individuals, 20 patients without calcification, and 53 patients with calcification, respectively. Analysis of the cross-table chi-square test showed cardiovascular calcification is not correlated with levels of serum IL-1β in patients with ESRD (p = 0.533). In response to IL-1β, VSMCs showed a senescence-like phenotype, such as flat and enlarged morphology, increased expression of p21, an increased activity of SA-β-gal, and increased levels of ROS. IL-1β-induced senescence of VSMCs was required for the activation of IL-1β/NF-κB/p53/p21 signaling pathway. IL-1β-induced senescent VSMCs underwent calcification due to osteoblastic transition mainly depending upon the upregulation of [[BMP2]]. Resveratrol, an activator of sirtuin-1, postponed the IL-1β-induced senescence through blocking the NF-κB/p53/p21 pathway and attenuated the osteoblastic transition and calcification in VSMCs. High levels of IL-1β in medial smooth muscles of arteries may play roles in inducing senescence-associated calcification. IL-1β-induced senescence depending on the activation of the NF-κB/p53/p21 signaling pathway and contributing to osteoblastic transition of VSMCs.
+|mesh-terms=* Adult
+* Aged
+* Aged, 80 and over
 * Female
 * Humans
-* Inflammation
+* Interleukin-1beta
-* Interferon Type I
-* Interleukin-6
 * Male
-* Pandemics
+* Middle Aged
-* Peptidyl-Dipeptidase A
+* Muscle, Smooth, Vascular
-* Pneumonia, Viral
+* Osteoblasts
-* SARS-CoV-2
+|keywords=* Interleukin-1β
-* Severe Acute Respiratory Syndrome
+* Osteoblastic transition
-|keywords=* COVID-19
+* Senescence
-* Cardiovascular diseases
+* Vascular calcification
-* Host-directed therapies
+|full-text-url=https://sci-hub.do/10.1159/000504298
-* Inflamm-aging
-* SARS-CoV-2
-* interleukin-6
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7252014
 }}
-{{medline-entry
+==BOC==
-|title=Restoration of the Renin-Angiotensin System Balance Is a Part of the Effect of Fasting on Cardiovascular Rejuvenation: Role of Age and Fasting Models.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31571520
-|keywords=* aging
-* cardiac hypertrophy index
-* intermittent fasting
-* renin–angiotensin system (RAS)
-|full-text-url=https://sci-hub.do/10.1089/rej.2019.2254
-}}
 {{medline-entry
-|title=Angiotensin 1-7 alleviates aging-associated muscle weakness and bone loss, but is not associated with accelerated aging in [[ACE2]]-knockout mice.
+|title=Protein Requirements of Elderly Chinese Adults Are Higher than Current Recommendations.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31519791
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32140711
+|abstract=Due to a lack of research data on the protein requirements of the elderly in China, the estimated average requirement (EAR) and the recommended nutrient intake (RNI) of protein in the elderly remain the same as those in young and middle-aged people at 0.98 g/(kg·d). The objective of this study was to determine the protein requirements of healthy Chinese adults >65y old through use of the indicator amino acid oxidation (IAAO) method. Seven healthy adult men and 7 healthy adult women participated in the study, with protein intakes ranging from 0.3 to 1.8 g/(kg·d). The diets were isocaloric and provided energy at a 1.5 resting energy expenditure. Protein was given based on the lactalbumin. Phenylalanine and tyrosine were added to protein doses of 0.3-1.5 g/kg according to the highest dose of protein content [1.8 g/(kg·d)]. Phenylalanine and tyrosine concentrations were kept constant at each protein dose. The mean protein requirement was determined by applying a nonlinear mixed-effects model analysis to the F13CO2, which identified a breakpoint in F13CO2 in response to graded amounts of protein. This trial was registered with the Chinese clinical trial registry as ChiCTR-[[BOC]]-17010930. Protein EAR and RNI for healthy elderly Chinese adults were determined to be 0.91 and 1.17 g/(kg·d), respectively, based on the indicator amino acid oxidation technique. The estimates of protein requirements for Chinese adults >65 y in the present study are 3.4% and 19.4% higher than the current estimated requirements, 0.88 g/(kg·d) for EAR and 0.98 g/(kg·d) for RNI.
-|mesh-terms=* Adipose Tissue
+|mesh-terms=* Aged
 * Aging
-* Angiotensin I
+* Amino Acids
-* Angiotensin-Converting Enzyme 2
-* Animals
 * Body Weight
-* Bone Resorption
+* China
-* Cyclin-Dependent Kinase Inhibitor p16
+* Dietary Proteins
-* Forelimb
+* Energy Intake
-* Gene Deletion
+* Energy Metabolism
-* Hand Strength
+* Female
+* Humans
 * Male
-* Mice, Inbred C57BL
+* Nutritional Requirements
-* Mice, Knockout
+* Oxidation-Reduction
-* Muscle Weakness
+* Phenylalanine
-* Muscles
+* Recommended Dietary Allowances
-* Organ Size
+* Tyrosine
-* PAX3 Transcription Factor
+|keywords=* indicator amino acid oxidation
-* Peptide Fragments
+* older adults
-* Peptidyl-Dipeptidase A
+* phenylalanine oxidation
-* Proto-Oncogene Proteins
+* protein requirement
-* Receptors, G-Protein-Coupled
+* stable isotope
-* Renin-Angiotensin System
+|full-text-url=https://sci-hub.do/10.1093/jn/nxaa031
-* Time Factors
-|keywords=* Angiotensin 1-7
-* Angiotensin Converting Enzyme 2
-* Mas receptor
-* Muscle weakness
-* osteoporosis
-|full-text-url=https://sci-hub.do/10.1042/CS20190573
 }}
-==ACLY==
+==C3==
 {{medline-entry
-|title=In S. cerevisiae hydroxycitric acid antagonizes chronological aging and apoptosis regardless of citrate lyase.
+|title=Reduced sialylation triggers homeostatic synapse and neuronal loss in middle-aged mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32666259
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32087947
+|abstract=Sialic acid-binding Ig-like lectin (Siglec) receptors are linked to neurodegenerative processes, but the role of sialic acids in physiological aging is still not fully understood. We investigated the impact of reduced sialylation in the brain of mice heterozygous for the enzyme glucosamine-2-epimerase/N-acetylmannosamine kinase (GNE+/-) that is essential for sialic acid biosynthesis. We demonstrate that GNE+/- mice have hyposialylation in different brain regions, less synapses in the hippocampus and reduced microglial arborization already at 6 months followed by increased loss of neurons at 12 months. A transcriptomic analysis revealed no pro-inflammatory changes indicating an innate homeostatic immune process leading to the removal of synapses and neurons in GNE+/- mice during aging. Crossbreeding with complement [[C3]]-deficient mice rescued the earlier onset of neuronal and synaptic loss as well as the changes in microglial arborization. Thus, sialic acids of the glycocalyx contribute to brain homeostasis and act as a recognition system for the innate immune system in the brain.
+|mesh-terms=* Aging
+* Animals
+* Brain
+* Homeostasis
+* Immunity, Innate
+* Mice, Transgenic
+* Neurons
+* Racemases and Epimerases
+* Sialic Acid Binding Immunoglobulin-like Lectins
+* Sialic Acids
+* Synapses
 |keywords=* Aging
-* Apoptosis/necrosis
+* GNE
-* Caloric restriction mimetics
+* Glycocalyx
-* Hydroxycitric acid
+* Microglia
-* Oxidative stress
+* Neurodegeneration
-* Sch9 and Ras2 pathways
+* Neuroinflammation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7527365
+* Sialic acid
+|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.01.008
 }}
-==ACR==
+==CA1==
 {{medline-entry
-|title=Progenitor cell niche senescence reflects pathology of the parotid salivary gland in primary Sjögren's syndrome.
+|title=Functional Connectivity of Hippocampal CA3 Predicts Neurocognitive Aging via [[CA1]]-Frontal Circuit.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32159757
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32239141
+|abstract=The CA3 and [[CA1]] principal cell fields of the hippocampus are vulnerable to aging, and age-related dysfunction in CA3 may be an early seed event closely linked to individual differences in memory decline. However, whether the differential vulnerability of CA3 and [[CA1]] is associated with broader disruption in network-level functional interactions in relation to age-related memory impairment, and more specifically, whether CA3 dysconnectivity contributes to the effects of aging via [[CA1]] network connectivity, has been difficult to test. Here, using resting-state fMRI in a group of aged rats uncontaminated by neurodegenerative disease, aged rats displayed widespread reductions in functional connectivity of CA3 and [[CA1]] fields. Age-related memory deficits were predicted by connectivity between left CA3 and hippocampal circuitry along with connectivity between left [[CA1]] and infralimbic prefrontal cortex. Notably, the effects of CA3 connectivity on memory performance were mediated by [[CA1]] connectivity with prefrontal cortex. We additionally found that spatial learning and memory were associated with functional connectivity changes lateralized to the left CA3 and [[CA1]] divisions. These results provide novel evidence that network-level dysfunction involving interactions of CA3 with [[CA1]] is an early marker of poor cognitive outcome in aging.
+|keywords=* aging
-|keywords=* p16
+* functional connectivity
-* primary Sjögren’s syndrome
+* hippocampus
-* salivary gland
+* spatial memory
-* salivary gland progenitor cells
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7325802
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7516109
 }}
 {{medline-entry
-|title=Jumping Joints: The Complex Relationship Between Osteoarthritis and Jumping Mechanography.
+|title=Integration of qRT-PCR and Immunohistochemical Techniques for mRNA Expression and Localization of m1AChR in the Brain of Aging Rat.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31655874
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32219760
+|abstract=The neurotransmitter acetylcholine (ACh) is involved in memory and cognitive functions, which normally decline with age. In this chapter, we describe qRT-PCR and immunohistochemical protocols for measurement of muscarinic ACh receptor M1 (m1AChR) levels in the brains of middle-aged rats, with and without administration of grape seed proanthocyanidin extract (GSPE) and exercise training. The analyses revealed that the interventions led to an increase in m1AChR mRNA and protein levels in the [[CA1]] subfield of hippocampus. This would be expected to enhance Ach levels at synapses and thereby boost cognitive ability. The protocols can be applied to m1AChR measurements in neurodegenerative diseases and dementia.
+|keywords=* Acetylcholine
-|keywords=* Aging
+* Aging
-* Jumping mechanography
+* Brain
-* Muscle
+* Immunohistochemistry
-* Osteoarthritis
+* m1AChR
-* Sarcopenia
+* qRT-PCR
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6994439
+|full-text-url=https://sci-hub.do/10.1007/978-1-0716-0471-7_23
 }}
-==ACVR1==
 {{medline-entry
-|title=Fibrodysplasia Ossificans Progressiva (FOP): A Segmental Progeroid Syndrome.
+|title=Role of Eclipta prostrata extract in improving spatial learning and memory deficits in D-galactose-induced aging in rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31998237
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32186114
+|abstract=To investigate the role of Eclipta prostrata (E. prostrata) extract in improving spatial learning and memory deficits in D-galactose-induced aging in rats. Rats were divided into five groups, with 10 animals in each group. Aging rats were produced by treatment with 100 mg·kg-1·d-1 of D-galactose for 6 weeks. Rats in the E. prostrata treatment groups received an aqueous extract of E. prostrata orally at a concentration of 50, 100, or 200 mg·kg-1·d-1 for 3 weeks. Animals in both the normal and model groups were treated with similar volumes of saline. Spatial memory performance was measured using the Morris water maze. The mRNA levels and enzyme activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) were analyzed using real-time quantitative PCR and spectrophotometry, respectively. The levels of induced nitric oxide synthase (iNOS), nitric oxide (NO), dopamine (DA), norepinephrine (NE), and serotonin (5-HT) were determined using enzyme-linked immunosorbent assay and spectrophotometry. Compared with the normal group, rats in the D-galactose-treated model group exhibited significant memory loss. There was severe damage to the hippocampal [[CA1]] area, and expression levels of SOD, CAT, GPx, and GR were significantly decreased in the model group compared with the normal group. In the model group, levels of iNOS and NO were significantly increased compared with the normal group. However, treatment with E. prostrata extract reversed the conditions caused by D-galactose-induced aging, especially in the groups with higher treatment concentrations. Compared with the normal group, the levels of DA, NE, and 5-HT were significantly lower in the D-galactose-treated model group. In the E. prostrata extract-treated groups, however, there was a dose-dependent upregulation of DA, NE, and 5-HT expression. Our results suggest that administration of E. prostrata extract can result in an improvement in the learning and memory impairments that are induced by D-galactose treatment in rats. This improvement may be the result of enhanced antioxidative ability, decreased iNOS and NO levels, and the induction of DA, NE, and 5-HT expression in the brain.
+|mesh-terms=* Aging
+* Animals
+* Behavior, Animal
+* CA1 Region, Hippocampal
+* Catalase
+* Dopamine
+* Eclipta
+* Galactose
+* Gene Expression Regulation, Enzymologic
+* Glutathione Peroxidase
+* Glutathione Reductase
+* Male
+* Memory Disorders
+* Nitric Oxide
+* Nitric Oxide Synthase Type II
+* Norepinephrine
+* Plant Extracts
+* RNA, Messenger
+* Rats
+* Rats, Sprague-Dawley
+* Serotonin
+* Spatial Learning
+* Superoxide Dismutase
+|keywords=* Antioxidants
+* Eclipta
+* Galactose
+* Memory disorders
+* Spatial learning
-|keywords=* ACVR1
-* activin A
-* cell senescence
-* fibrodysplasia ossificans progressiva
-* progeroid syndrome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6966325
 }}
-==ADA==
 {{medline-entry
-|title=Adenosine Metabolism in the Cerebral Cortex from Several Mice Models during Aging.
+|title=Differential annualized rates of hippocampal subfields atrophy in aging and future Alzheimer's clinical syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33023260
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32107063
+|abstract=Several studies have investigated the differential vulnerability of hippocampal subfields during aging and Alzheimer's disease (AD). Results were often contradictory, mainly because these works were based on concatenations of cross-sectional measures in cohorts with different ages or stages of AD, in the absence of a longitudinal design. Here, we investigated 327 participants from a population-based cohort of nondemented older adults with a 14-year clinical follow-up. MRI at baseline and 4 years later were assessed to measure the annualized rates of hippocampal subfields atrophy in each participant using an automatic segmentation pipeline with subsequent quality control. On the one hand, CA4 dentate gyrus was significantly more affected than the other subfields in the whole population ([[CA1]]-3: -0.68%/year; subiculum: -0.99%/year; and CA4-DG: -1.39%/year; p < 0.0001). On the other hand, the annualized rate of [[CA1]]-3 atrophy was associated with an increased risk of developing Alzheimer's clinical syndrome over time, independently of age, gender, educational level, and ApoE4 genotype (HR = 2.0; CI 95% 1.4-3.0). These results illustrate the natural history of hippocampal subfields atrophy during aging and AD by showing that the dentate gyrus is the most vulnerable subfield to the effects of aging while the cornu-ammonis is the primary target of AD pathophysiological processes, years before symptom onset.
+|mesh-terms=* Aged
-|keywords=* adenosine metabolism
+* Aging
-* aging
+* Alzheimer Disease
-* animal models
+* Atrophy
-* glutamate
+* Cohort Studies
-* purinergic signaling
+* Cross-Sectional Studies
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7582336
+* Dentate Gyrus
+* Female
+* Hippocampus
+* Humans
+* Magnetic Resonance Imaging
+* Male
+* Neuropsychological Tests
+* Risk
+|keywords=* Aging
+* Alzheimer's disease
+* Hippocampal subfields
+* MRI
+|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.01.011
 }}
-==ADAM10==
+==CCK==
 {{medline-entry
-|title=NKG2D Ligand Shedding in Response to Stress: Role of [[ADAM10]].
+|title=Effects of Age on Acute Appetite-Related Responses to Whey-Protein Drinks, Including Energy Intake, Gastric Emptying, Blood Glucose, and Plasma Gut Hormone Concentrations-A Randomized Controlled Trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32269567
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32268554
+|abstract=Protein-rich supplements are used commonly to increase energy intake in undernourished older people. This study aimed to establish age effects on energy intake, appetite, gastric emptying, blood glucose, and gut hormones in response to protein-rich drinks. In a randomized double-blind, order, 13 older men (age: 75 ± 2 yrs, body mass index (BMI): 26 ± 1 kg/m ) and 13 younger (23 ± 1 yrs, 24 ± 1 kg/m ) men consumed (i) a control drink (~2 kcal) or drinks (450 mL) containing protein/fat/carbohydrate: (ii) 70 g/0 g/0 g (280 kcal/'P ), (iii) 14 g/12.4 g/28 g (280 kcal/'M ), (iv) 70 g/12.4 g/28 g (504 kcal/'M ), on four separate days. Appetite (visual analog scales), gastric emptying (3D ultrasonography), blood glucose, plasma insulin, ghrelin, cholecystokinin ([[CCK]]), glucagon-like peptide-1 (GLP-1) concentrations (0-180 min), and ad-libitum energy intake (180-210 min) were determined. Older men, compared to younger men, had higher fasting glucose and [[CCK]] concentrations and lower fasting GLP-1 concentrations (all [i]p[/i] < 0.05). Energy intake by P  compared to control was less suppressed in older men (increase: 49 ± 42 kcal) than it was in younger men (suppression: 100 ± 54 kcal, [i]p[/i] = 0.038). After the caloric drinks, the suppression of hunger and the desire to eat, and the stimulation of fullness was less ([i]p[/i] < 0.05), and the stimulation of plasma GLP-1 was higher ([i]p[/i] < 0.05) in older men compared to younger men. Gastric emptying, glucose, insulin, ghrelin, and [[CCK]] responses were similar between age groups. In conclusion, ageing reduces the responses of caloric drinks on hunger, the desire to eat, fullness, and energy intake, and protein-rich nutrition supplements may be an effective strategy to increase energy intake in undernourished older people.
+|keywords=* aging
-|keywords=* ADAM10
+* appetite
-* NKG2D
+* energy intake
-* NKG2D ligands
+* gastric emptying
-* cancer
+* glucose
-* chemotherapy
+* gut hormones
-* senescence
+* whey protein
-* shedding
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7231005
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7109295
 }}
+==CCL20==
 {{medline-entry
-|title=Chronic Mild Stress Modified Epigenetic Mechanisms Leading to Accelerated Senescence and Impaired Cognitive Performance in Mice.
+|title=p53 and p53-related mediators PAI-1 and IGFBP-3 are downregulated in peripheral blood mononuclear cells of HIV-patients exposed to non-nucleoside reverse transcriptase inhibitors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32050516
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32272174
+|abstract=The improved effectiveness and safety of the combined antiretroviral therapy (cART) has largely diminished mortality and AIDS-defining morbidity of HIV-patients. Nevertheless, chronic age-related diseases in these individuals are more common and their underlying pathogenic mechanisms of these actions seem to involve accelerated aging and enhanced inflammation. The present study explores markers of these processes in a heterogenous Spanish HIV cohort using peripheral blood samples of HIV-patients and matched uninfected controls. We isolated periheral blood mononuclear cells (PBMCs) and i) compared the expression of a panel of 14 genes related to inflammation and senescence in PBMCs of HIV-patients vs matched uninfected controls, ii) analyzed the expression in HIV-patients in association with a number of demographic, biochemical and immunological parameters and iii) in relation with the current cART they received. PBMCs of HIV-patients displayed significantly increased expression of general inflammatory genes (IL6, IL18 and CXCL10) and this occurs irrespectively of the antiviral therapy they have been receiving. Conversely, levels of senescence-associated genes TP53, SERPINE1andIGFBP3 were slightly but significantly reduced in patients compared to uninfected matched individuals and this effect is related to NNRTI-containing treatments. The expression of the inflammatory markers IL6, IL18, IL1B, TNFA, RELA, CCL2, [[CCL20]] and CXCL10 displayed correlation with certain demographic, morbidity- and HIV infection-related parameters. The levels of TP53 mRNA were positively associated only with plasma LDL. Correlation analysis between the expressions of pairs of genes revealed a different pattern between HIV-patients and controls. The diminished expression of TP53 and SERPINE1 in HIV-patients was also observed at a protein level, and the correlation between the two proteins (p53 and PAI1) in patients and controls showed the opposite trend. In conclusion, HIV-patients show dysregulation of p53 and p53-related mediators, a phenomenon which may be of pathophysiological relevance and could be related to the shorter health- and/or life-span observed in these individuals.
-|mesh-terms=* ADAM10 Protein
+|keywords=* Aging
-* Aging
+* Antiretroviral drugs
-* Amyloid Precursor Protein Secretases
+* HIV
-* Animals
+* Inflammation
-* Cognition
+* NNRTI
-* Epigenesis, Genetic
+* Senescence
-* Female
+* p53
-* Glial Fibrillary Acidic Protein
+|full-text-url=https://sci-hub.do/10.1016/j.antiviral.2020.104784
-* Glycogen Synthase Kinase 3 beta
-* Mechanistic Target of Rapamycin Complex 1
-* Membrane Proteins
-* Mice
-* MicroRNAs
-* NF-kappa B
-* Reactive Oxygen Species
-* Signal Transduction
-* Stress, Psychological
-|keywords=* Alzheimer’s disease
-* SAMP8
-* SAMR1
-* age-related cognitive decline
-* autophagy
-* cognition
-* epigenetics
-* inflammation
-* oxidative stress
-* senescence
-* stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7037343
 }}
-==ADAM17==
+==CCL28==
 {{medline-entry
-|title=ACE2/[[ADAM17]]/TMPRSS2 Interplay May Be the Main Risk Factor for COVID-19.
+|title=Age-related chemokine alterations affect IgA secretion and gut immunity in female mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33117379
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32277312
+|abstract=The chemokines CCL25 and [[CCL28]], which promote immune cell migration, are primarily expressed in the small and large intestines and play critical roles in sustaining gut immunity. In particular, these chemokines are closely related to intestinal IgA secretion. However, there is no research regarding the effects of aging on CCL25 and [[CCL28]] expression and function. Therefore, in the present study, we investigated the effects of aging on production of CCL25 and [[CCL28]], and on gut immunity, especially IgA secretion, using young and aged female mice. By aging, the levels of small intestinal mRNA and protein of CCL25 lowered, while these levels of [[CCL28]] in colon became higher. Moreover, the number of IgA-antibody secreting cells (IgA-ASCs) and total IgA concentration decreased in the small intestine due to the age-associated reduction of CCL25. In contrast, colonic IgA production was increased due to up-regulation of [[CCL28]], while the number of colonic IgA-ASCs was unchanged with aging. These results clearly demonstrate that aging-associated decrease in small intestinal CCL25 production and increase in colonic [[CCL28]] production c be involved in aging-associated deterioration of gut immunity.
-|mesh-terms=* ADAM17 Protein
+|keywords=* Aging
-* Aged
+* CCL25
-* Aging
+* CCL28
-* Angiotensin-Converting Enzyme 2
+* Gut immunity
-* Betacoronavirus
+* IgA
-* COVID-19
+|full-text-url=https://sci-hub.do/10.1007/s10522-020-09877-9
-* Comorbidity
-* Coronavirus Infections
-* Female
-* Humans
-* Male
-* Pandemics
-* Peptidyl-Dipeptidase A
-* Pneumonia, Viral
-* Receptors, Interleukin-6
-* Risk Factors
-* SARS-CoV-2
-* Serine Endopeptidases
-* Tumor Necrosis Factor-alpha
-|keywords=* ACE2
-* ADAM17
-* COVID-19 pathophysiology
-* SARS-CoV-2
-* TMPRSS2
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7575774
 }}
-==ADH5==
+==CCR2==
 {{medline-entry
-|title=Can Serum Nitrosoproteome Predict Longevity of Aged Women?
+|title=Tet2-mediated clonal hematopoiesis in nonconditioned mice accelerates age-associated cardiac dysfunction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33260845
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32154790
+|abstract=Clonal hematopoiesis of indeterminate potential is prevalent in elderly individuals and associated with increased risks of all-cause mortality and cardiovascular disease. However, mouse models to study the dynamics of clonal hematopoiesis and its consequences on the cardiovascular system under homeostatic conditions are lacking. We developed a model of clonal hematopoiesis using adoptive transfer of unfractionated ten-eleven translocation 2-mutant (Tet2-mutant) bone marrow cells into nonirradiated mice. Consistent with age-related clonal hematopoiesis observed in humans, these mice displayed a progressive expansion of Tet2-deficient cells in multiple hematopoietic stem and progenitor cell fractions and blood cell lineages. The expansion of the Tet2-mutant fraction was also observed in bone marrow-derived [[CCR2]]+ myeloid cell populations within the heart, but there was a negligible impact on the yolk sac-derived [[CCR2]]- cardiac-resident macrophage population. Transcriptome profiling revealed an enhanced inflammatory signature in the donor-derived macrophages isolated from the heart. Mice receiving Tet2-deficient bone marrow cells spontaneously developed age-related cardiac dysfunction characterized by greater hypertrophy and fibrosis. Altogether, we show that Tet2-mediated hematopoiesis contributes to cardiac dysfunction in a nonconditioned setting that faithfully models human clonal hematopoiesis in unperturbed bone marrow. Our data support clinical findings that clonal hematopoiesis per se may contribute to diminished health span.
-|keywords=* aging
-* cardiovascular disease
-* muscle atrophy
-* nitrosative stress
-* proteomics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7731247
-}}
-==ADM==
-{{medline-entry
-|title=Assessment of age-related differences in decomposition-based quantitative EMG in the intrinsic hand muscles: A multivariate approach.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32693193
 |keywords=* Aging
-* Decomposition-based quantitative electromyography (DQEMG)
+* Bone marrow transplantation
-* Hand muscle
+* Cardiology
-* Jiggle
+* Hematopoietic stem cells
-* Motor unit potential (MUP)
+* Macrophages
-* Multivariate
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7213793
-|full-text-url=https://sci-hub.do/10.1016/j.clinph.2020.06.017
 }}
-{{medline-entry
+==CD27==
-|title=Evaluation of transcriptional levels of the natriuretic peptides, endothelin-1, adrenomedullin, their receptors and long non-coding RNAs in rat cardiac tissue as cardiovascular biomarkers of aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31629715
-|keywords=* ADM system
-* Aging
-* Biomarkers
-* ET-1system
-* LncRNA
-* NP system
-|full-text-url=https://sci-hub.do/10.1016/j.peptides.2019.170173
-}}
-==ADORA2B==
 {{medline-entry
-|title=Adenosine A2B receptor: A pathogenic factor and a therapeutic target for sensorineural hearing loss.
+|title=The Interplay between [[CD27]]  and [[CD27]]  B Cells Ensures the Flexibility, Stability, and Resilience of Human B Cell Memory.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33131093
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32130900
+|abstract=Memory B cells (MBCs) epitomize the adaptation of the immune system to the environment. We identify two MBC subsets in peripheral blood, [[CD27]]  and [[CD27]]  MBCs, whose frequency changes with age. Heavy chain variable region (VH) usage, somatic mutation frequency replacement-to-silent ratio, and CDR3 property changes, reflecting consecutive selection of highly antigen-specific, low cross-reactive antibody variants, all demonstrate that [[CD27]]  and [[CD27]]  MBCs represent sequential MBC developmental stages, and stringent antigen-driven pressure selects [[CD27]]  into the [[CD27]]  MBC pool. Dynamics of human MBCs are exploited in pregnancy, when 50% of maternal MBCs are lost and [[CD27]]  MBCs transit to the more differentiated [[CD27]]  stage. In the postpartum period, the maternal MBC pool is replenished by the expansion of persistent [[CD27]]  clones. Thus, the stability and flexibility of human B cell memory is ensured by [[CD27]]  MBCs that expand and differentiate in response to change.
+|keywords=* CD27
-|keywords=* ADA-deficiency
+* VH repertoire
-* adenosine deaminase deficiency
 * aging
-* myelin protein zero
+* germinal center
-* myelination
+* immunodeficiency
-|full-text-url=https://sci-hub.do/10.1096/fj.202000939R
+* immunological memory
+* memory B cells
+* pregnancy
+* spleen
+* vaccine
+|full-text-url=https://sci-hub.do/10.1016/j.celrep.2020.02.022
 }}
-==ADRA2A==
+==CD28==
 {{medline-entry
-|title=α2A-Adrenergic Receptor Inhibits the Progression of Cervical Cancer Through Blocking PI3K/AKT/mTOR Pathway.
+|title=Immunosenescent characteristics of T cells in young patients following haploidentical haematopoietic stem cell transplantation from parental donors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33116632
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32280463
+|abstract=Paediatric and adolescent patients in need of allogeneic haematopoietic stem cell transplantation (HSCT) generally receive stem cells from older, unrelated or parental donors when a sibling donor is not available. Despite encouraging clinical outcomes, it has been suggested that immune reconstitution accompanied by increased replicative stress and a large difference between donor and recipient age may worsen immunosenescence in paediatric recipients. In this study, paired samples were collected at the same time from donors and recipients of haploidentical haematopoietic stem cell transplantation (HaploSCT). We then conducted flow cytometry-based phenotypic and functional analyses and telomere length (TL) measurements of 21 paired T-cell sets from parental donors and children who received T-cell-replete HaploSCT with post-transplant cyclophosphamide (PTCy). Senescent T cells, [[CD28]]  or CD57  cells, were significantly expanded in patients. Further, not only CD4 [[CD28]]  T cells, but also CD4 [[CD28]]  T cells showed reduced cytokine production capacity and impaired polyfunctionality compared with parental donors, whereas their TCR-mediated proliferation capacity was comparable. Of note, the TL in patient T cells was preserved, or even slightly longer, in senescent T cells compared with donor cells. Regression analysis showed that senescent features of CD4  and CD8  T cells in patients were influenced by donor age and the frequency of [[CD28]]  cells, respectively. Our data suggest that in paediatric HaploSCT, premature immunosenescent changes occur in T cells from parental donors, and therefore, long-term immune monitoring should be conducted.
+|keywords=* CD28− T cells
-|keywords=* ADRA2A
+* HaploSCT
-* PI3K/Akt/mTOR pathway
+* immune monitoring
-* cervical cancer
+* immunosenescence
-* metastasis
+* telomere length
-* proliferation
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7142179
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7574911
 }}
-==AFM==
 {{medline-entry
-|title=Photocatalytic aging process of Nano-TiO  coated polypropylene microplastics: Combining atomic force microscopy and infrared spectroscopy ([[AFM]]-IR) for nanoscale chemical characterization.
+|title=Diagnosis-independent loss of T-cell costimulatory molecules in individuals with cytomegalovirus infection.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33080556
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32209361
+|abstract=Major depressive disorder (MDD) is associated with physiological changes commonly observed with increasing age, such as inflammation and impaired immune function. Age-related impaired adaptive immunity is characterized by the loss of naive T-cells and the reciprocal accumulation of memory T-cells together with the loss of T-cell co-stimulatory molecules. Additionally, the presence and activity of cytomegalovirus (CMV) alters the architecture of the T-cell compartment in a manner consistent with premature aging. Because CMV is also thought to reactivate with psychological stress, this study tested whether MDD influences age-related phenotypes of T-cell populations in the context of CMV infection in young and middle-aged adults. Morning blood samples from volunteers with a DSM-IV diagnosis of MDD (n = 98, mean age(SD) = 36(10) years, 74.5% female, 57.1% CMV ) and comparison controls (n = 98, mean age(SD) = 34(10) years, 68.4% female, 51.0% CMV ) were evaluated for CMV IgG antibody status and the distribution of late differentiated (CD27 [[CD28]] ) cells within CD4  and CD8  T-cell subsets, i.e. naive (CCR7 CD45RA ), effector memory (EM, CCR7 CD45RA ), central memory (CM, CCR7 CD45RA ) and effector memory cells re-expressing CD45RA (EMRA, CCR7 CD45RA ). Mixed linear regression models controlling for age, sex, ethnicity and flow cytometry batch showed that CMV seropositivity was associated with a reduction in naive T-cells, expansion of EMRA T-cells, and a greater percent distribution of CD27 [[CD28]]  cells within CD4  and CD8  memory T-cell subsets (p's < 0.004), but there was no significant effect of MDD, nor any significant interaction between CMV and diagnosis. Unexpectedly, depressed men were less likely to be CMV  and depressed women were more likely to be CMV  than sex-matched controls suggesting a possible interaction between sex and MDD on CMV susceptibility, but this three-way interaction did not significantly affect the T-cell subtypes. Our findings suggest that depression in young and middle-aged adults does not prematurely advance aging of the T-cell compartment independently of CMV, but there may be significant sex-specific effects on adaptive immunity that warrant further investigation.
+|keywords=* Biological aging
-|keywords=* AFM-IR
+* Cytomegalovirus
-* Aging process
+* Depression
-* Microplastics
+* Immunosenescence
-* Nanoscale characterization
+* Major depressive disorder
-* Polypropylene
+* Sex differences
-|full-text-url=https://sci-hub.do/10.1016/j.jhazmat.2020.124159
+* T-cells
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7594105
 }}
 {{medline-entry
-|title=Nanoscale infrared, thermal and mechanical properties of aged microplastics revealed by an atomic force microscopy coupled with infrared spectroscopy ([[AFM]]-IR) technique.
+|title=Accelerated immunosenescence in rheumatoid arthritis: impact on clinical progression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32702545
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32190092
+|abstract=Patients with rheumatoid arthritis (RA) develop features of accelerated ageing, including immunosenescence. These changes include decreased thymic functionality, expansion of late-differentiated effector T cells, increased telomeric attrition, and excessive production of cytokines (senescence-associated secretory phenotype). The progression of RA has been associated with the early development of age-related co-morbidities, including osteoporosis, cardiovascular complications, and cognitive impairment. Here I review data supporting the hypothesis that immune-senescence contributes to the aggravation of both articular and extra-articular manifestations. Of note, poor cognitive functions in RA were associated with senescent [[CD28]]- T cells, inflammaging, and autoantibodies against brain antigens. The pathways of immune-to-brain communication are discussed and provide the rationale for the cognitive impairment reported in RA.
+|keywords=* Ageing
-|keywords=* AFM-IR
+* Cell senescence
-* Aging process
+* Cognitive impairment
-* Mechanical properties
+* Immune ageing
-* Microplastics (MPs)
+* Rheumatoid arthritis
-* Thermal analysis
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7068869
-|full-text-url=https://sci-hub.do/10.1016/j.scitotenv.2020.140944
 }}
 {{medline-entry
-|title=Detecting zeta potential of polydimethylsiloxane (PDMS) in electrolyte solutions with atomic force microscope.
+|title=Accelerated immune aging was correlated with lupus-associated brain fog in reproductive-age systemic lupus erythematosus patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32521351
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32107852
+|abstract=Cognitive impairment is common in systemic lupus erythematosus (SLE) patients with substantial adverse effects on function and quality of life. One hypothesis to understand the mechanisms of cognitive impairment in SLE is accelerated immunosenescence. The aim of this study is to observe the correlation between immunosenescence with cognitive impairment in patients with SLE. Sixty-one female SLE patient were measured for CD4 and CD8 T cell-associated senescence markers, including percentage of end-stage differentiated T cells (CD4 and CD8 T cells expressing CD57  or loss of [[CD28]] expression), of naïve T cells (CD4  CD45RA  and CD8  CD45RA  ), memory T cells (CD4  CD45RO  and CD8  CD45RO  ), and antigen-experienced T cells (CD4  KLRG1  and CD8  KLRG1  ) which were measured using flow cytometry. One hallmark of immunosenescence called immune risk profile (IRP) was defined by an inverted ratio of CD4 and CD8. Cognitive functions were measured by Mini-Mental State Examination (MMSE) and Montréal Cognitive Assessment (MOCA) questionnaire. Thirty-six (59.1%) SLE patients who had IRP develop significantly lower attention and recall from both MMSE (P = .005 and P = .000) and MOCA (P = .017 and P = .000) examinations. Decreased visuospatial ability was also found in patients with IRP measured by MOCA (P = .046). There was a negative correlation between memory CD4  CD45RO  T cells with recall and visuospatial domain (R = -0.204, P = .039 and R = -0.250, P = .033; respectively), and negative correlation between CD8  [[CD28]]  T cells with recall and attention domain (R = -0.249, P = .027 and R = -0.145, P = .048, respectively). Systemic lupus erythematosus patients develop an accelerated immunosenescence which contributes to cognitive dysfunction, especially in attention, recall, and visuospatial domains.
+|keywords=* immunosenescence
-|keywords=* AFM
+* lupus-associated brain fog
-* Air plasma treatment
+* systemic lupus erythematosus
-* Liquid aging
+|full-text-url=https://sci-hub.do/10.1111/1756-185X.13816
-* PDMS
-* Zeta potential
-|full-text-url=https://sci-hub.do/10.1016/j.jcis.2020.05.061
 }}
 {{medline-entry
-|title=Recent Applications of Advanced Atomic Force Microscopy in Polymer Science: A Review.
+|title=T cells, aging and senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32429499
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32092501
+|abstract=The T cell compartment undergoes characteristic changes with age, which contribute to increased incidence and severity of infections and reduced immunogenicity and efficacy of many vaccines in the older population. Production of naïve T cells is severely impaired due to a decreased output of lymphoid cells from the bone marrow and the involution of the thymus. At the same time, antigen-experienced, highly differentiated T cells accumulate resulting in a diminished T cell receptor repertoire. These cells show some similarities with senescent cells, such as shorter telomers, accumulated DNA damage and metabolic changes. Latent infection with Cytomegalovirus also impacts the T cell compartment and aggravates several of its age-associated changes. Loss of [[CD28]] expression is one hallmark of T cells after repeated antigenic stimulation, but [[CD28]]  T cells cannot be considered truly senescent as e.g. they are still able to proliferate upon adequate stimulation. Several additional markers have been suggested in order to define a potential fully senescent T cell population, but no consensus definition has been reached so far. It has been postulated that highly differentiated senescent-like T cells are unable to eliminate other senescent cell types. Removal of senescent non-immune cells has been shown to be beneficial for the organism and a reliable definition of senescent T cells is essential for an extension of this concept to T cells.
+|keywords=* Aging
+* Senescence
+* T cells
+|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110887
+}}
+==CD38==
-|keywords=* AFM-IR
-* blends
-* nanoscale characterization
-* polymer aging
-* polymer composites
-* polymers
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7284686
-}}
 {{medline-entry
-|title=Active fractions of mannoproteins derived from yeast cell wall stimulate innate and acquired immunity of adult and elderly dogs.
+|title=[[CD38]] in Neurodegeneration and Neuroinflammation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32288071
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32085567
+|abstract=Neurodegenerative diseases are characterized by neuronal degeneration as well as neuroinflammation. While [[CD38]] is strongly expressed in brain cells including neurons, astrocytes as well as microglial cells, the role played by [[CD38]] in neurodegeneration and neuroinflammation remains elusive. Yet, [[CD38]] expression increases as a consequence of aging which is otherwise the primary risk associated with neurodegenerative diseases, and several experimental data demonstrated that [[CD38]] knockout mice are protected from neurodegenerative and neuroinflammatory insults. Moreover, nicotinamide adenine dinucleotide, whose levels are tightly controlled by [[CD38]], is a recognized and potent neuroprotective agent, and NAD supplementation was found to be beneficial against neurodegenerative diseases. The aims of this review are to summarize the physiological role played by [[CD38]] in the brain, present the arguments indicating the involvement of [[CD38]] in neurodegeneration and neuroinflammation, and to discuss these observations in light of [[CD38]] complex biology.
+|keywords=* ALS.
+* Alzheimer’s disease
+* CD38
+* NAD
+* Parkinson’s disease
+* aging
+* neurodegeneration
+* neuroinflammation
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072759
+}}
+==CD4==
-|keywords=* AFM, active fraction of mannoproteins
+{{medline-entry
-* ALP, alkaline phosphatase
+|title=The effects of advanced maternal age on T-cell subsets at the maternal-fetal interface prior to term labor and in the offspring: a mouse study.
-* ALT, alanine aminotransferase
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32279324
-* Ageing
+|abstract=Women who conceive at 35 years of age or older, commonly known as advanced maternal age, have a higher risk of facing parturition complications and their children have an increased risk of developing diseases later in life. However, the immunological mechanisms underlying these pathological processes have yet to be established. To fill this gap in knowledge, using a murine model and immunophenotyping, we determined the effect of advanced maternal age on the main cellular branch of adaptive immunity, T cells, at the maternal-fetal interface and in the offspring. We report that advanced maternal age impaired the process of labor at term, inducing dystocia and delaying the timing of delivery. Advanced maternal age diminished the number of specific proinflammatory T-cell subsets [T helper type 1 (Th1): [[CD4]]  IFN-γ  , CD8  IFN-γ  and Th9: [[CD4]]  IL-9  ], as well as [[CD4]]  regulatory T cells ([[CD4]]  CD25  FoxP3  T cells), at the maternal-fetal interface prior to term labor. Advanced maternal age also altered fetal growth and survival of the offspring in early life. In addition, infants born to advanced-age mothers had alterations in the T-cell repertoire but not in CD71  erythroid cells (CD3  CD71  TER119  cells). This study provides insight into the immune alterations observed at the maternal-fetal interface of advanced-age mothers and their offspring.
-* CBC, complete blood count
+|mesh-terms=* Adult
-* CD21+, B lymphocyte
+* Aging
-* CD4+, auxiliary T lymphocyte
+* Animals
-* CD5+, total T lymphocyte
+* Female
-* CD8+, cytotoxic lymphocyte
+* Humans
-* CO, cells only
+* Live Birth
-* Canine
+* Mice
-* DCHT, delayed cutaneous hypersensitivity test
+* Mice, Transgenic
-* FOSs, fructooligosaccharides
+* Placenta
-* GALT, gut-associated lymphoid tissue
+* Pregnancy
-* IL-12, interleukin 12
+* T-Lymphocyte Subsets
-* IgA, immunoglobulin A
+|keywords=* birth weight
-* Immunosenescence
+* neonate
-* LPS, bacterial lipopolysaccharide
+* offspring
-* MOSs, mannanoligosaccharides
+* pregnancy
-* NADPH, reduced nicotinamide adenine dinucleotide phosphate
+* preterm labor
-* NO, nitrogen monoxide
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7290081
-* NOS, nitric oxide synthase
-* OD, optical density
-* PMA, phorbol myristate acetate
-* Saccharomyces cerevisiae
-* Senescence
-* TNF-α, tumour necrosis factor alpha
-* Th1, helper T lymphocyte
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7126846
 }}
 {{medline-entry
-|title=The Effect of Waste Engine Oil and Waste Polyethylene on UV Aging Resistance of Asphalt.
+|title=Structural and Functional Changes in the Mesenteric Lymph Nodes in Humans during Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32155867
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32248450
+|abstract=Morphometric analysis of structural and functional changes in the human mesenteric lymph nodes during aging revealed the development of fibrous connective tissue, fragmentation of the lymphoid parenchyma, the absence of follicles with germinal centers, and a decrease in the level of lymphocyte proliferation, which was confirmed by the absence of Ki-67  cells. The paracortical zone lacked [[CD4]]  T helpers that regulate both cellular and humoral immunity. High content of plasma cells and eosinophilic granulocytes in the medullary cords and sinuses reflects the development of autoimmune processes associated with a decrease in the number of regulatory T lymphocytes. The development of fibrous connective tissue in the sinus system complicates lymph flow through the lymph node and impairs lymph filtration.
+|keywords=* age-related involution
-|keywords=* Fourier transform infrared spectroscopy
+* aging
-* atomic force microscopy
+* immune system
-* gel permeation chromatography
+* immunomorphology
-* ultraviolet aging
+* mesenteric lymph nodes
-* waste engine oil
+|full-text-url=https://sci-hub.do/10.1007/s10517-020-04782-0
-* waste polyethylene
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7182932
 }}
 {{medline-entry
-|title=Mechanical properties measured by atomic force microscopy define health biomarkers in ageing C. elegans.
+|title=Neurocognitive Functioning is Associated with Self-Reported and Performance-Based Treatment Management Abilities in People Living with HIV with Low Health Literacy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32098962
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32090235
+|abstract=People living with HIV (PLWH) are at higher risk for poorer neurocognitive functioning and health literacy than uninfected persons, which are associated with worse medical outcomes. Aging research suggests that the effect of neurocognitive functioning on health outcomes may be more pronounced in those with low health literacy. We aimed to determine whether low health literacy might amplify the adverse effects of neurocognitive functioning on treatment management outcomes in 171 PLWH aged 40+. In this cross-sectional, observational study, participants completed a well-validated battery of neurocognitive, health literacy, and treatment management measures. A binary health literacy variable (low vs. adequate) was determined via established cut points on the well-validated health literacy tests. Treatment management outcomes included biomarkers of HIV (i.e., [[CD4]] counts and viral load), self-management of HIV disease (i.e., self-reported medication adherence and self-efficacy for HIV disease management), and performance-based health-related decision-making. Forty-seven percent of the sample met the criteria for low health literacy. Multivariable regressions adjusting for clinicodemographic (e.g., race, socioeconomic status) covariates revealed significant interactions for self-efficacy for HIV disease management and health-related decision-making, such that neurocognitive functioning was associated with these outcomes among those with low, but not adequate health literacy. Findings suggest that low health literacy may increase the vulnerability of PLWH to the adverse effects of neurocognitive impairment on health outcomes, or conversely that adequate health literacy may provide a buffer against the health risks associated neurocognitive impairment. Interventions targeting health literacy in PLWH may mitigate the effects of neurocognitive impairment on health outcomes.
+|mesh-terms=* Adult
+* Cognition
+* Cross-Sectional Studies
+* HIV Infections
+* Health Literacy
+* Humans
+* Neuropsychological Tests
+* Self Report
+|keywords=* Adherence
+* Aging
+* Cognitive impairment
+* HIV/AIDS
+* Health illiteracy
+* Observational study
+|full-text-url=https://sci-hub.do/10.1093/arclin/acaa005
+}}
+{{medline-entry
+|title=Blockade of Stat3 oncogene addiction induces cellular senescence and reveals a cell-nonautonomous activity suitable for cancer immunotherapy.
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32064174
+|abstract=Stat3 is constitutively activated in several tumor types and plays an essential role in maintaining their malignant phenotype and immunosupression. To take advantage of the promising antitumor activity of Stat3 targeting, it is vital to understand the mechanism by which Stat3 regulates both cell autonomous and non-autonomous processes. Here, we demonstrated that turning off Stat3 constitutive activation in different cancer cell types induces senescence, thus revealing their Stat3 addiction. Taking advantage of the senescence-associated secretory phenotype (SASP) induced by Stat3 silencing (SASP-siStat3), we designed an immunotherapy. The administration of SASP-siStat3 immunotherapy induced a strong inhibition of triple-negative breast cancer and melanoma growth associated with activation of [[CD4]] + T and NK cells. Combining this immunotherapy with anti-PD-1 antibody resulted in survival improvement in mice bearing melanoma. The characterization of the SASP components revealed that type I IFN-related mediators, triggered by the activation of the cyclic GMP-AMP synthase DNA sensing pathway, are important for its immunosurveillance activity. Overall, our findings provided evidence that administration of SASP-siStat3 or low dose of Stat3-blocking agents would benefit patients with Stat3-addicted tumors to unleash an antitumor immune response and to improve the effectiveness of immune checkpoint inhibitors.
-|mesh-terms=* Aging
+|keywords=* Stat3
-* Animal Feed
+* immune checkpoint blockade
-* Animals
+* immunotherapy
-* Bacillus subtilis
+* oncogene addiction
-* Biomarkers
+* senescence
-* Caenorhabditis elegans
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996562
-* Caenorhabditis elegans Proteins
-* Comamonas
-* Escherichia coli
-* Forkhead Transcription Factors
-* Hot Temperature
-* Insulin
-* Microbiota
-* Microscopy, Atomic Force
-* Mutation
-* Receptor, Insulin
-* Signal Transduction
-* Ultraviolet Rays
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7042263
 }}
 {{medline-entry
-|title=Nanomechanical insights: Amyloid beta oligomer-induced senescent brain endothelial cells.
+|title=Age-related changes in T lymphocytes of patients with head and neck squamous cell carcinoma.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31513781
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32082401
+|abstract=The number of aging cancer patients has increased continuously and will do so further in the future. The immune system of elderly people experiences critical changes over the time. Therefore, tumor-induced changes in the immune system are believed to differ in young and elderly cancer patients as well. The effect of aging on the immune system was measured in peripheral blood lymphocytes (PBL) of healthy volunteers ([i]n[/i] = 48, 21-84 yrs.) divided into three different age groups. Seventy years was set as a cut-off for defining subjects as elderly. Results were compared to two groups of adult cancer patients, which donated PBL and tumor infiltrating lymphocytes (TIL): young cancer patients (40-69 yrs.; blood: [i]n[/i] = 13; TIL: [i]n[/i] = 17) and elderly cancer patients (70-90 yrs.; blood: [i]n[/i] = 20; TIL: [i]n[/i] = 15) with head and neck squamous cell carcinoma (HNSCC). Frequencies and phenotypes of [[CD4]]  and CD8  T cells as well as regulatory T cells (T ) were assessed by flow cytometry. We observed lower frequencies of CD8  cytotoxic T cells during aging in both groups. Frequencies of tumor infiltrating regulatory T cells were significantly higher than in the peripheral blood but showed a significant decline in older tumor patients. With increasing age, expression of immunosuppressive CD73 and CCR7 was lower and expression of PD1 elevated on peripheral T cells in healthy volunteers and tumor patients. Immunosenescence takes place in healthy donors and cancer patients. Our results suggest that in elderly tumor patients, the immune system is impaired and the tumor-induced immune escape is less pronounced. The increased expression of PD1 implies the potential for effective immunotherapies in elderly, as treatment with checkpoint inhibitors could be more beneficial for elderly HNSCC patients.
-|mesh-terms=* Alzheimer Disease
+|keywords=* Aging
-* Amyloid beta-Peptides
+* Head and neck cancer
-* Biomechanical Phenomena
+* Immune escape
-* Brain
+* Immunosenescence
-* Cell Culture Techniques
+* T cells
-* Cell Membrane
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7017629
-* Cellular Senescence
-* Endothelial Cells
-* Endothelium, Vascular
-* Humans
-* Microscopy, Atomic Force
-* Vascular Endothelial Growth Factor A
-|keywords=* Amyloid beta oligomer
-* Atomic force microscopy
-* Brain endothelial cells
-* Nanoindentation
-* Nanomechanical properties
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6791778
 }}
-==AGER==
+==CD68==
 {{medline-entry
-|title=Vitamin D3 regulates apoptosis and proliferation in the testis of D-galactose-induced aged rat model.
+|title=Cellular senescence in recurrent tonsillitis and tonsillar hypertrophy in children.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31575929
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32200310
+|abstract=To observe the difference in cellular senescence patterns between recurrent tonsillitis and tonsillar hypertrophy. Forty-three patients diagnosed with recurrent tonsillitis or tonsillar hypertrophy, based on medical history and symptoms, underwent tonsillectomy. The specimens were collected and examined using senescence β-galactosidase staining for cellular senescence. Macrophages were detected by immunochemistry. Cellular senescence was found in both recurrent tonsillitis and tonsillar hypertrophy groups. The comparison of cellular senescence in microcompartments of tonsil tissue (germinal centre, mantle zone, subepithelial and intraepithelial) revealed a significant increase of senescent cells in germinal centres in tonsillar hypertrophy compared with that in tonsillar hypertrophy. The majority of senescent cells in both groups were [[CD68]]-positive. Different cellular senescence patterns were found between the two studied paediatric tonsillar diseases. Macrophage senescence may play a role in the pathogenesis of these diseases.
+|mesh-terms=* Antigens, CD
+* Antigens, Differentiation, Myelomonocytic
+* Cellular Senescence
+* Child
+* Germinal Center
+* Humans
+* Hypertrophy
+* Macrophages
+* Palatine Tonsil
+* Recurrence
+* Tonsillectomy
+* Tonsillitis
+|keywords=* Cellular senescence
+* Recurrent tonsillitis
+* Tonsillar hypertrophy
+|full-text-url=https://sci-hub.do/10.1016/j.ijporl.2020.110004
+}}
+==CD80==
+{{medline-entry
+|title=The aging common marmoset's immune system: From junior to senior.
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32246726
+|abstract=The social, health, and economic challenges of a steadily increasing aging population demand the use of appropriate translational animal models to address questions like healthy aging, vaccination strategies, or potential interventions during the aging process. Due to their genetic proximity to humans, especially nonhuman primates (NHPs) with a relatively short generation period compared to humans, qualify as excellent animal models for these purposes. The use of common marmosets (Callithrix jacchus) in gerontology research steadily increased over the last decades, yet important information about their aging parameters are still missing. We therefore aimed to characterize their aging immune system by comprehensive flow cytometric phenotyping of blood immune cells from juvenile, adult, aging, and geriatric animals. Aged and geriatric animals displayed clear signs of immunosenescence. A decline in CD4/CD8 ratio, increased expression of HLA-DR and PD-1, higher frequencies of CD95  memory cells, alterations in cytokine secretion, and a decline in the proliferative capacity proved T cell senescence in aging marmosets. Also, the B cell compartment was affected by age-related changes: while overall B cell numbers remained stable with advancing age, expression of the activation marker [[CD80]] increased and immunoglobulin M expression decreased. Interestingly, marmoset B cell memory subset distribution rather mirrored the human situation than that of other NHP. CD21  CD27  naïve B cell frequencies decreased while those of CD21  CD27  tissue memory B cells increased with age. Furthermore, frequencies and numbers of NK cells as part of the innate immune system declined with advancing age. Thus, the observed immunological changes in common marmosets over their life span revealed several similarities to age-related changes in humans and encourages further studies to strengthen the common marmoset as a potential aging model.
 |mesh-terms=* Aging
 * Animals
-* Antioxidants
+* CD4-CD8 Ratio
-* Apoptosis
+* Callithrix
-* Cell Proliferation
+* Female
-* Cholecalciferol
+* Flow Cytometry
-* Down-Regulation
+* Immune System
-* Galactose
+* Longevity
 * Male
-* Oxidative Stress
+* Models, Animal
-* Rats
+* Sex Factors
-* Spermatogenesis
+|keywords=* aging
-* Testis
+* common marmoset
+* immune system
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6773724
+* immunosenescence
+* innate and adaptive immunity
+* sex
+|full-text-url=https://sci-hub.do/10.1002/ajp.23128
 }}
-==AGT==
+==CD81==
 {{medline-entry
-|title=SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence.
+|title=Increased production of functional small extracellular vesicles in senescent endothelial cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31441382
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32101370
+|abstract=Small extracellular vesicles (EVs) are novel players in vascular biology. However, a thorough understanding of their production and function remains elusive. Endothelial senescence is a key feature of vascular ageing and thus, is an attractive therapeutic target for the treatment of vascular disease. In this study, we sought to characterize the EV production of senescent endothelial cells. To achieve this, Human Umbilical Vascular Endothelial Cells (HUVECs) were replicated until they reached senescence, as determined by measurement of Senescence-Associated β-Galactosidase activity via microscopy and flow cytometry. Expression of the endosomal marker Rab7 and the EV marker CD63 was determined by immunofluorescence. Small EVs were isolated by ultracentrifugation and characterized using electron microscopy, nanoparticle tracking analysis and immunoassays to assess morphology, size, concentration and expression of exosome markers CD9 and [[CD81]]. Migration of HUVECs in response to EVs was studied using a transwell assay. The results showed that senescent endothelial cells express higher levels of Rab7 and CD63. Moreover, senescent endothelial cells produced higher levels of CD9- and [[CD81]]-positive EVs. Additionally, small EVs from both young and senescent endothelial cells promoted HUVEC migration. Overall, senescent endothelial cells produce an increased number of functional small EVs, which may have a role in vascular physiology and disease.
+|keywords=* endothelium
-|keywords=* Aging
+* exosomes
-* SQSTM1
+* extracellular vesicles
-* autophagy
-* oxidative stress
 * senescence
-* vascular biology
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7176858
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7469683
 }}
-==AHR==
+==CDK2==
 {{medline-entry
-|title=Indoles from the commensal microbiota act via the [[AHR]] and IL-10 to tune the cellular composition of the colonic epithelium during aging.
+|title=p57  is a master regulator of human adipose derived stem cell quiescence and senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32817517
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32224418
+|abstract=Although human adipose derived stem cells (hADSCs) hold great promises for regenerative medicine, their key biological properties remain poorly understood. In particular, proliferation defects resulted from deep quiescence (dormancy) and senescence represent a major hurdle in hADSC production and clinical application. We have developed a model system for mechanistic dissection of hADSC quiescence and senescence. p57 , a major CDK inhibitor, was highly expressed in quiescent and senescent hADSCs but its level quickly declined upon stem cell activation. p57  overexpression induced quiescence in spite of proliferative signals and its knockdown promoted cell cycle reentry even with induction of quiescence presumably through modulating the [[CDK2]]-CyclinE1 complex. Given its key role in quiescence and senescence, p57  may be exploited for innovative strategies to amplify hADSCs of high quality for clinics.
-|mesh-terms=* Aging
+|keywords=* Human adipose derived stem cells
-* Animals
+* Quiescence
-* Bacteria
+* Senescence
-* Cell Differentiation
+* p57(Kip2)
-* Epithelial Cells
+|full-text-url=https://sci-hub.do/10.1016/j.scr.2020.101759
-* Female
-* Goblet Cells
-* Indoles
-* Interleukin-10
-* Interleukins
-* Male
-* Mice
-* Mice, Inbred BALB C
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Microbiota
-* Mucus
-* Receptors, Aryl Hydrocarbon
-* Signal Transduction
-|keywords=* aging
-* goblet cell
-* intestinal homeostasis
-* mucus
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7474656
 }}
-{{medline-entry
+==CDKN1A==
-|title=Role of the Aryl Hydrocarbon Receptor in Environmentally Induced Skin Aging and Skin Carcinogenesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31795255
-|mesh-terms=* Animals
-* Environmental Exposure
-* Extracellular Matrix
-* Humans
-* Receptors, Aryl Hydrocarbon
-* Skin Aging
-* Skin Neoplasms
-|keywords=* DNA damage
-* UV radiation
-* extracellular matrix
-* extrinsic skin aging
-* melanoma
-* particulate matter
-* pigmentation
-* polycyclic aromatic hydrocarbons
-* squamous cell carcinoma
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6928879
-}}
-==AIP==
 {{medline-entry
-|title=[Aryl hydrocarbon receptor interacting protein ([[AIP]]) in human dermis during aging.]
+|title=Involvement of [[CDKN1A]] (p21) in cellular senescence in response to heat and irradiation stress during preimplantation development.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33280328
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32253738
+|abstract=This study examined the role of cyclin-dependent kinase inhibitor 1a (CDK1A, p21) in response to exogenous stressors during mouse preimplantation embryo development. [[CDKN1A]] knockdown (KD) one-cell zygotes were exposed to 39 °C heat stress (HS) for 4 days or irradiated by 1 (1-Gy) or 3 (3-Gy) Gy X-rays, and their developmental competence and gene expression were compared with control embryos. [[CDKN1A]] KD and HS did not influence early cleavage or subsequent embryonic development; however, HS delayed cavitation and induced elevated Cdkn1a expression in control embryos. Exposure to 1- or 3-Gy had no effect on development to the morula stage; however, a significant number of morulae failed to develop to the blastocyst stage. Interestingly, under the 1-Gy condition, the blastocyst rate of [[CDKN1A]] KD embryos (77.7%) was significantly higher than that of the controls (44.4%). In summary, exposure to cellular stressors resulted in the upregulation of Cdkn1a in embryos exposed to HS or X-ray irradiation, particularly in response to heat stress or low-dose X-ray irradiation, and depleting Cdkn1a mRNA alleviated cell cycle arrest. These findings suggest that [[CDKN1A]] plays a vital role in cellular senescence during preimplantation embryo development.
-|keywords=* AIP
-* PCNA
-* aging
-* fibroblasts
-* skin
+|keywords=* Cdkn1a
+* Heat stress
+* Irradiation
+* Preimplantation
+* Senescence
+* p21
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7193008
 }}
-{{medline-entry
+==CFI==
-|title=Sex-Specific Association between Serum Vitamin D Status and Lipid Profiles: A Cross-Sectional Study of a Middle-Aged and Elderly Chinese Population.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32350171
-|keywords=* atherogenic index of plasma
-* dyslipidaemia
-* gerontology
-* sex difference
-* vitamin D
-|full-text-url=https://sci-hub.do/10.3177/jnsv.66.105
-}}
 {{medline-entry
-|title=The oblique effect: The relationship between profiles of visuospatial preference, cognition, and brain connectomics in older adults.
+|title=The decision about retirement: A scale to describe representations and practices of medical doctors and nurses.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31654648
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32258559
+|abstract=New reliable and valid instrument to describe health professionals representations about retirement.A valid instrument that can be used to compare different health professionals.Job satisfaction is the major factor associated with positions about general policies about retirement. To test the psychometric properties of a newly designed instrument to describe the REpresentations and Practices About REtirement (the PREPARE instrument). Participants were nurses and doctors working in the two public hospitals of Porto, aged 55-65 years, in 2011. Among the 367 eligible participants, 231 (65.9%) participated in the study. The PREPARE instrument consists of four sections: 9, 5 and 12, respectively. A principal component analysis was performed to evaluate the scale's dimensionality, followed by a confirmatory factor analysis to test the fit using different indexes (TLI - Tucker-Lewis Index and [[CFI]] - Confirmatory fit index). Principal confirmatory analysis and confirmatory factor analysis identified 3, 1 and 2 factors for section 1, 2 and 3. All confirmatory factor analysis models had a value of [[CFI]] and TLI higher than 0.9. Section 1 showed a first factor related with items about the importance of personal competences, a second factor related with items about the importance of relationships with patients, and third factor related with items about the importance of following ethical and directive rules; section 2 showed a general factor about the features you valued most in the other health professional group; and, finally, in section 3, the first factor was related with items about satisfaction with the work environment and the second factor with items about satisfaction with professional career. The PREPARE instrument has the basic requirements of a valid and reliable measurement of a scale to describe medical doctors and nurses representations and practices about the decision regarding retirement.
-|mesh-terms=* Aged
-* Brain
-* Cognition
-* Connectome
-* Diffusion Tensor Imaging
-* Executive Function
-* Female
-* Humans
-* Judgment
-* Male
-* Middle Aged
-* Neuropsychological Tests
-* Pattern Recognition, Visual
-* Spatial Processing
 |keywords=* Aging
-* Executive function
+* Job satisfaction
-* Oblique effect
+* Retirement
-* Perception
+* Scale
-* Structural connectivity
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6806742
-* Visuospatial processing
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6887099
 }}
-==ALAS1==
+==CIT==
 {{medline-entry
-|title=Heterozygous disruption of [[ALAS1]] in mice causes an accelerated age-dependent reduction in free heme, but not total heme, in skeletal muscle and liver.
+|title=The Relationship Between the Striatal Dopaminergic Neuronal and Cognitive Function With Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33307066
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32184717
+|abstract=Both cognitive function and striatal dopamine function decline by normal aging. However, the relationship among these three factors remains unclear. The aim of this study was to elucidate the association among age-related changes in the striatal dopamine transporter (DAT) and cognitive function in healthy subjects. The 30 healthy volunteers were enrolled in this research, the age ranged from 41 to 82 (64.5 ± 11.5, mean ± SD). All subjects were scanned with both T1-weighted magnetic resonance imaging (MRI) and  I-FP-[[CIT]] single-photon emission computed tomography (SPECT) images. The Wechsler Adult Intelligence Scale-Third Edition (WAIS-III) was used to evaluate cognitive function. Six spherical regions of interest (ROI) using 10 mm in diameter on the caudate nucleus, anterior putamen and posterior putamen were manually drawn on MRI image which was applied onto SPECT image. The relationship between striatal occipital ratio (SOR) values and WAIS-III subscore were analyzed by multiple regression analysis. Subscores which was significant were further analyzed by path analyses. Full intelligence quotient (IQ), verbal IQ, verbal comprehension were all positively correlated with age-adjusted striatal DAT binding ([i]P[/i] < 0.01). Multiple regression analyses revealed that the coding digit symbol correlated with all striatal regions except for the left caudate ([i]P[/i] < 0.04). Picture completion and right caudate, similarities and left caudate also showed a positive correlation ([i]P[/i] < 0.04). Path analysis found that the right caudate and picture completion; the left caudate and similarities were correlated independently from age, whereas the models of coding digit symbol were not significant. These results suggest that age-based individual diversity of striatal DAT binding was associated with verbal function, and the caudate nucleus plays an important role in this association.
+|keywords=* SPECT
-|keywords=* 5-Aminolevulinate synthase 1 (ALAS1)
+* Wechsler Adult Intelligence Scale
-* 5-Aminolevulinic acid (ALA)
+* aging
-* Aging
+* cognitive function
-* Free heme
+* dopamine transporter
-* Liver
+* verbal function
-* Skeletal muscle
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7058549
-|full-text-url=https://sci-hub.do/10.1016/j.abb.2020.108721
 }}
-==ALB==
+==COPE==
 {{medline-entry
-|title=Effects of Age on Inflammatory Profiles and Nutrition/Energy Metabolism in Domestic Cats.
+|title=Patterns and characteristics of cognitive functioning in older patients approaching end stage kidney disease, the [[COPE]]-study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33262938
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32272897
+|abstract=The prevalence of impaired cognitive functioning in older patients with end stage kidney disease (ESKD) is high. We aim to describe patterns of memory, executive function or psychomotor speed and to identify nephrologic, geriatric and neuroradiologic characteristics associated with cognitive impairment in older patients approaching ESKD who have not yet started with renal replacement therapy (RRT). The [[COPE]]-study (Cognitive Decline in Older Patients with ESRD) is a prospective cohort study including 157 participants aged 65 years and older approaching ESKD (eGFR ≤20 ml/min/1.73 m ) prior to starting with RRT. In addition to routinely collected clinical parameters related to ESKD, such as vascular disease burden and parameters of metabolic disturbance, patients received a full geriatric assessment, including extensive neuropsychological testing. In a subgroup of patients (n = 93) a brain MRI was performed. The median age was 75.3 years. Compared to the normative data of neuropsychological testing participants memory performance was in the 24th percentile, executive function in the 18th percentile and psychomotor speed in the 20th percentile. Independent associated characteristics of impairment in memory, executive and psychomotor speed were high age, low educational level and low functional status (all p-values < 0.003). A history of vascular disease (p = 0.007) and more white matter hyperintensities on brain MRI (p = 0.013) were associated with a lower psychomotor speed. Older patients approaching ESKD have a high prevalence of impaired memory, executive function and psychomotor speed. The patterns of cognitive impairment and brain changes on MRI are suggestive of vascular cognitive impairment. These findings could be of potentially added value in the decision-making process concerning patients with ESKD.
+|keywords=* Cognitive function
-|keywords=* M/L ratio
+* End stage renal disease
-* SAA
+* Geriatric assessment
-* aging
+* Geriatrics
-* domestic cats
+* Older patients
-* obesity
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7147053
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7695597
 }}
-==ALK==
+==CPM==
 {{medline-entry
-|title=Catalog of Lung Cancer Gene Mutations Among Chinese Patients.
+|title=Age does not affect sex effect of conditioned pain modulation of pressure and thermal pain across 2 conditioning stimuli.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32850378
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32072094
+|abstract=Conditioned pain modulation ([[CPM]]) is a laboratory test resulting in pain inhibition through activation of descending inhibitory mechanisms. Older adults consistently demonstrate reduced [[CPM]] compared with younger samples; however, studies of sex differences in younger cohorts have shown mixed results. This study tested for sex differences in [[CPM]] within samples of younger and older adults. Participants were 67 younger adults (mean age = 25.4 years) and 50 older adults (66.4 years). Study conditioning paradigms were the cold-pressor test and contact heat pain administered in separate sessions. Pressure pain threshold and ramping suprathreshold heat were the test stimuli across three time points after presentation of the conditioning stimuli (CS). Significant inhibition was observed during both testing sessions. The hypothesis for sex differences across both age cohorts was supported only for ∆PPTh. However, sex differences did not reach significance for either paradigm using ascending suprathreshold heat as the test stimuli. The overall trend was that younger males experienced the strongest [[CPM]] and older females the weakest. From a methodological perspective, duration differences were seen in [[CPM]], with inhibition decaying more quickly for PPTh than for suprathreshold heat pain. Furthermore, there were no differences in inhibition induced by cold-pressor test and contact heat pain as CS. Sex differences were similar across both age cohorts with males experiencing greater inhibition than females. Cross-sectional associations were also demonstrated between [[CPM]] inhibition and measures of recent pain, further supporting [[CPM]] as an experimental model with clinical utility.
+|keywords=* Aging
-|keywords=* China
+* CPM duration
-* aging
+* Conditioned pain modulation
-* gene mutation
+* Conditioning stimulus
-* lung cancer
+* Sex differences
-* pathology
+* Test stimulus
-* tobacco smoking
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7004505
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7417348
 }}
-==ALKBH8==
+==CRABP2==
 {{medline-entry
-|title=Loss of epitranscriptomic control of selenocysteine utilization engages senescence and mitochondrial reprogramming .
+|title=Preconception resveratrol intake against infertility: Friend or foe?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31765888
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32273814
+|abstract=Resveratrol is an antiaging, antioxidant, anti-inflammatory, and insulin-sensitizing natural polyphenolic compound. Growing evidence indicates that resveratrol has potential therapeutic effects in infertile women with diminished ovarian function, polycystic ovary syndrome (PCOS), or endometriosis. However, only one clinical trial in women undergoing in vitro fertilization (IVF) cycles using resveratrol has ever been reported. This review focuses on the potential therapeutic effects of resveratrol on pregnancy and on its advantages and disadvantages in pregnancy outcomes during infertility treatment. We performed a literature review to describe the known impacts of resveratrol on the ovary and endometrium. Resveratrol upregulates sirtuin (SIRT)1 expression in ovaries, which is associated with protection against oxidative stress. It leads to the activation of telomerase activity and mitochondrial function, improving ovarian function. In the endometrium, resveratrol downregulates the [[CRABP2]]-RAR pathway leading to suppressing decidual and senescent changes of endometrial cells, which is essential for embryo implantation and placentation. Moreover, resveratrol may also induce deacetylation of important decidual-related genes. Resveratrol has potential therapeutic effects for improving ovarian function; however, it also has anti-deciduogenic actions in uterine endometrium. In addition, its teratogenicity has not yet been ruled out; thus, resveratrol should be avoided during the luteal phase and pregnancy.
-|mesh-terms=* AlkB Homolog 8, tRNA Methyltransferase
+|keywords=* aging
-* Animals
+* assisted reproductive technology
-* Cells, Cultured
+* infertility
-* Cellular Senescence
+* resveratrol
-* Epigenesis, Genetic
+* sirtuin
-* Gene Deletion
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7138940
-* Gene Expression Profiling
-* Humans
-* Mice
-* Mitochondria
-* Oxygen Consumption
-* Selenocysteine
-* Uncoupling Protein 2
-|keywords=* Epitranscriptome
-* Mitochondria
-* Selenium
-* Senescence
-* Uncoupling protein
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6904832
 }}
-==ALOX12==
+==CRP==
 {{medline-entry
-|title=Arachidonate 12-lipoxygenase and 12-hydroxyeicosatetraenoic acid contribute to stromal aging-induced progression of pancreatic cancer.
+|title=The Impact of Age on the Prevalence of Sarcopenic Obesity in Bariatric Surgery Candidates.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32265301
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32249368
+|abstract=Sarcopenia pre-dating bariatric surgery (BS) has been suggested as concern for the use of BS in older-adults with morbid obesity. To evaluate the impact of age on the prevalence of sarcopenic obesity (SO) in BS-candidates. Cross-sectional study including 1370 consecutive BS-candidates aged ≥18, and grouped according to age: 18-39 (reference group), 40-49, 50-59 and ≥ 60 years. From body composition analysis data obtained using bioelectrical impedance, skeletal muscle mass (SMM), SMM index (SMMI=SMM/height ), and percentage of SMM (%SMM = SMM/BW*100) were calculated. Class I or class II SO was adjudicated, respectively, when a value between > - 1 and - 2, or > -2 standard deviations from the regression line from the gender-specific distribution of the relationship between BMI and SMMI or the %SMM in the reference group was encountered. According to the SMMI distribution, prevalence of class I and class II SO in the whole cohort was respectively 16.4% and 4.6%. SO was more prevalent in females (p < 0.005). Proportion of subjects with SO positively correlated with older age category in females (Tau-c = 0.149, p < 0.001) but not in males. In females aged ≥60, class I SO was present in 29.1%, and class II in 12.8%. Similar results were obtained when %SMM was used (Cohen's k-coefficient = 0.886, p < 0.001). Age and female gender were identified as independent preditors of SO, whereas [[CRP]] or the presence of obesity-associated comorbidities were not. Age is a risk factor for SO in BS-candidates. SO is fairly common in female subjects aged >60 years that are candidates to BS.
+|keywords=* Aging
-|keywords=* aging
+* Bariatric surgery
-* arachidonic acid (AA) (ARA)
+* Elderly
-* cancer biology
+* Obesity
-* cell proliferation
+* Sarcopenia
-* fibroblast
+|full-text-url=https://sci-hub.do/10.1007/s11695-019-04198-4
-* pancreatic cancer
-* stromal cell
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7242692
 }}
-==ALOX5==
 {{medline-entry
-|title=Functional Characterization of Knock-In Mice Expressing a 12/15-Lipoxygenating Alox5 Mutant Instead of the 5-Lipoxygenating Wild-Type Enzyme.
+|title=Intake of dietary advanced glycation end products influences inflammatory markers, immune phenotypes, and antiradical capacity of healthy elderly in a little-studied population.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31642348
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32148813
+|abstract=Dietary advanced glycation end products (dAGE) have profound negative effects on overall health, and their intake must be assessed. In this cross-sectional study, we investigated dAGE intake of 337 adult participants (180/157:M/F; age range 50-73 years). Data were collected on anthropometrics, body composition, dietary intake, selected blood biochemistry, immunological parameters, and antiradical capacity (50% hemolysis time; HT ). From the dietary data, dAGEs and phytochemical index (PI) were calculated. Mean BMI, % body fat (%BF), and fasting plasma glucose were all within the accepted normal range. Subjects with high dAGE intake had higher %BF, higher energy intake, and lower PI. They tended to have lower CD4/CD8 ratios and higher proportions of B cells and NK cells, but had significantly higher hs-[[CRP]] levels and lower HT  values. Results on HT  suggested that being >60 years of age enhanced dAGE-associated impairment of defense capacity in both those with low and high HT  compared with those <60 years of age. Thus, overall dAGE consumption was high, but elderly participants had lower dAGE intake than younger adults. Indicators of nutritional status and immunological parameters of the subjects were found to be associated with dAGE intake, suggesting a potential impact on health.
-|mesh-terms=* Aging
+|keywords=* CRP
-* Alanine
+* advanced glycationed end products
-* Animals
+* aging
-* Arachidonate 5-Lipoxygenase
+* dAGE
-* Asparagine
+* immunity
-* Body Weight
-* Female
-* Gene Knock-In Techniques
-* Leukotrienes
-* Linoleic Acid
-* Male
-* Mice
-* Mutation
-* PPAR gamma
-* Phenylalanine
-|keywords=* eicosanoids
 * inflammation
-* leukotrienes
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7020308
-* lipoxygenase
-* resolvins
-|full-text-url=https://sci-hub.do/10.1089/ars.2019.7751
 }}
-==AMH==
 {{medline-entry
-|title=Beyond premature ovarian insufficiency: Staging reproductive aging in adolescent and young adult cancer survivors.
+|title=Intentional Switching Between Bimanual Coordination Patterns in Older Adults: Is It Mediated by Inhibition Processes?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33141175
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32132919
+|abstract=The study investigated the consequences of age-related decline in inhibition processes on intentional switching between bimanual coordination patterns. Fifteen young (24±2.8 years) and 20 older adults (69±5.3 years) performed Stroop tasks and bimanual coordination tasks. Stroop tasks included neutral, congruent, and incongruent conditions. Response time and error rate were measured. Bimanual coordination tasks consisted of performing in-phase (IP) and anti-phase (AP) patterns. Participants were requested to switch as quickly as possible from one pattern to the other, resulting in two different switching directions (AP to IP; IP to AP). Mean and standard deviation (SD) of the continuous relative phase ([[CRP]]) were calculated pre- and post-switching for each participant. Total switching time (TST) was measured. The switching phase was also decomposed into reaction time (RT) and reversal time (REvT). Pearson correlation analyses were performed to test for correlations between: (i) SD of [[CRP]] and response time in Stroop tasks, and (ii) switching times (TST, RT, RevT) and response time in Stroop task, respectively. In addition, parallel mediation analyses were conducted. Results showed that: (i) the AP pattern was less stable than the IP pattern in both young and older adults, (ii) coordination patterns were less stable in older adults, (iii) response times in Stroop task were longer in the incongruent condition, and (iv) RespTs were longer in older than in young participants, whatever the condition. In the bimanual coordination task, RT, RevT, and TST increased with age. The stability of the IP pattern was correlated with the response times observed in neutral and congruent conditions, while the stability of the AP pattern was correlated with response time observed in the incongruent condition. Correlation and mediation analyses showed that, in the AP to IP switching direction, RT and RevT were both significantly correlated with response times observed in the incongruent condition of Stroop task. These findings suggest that inhibition processes are involved in switching between bimanual coordination patterns, at least to trigger the early phase of switching. They also support the hypothesis that inhibition processes are more involved in maintaining the AP pattern and switching to the IP pattern. Finally, age-related changes in switching times seem to be prominently mediated by alterations of inhibition processes.
+|keywords=* Stroop task
-|keywords=* STRAW
+* aging
-* adolescent and young adult cancer
+* bimanual coordination
-* menopausal transition
+* inhibition
-* premature ovarian insufficiency
+* mediation analysis
-* reproductive aging
+* switching
-|full-text-url=https://sci-hub.do/10.1210/clinem/dgaa797
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7041435
 }}
 {{medline-entry
-|title=Correlates and Timing of Reproductive Aging Transitions in a Global Cohort of Midlife Women With Human Immunodeficiency Virus: Insights From the REPRIEVE Trial.
+|title=Shorter Telomere Length in Peripheral Blood Leukocytes Is Associated with Post-Traumatic Chronic Osteomyelitis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32645159
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32125944
+|abstract= This study investigated the association between post-traumatic chronic osteomyelitis (COM) and peripheral leukocyte telomere length (PLTL) and explored factors associated with PLTL in COM.   A total of 56 patients with post-traumatic COM of the extremity and 62 healthy control subjects were recruited. The PLTL was measured by real-time PCR. Binary logistic regression analysis was used to identify factors in correlation with telomere length. Sex, age, white blood cell (WBC) count, erythrocyte sedimentation rate (ESR), C-reactive protein ([[CRP]]), and infection duration were included as independent variables in the logistic regression model.   Post-traumatic COM patients had significantly shorter PLTLs (5.39 ± 0.40) than healthy control subjects (5.69 ± 0.46; p < 0.001). Binary logistic regression analysis showed that PLTL had a statistically significant association with age ([i]B[/i] = -0.072; p = 0.013) and [[CRP]] ([i]B[/i] = -0.061; p = 0.033). The logistic regression model was statistically significant and explained 31.4% (Nagelkerke R ) of the change in telomere length and correctly classified 69.6% of the cases.   Patients with post-traumatic COM have shorter PLTLs than healthy subjects. The PLTL erosion of post-traumatic COM was partially explained by age and [[CRP]].
+|keywords=* aging
+* post-traumatic chronic osteomyelitis
+* telomere
+|full-text-url=https://sci-hub.do/10.1089/sur.2019.326
+}}
+==CTSB==
-|keywords=* Cardiometabolic Risk
+{{medline-entry
-* HIV
+|title=Myocardial cathepsin D is downregulated in sudden cardiac death.
-* Menopause
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32176724
-* Reproductive Aging
+|abstract=Cathepsins are the major lysosomal proteases that maintain intracellular homeostasis. Herein, we investigated the alterations in myocardial cathepsin expression during aging, cardiac hypertrophy, and sudden cardiac death (SCD). Cardiac tissue and blood were sampled from autopsy cases. Subjects were classified into three groups: SCD with cardiac hypertrophy (SCH), compensated cardiac hypertrophy (CCH), and control. Immunoblotting was performed for the major cardiac cathepsins and their targets: cathepsin B, D, and L ([[CTSB]]/D/L), p62, ATP synthase subunit c (ATPSC), and α-synuclein (ASNC). Immunohistochemical analysis and ELISA using serum samples were performed for CTSD. Cardiac [[CTSB]] and CTSD were upregulated with age (r = 0.63 and 0.60, respectively), whereas the levels of CTSL, p62, ATPSC, and ASNC remained unchanged. In age-matched groups, cardiac CTSD was significantly downregulated in SCH (p = 0.006) and CTSL was moderately downregulated in CCH (p = 0.021); however, p62, ATPSC, and ASNC were not upregulated in cardiac hypertrophy. Immunohistochemistry also revealed decreased myocardial CTSD levels in SCH, and serum CTSD levels were relatively lower in SCH cases. Overall, these results suggest that upregulation of cardiac [[CTSB]] and CTSD with age may compensate for the elevated proteolytic demand, and that downregulation of CTSD is potentially linked to SCH.
-* Sex
+|mesh-terms=* Adult
-* Women
+* Aged
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7347076
+* Aged, 80 and over
+* Aging
+* Cathepsin D
+* Death, Sudden, Cardiac
+* Down-Regulation
+* Female
+* Humans
+* Male
+* Middle Aged
+* Myocardium
+* Substrate Specificity
+|keywords=#f
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7075574
 }}
+==CX3CR1==
 {{medline-entry
-|title=Epigenetic clock measuring age acceleration via DNA methylation levels in blood is associated with decreased oocyte yield.
+|title=Monocytes present age-related changes in phospholipid concentration and decreased energy metabolism.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32285295
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32107839
+|abstract=Age-related changes at the cellular level include the dysregulation of metabolic and signaling pathways. Analyses of blood leukocytes have revealed a set of alterations that collectively lower their ability to fight infections and resolve inflammation later in life. We studied the transcriptomic, epigenetic, and metabolomic profiles of monocytes extracted from younger adults and individuals over the age of 65 years to map major age-dependent changes in their cellular physiology. We found that the monocytes from older persons displayed a decrease in the expression of ribosomal and mitochondrial protein genes and exhibited hypomethylation at the HLA class I locus. Additionally, we found elevated gene expression associated with cell motility, including the [[CX3CR1]] and ARID5B genes, which have been associated with the development of atherosclerosis. Furthermore, the downregulation of two genes, PLA2G4B and ALOX15B, which belong to the arachidonic acid metabolism pathway involved in phosphatidylcholine conversion to anti-inflammatory lipoxins, correlated with increased phosphatidylcholine content in monocytes from older individuals. We found age-related changes in monocyte metabolic fitness, including reduced mitochondrial function and increased glycose consumption without the capacity to upregulate it during increased metabolic needs, and signs of increased oxidative stress and DNA damage. In conclusion, our results complement existing findings and elucidate the metabolic alterations that occur in monocytes during aging.
+|keywords=* DNA methylation
-|keywords=* Aging
+* aging
-* DNA methylation
+* glucose metabolism
-* Epigenetic clock
+* monocytes
-* Epigenetics
+* phosphatidylcholines
-* Infertility
+* transcriptome
-* Methylome
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189998
-* Ovarian aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244694
 }}
 {{medline-entry
-|title=Modeling Variation in the Reproductive Lifespan of Female Adolescent and Young Adult Cancer Survivors Using [[AMH]].
+|title=Muscle Injury Induces Postoperative Cognitive Dysfunction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32270202
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32066806
+|abstract=Postoperative cognitive dysfunction (POCD) is a major complication affecting patients of any age undergoing surgery. This syndrome impacts everyday life up to months after hospital discharge, and its pathophysiology still remains unclear. Translational research focusing on POCD is based on a wide variety of rodent models, such as the murine tibial fracture, whose severity can limit mouse locomotion and proper behavioral assessment. Besides, influence of skeletal muscle injury, a lesion encountered in a wide range of surgeries, has not been explored in POCD occurrence. We propose a physical model of muscle injury in [[CX3CR1]]  mice (displaying green fluorescent microglial cells) to study POCD, with morphological, behavioral and molecular approaches. We highlighted: alteration of short- and long-term memory after muscle regeneration, wide microglial reactivity in the brain, including hippocampus area, 24 hours after muscle injury, and an alteration of central brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) balance, 28 days after muscle injury. Our results suggest for the first time that muscle injury can have early as well as late impacts on the brain. Our [[CX3CR1]]  model can also facilitate microglial investigation, more specifically their pivotal role in neuroinflammation and synaptic plasticity, in the pathophysiology of POCD.
+|mesh-terms=* Aging
+* Animals
+* Brain
+* Brain-Derived Neurotrophic Factor
+* CX3C Chemokine Receptor 1
+* Cytokines
+* Disease Models, Animal
+* Hippocampus
+* Humans
+* Male
+* Mice
+* Microglia
+* Muscle, Skeletal
+* Nerve Growth Factor
+* Postoperative Cognitive Complications
+* Postoperative Complications
+|keywords=#f
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7026159
+}}
+==CYP2E1==
+{{medline-entry
+|title=DNA methylation and histone acetylation changes to cytochrome P450 2E1 regulation in normal aging and impact on rates of drug metabolism in the liver.
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32221779
+|abstract=Aging is associated with reduced liver function that may increase the risk for adverse drug reactions in older adults. We hypothesized that age-related changes to epigenetic regulation of genes involved in drug metabolism may contribute to this effect. We reviewed published epigenome-wide studies of human blood and identified the cytochrome P450 2E1 ([[CYP2E1]]) gene as a top locus exhibiting epigenetic changes with age. To investigate potential functional changes with age in the liver, the primary organ of drug metabolism, we obtained liver tissue from mice aged 4-32 months from the National Institute on Aging. We assayed global DNA methylation (5-methylcytosine, 5mC), hydroxymethylation (5-hydroxymethylcytosine, 5hmC), and locus-specific 5mC and histone acetylation changes around mouse Cyp2e1. The mouse livers exhibit significant global decreases in 5mC and 5hmC with age. Furthermore, 5mC significantly increased with age at two regulatory regions of Cyp2e1 in tandem with decreases in its gene and protein expressions. H3K9ac levels also changed with age at both regulatory regions of Cyp2e1 investigated, while H3K27ac did not. To test if these epigenetic changes are associated with varying rates of drug metabolism, we assayed clearance of the [[CYP2E1]]-specific probe drug chlorzoxazone in microsome extracts from the same livers. [[CYP2E1]] intrinsic clearance is associated with DNA methylation and H3K9ac levels at the Cyp2e1 locus but not with chronological age. This suggests that age-related epigenetic changes may influence rates of hepatic drug metabolism. In the future, epigenetic biomarkers could prove useful to guide dosing regimens in older adults.
-|keywords=* AMH
+|keywords=* Aging
-* adolescent and young adult cancer
+* Cyp2e1
-* functional principal components analysis
+* DNA methylation
-* ovarian reserve
+* Drug metabolism
-* reproductive lifespan
+* Histone acetylation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7329316
+* Pharmacokinetics
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7287002
 }}
+==DCX==
 {{medline-entry
-|title=Improving Prediction of Age at Menopause Using Multiple Anti-Müllerian Hormone Measurements: the Tehran Lipid-Glucose Study.
+|title=Doublecortin and IGF-1R protein levels are reduced in spite of unchanged DNA methylation in the hippocampus of aged rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109280
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32236698
+|abstract=The aim of the current study was to investigate whether doublecortin ([[DCX]]), insulin-like growth factor receptor 1 (IGF-1R) and metabotropic glutamate receptor 5 (mGluR5) levels are indeed modified in the aging rat hippocampal individual subareas (rather than total hippocampal tissue as in previous reports) at the protein and mRNA level and whether the methylation status contributes to these changes. Since the aging population is not homogeneous in terms of spatial memory performance, we examined whether changes in [[DCX]], IGF-1R and mGluR5 are linked to cognitive aging. Aged (22 months) male Sprague Dawley rats were trained in the hole-board, a spatial memory task, and were subdivided according to performance to aged impaired and aged unimpaired groups. Age- and memory performance-dependent changes in mRNA steady-state levels, protein levels and DNA methylation status of [[DCX]], IGF-1R and mGluR5 were evaluated by RT-PCR, immunoblotting and bisulfite pyrosequencing. Extending previous findings, we detected decreased [[DCX]] protein and mRNA levels in dentate gyrus (DG) of aged animals. IGF-1 signaling is a key event and herein we show that mRNA levels for IGF-1R were unchanged although reduced at the protein level. This finding may simply reflect that these protein levels are regulated at the level of protein synthesis as well as protein degradation. We provide evidence that promoter methylation is not involved in regulation of mRNA and protein levels of [[DCX]], IGF-1R and mGluR5 during aging. Moreover, there was no significant difference between aged rats with impaired and aged rats with unimpaired memory at the protein and mRNA level. Findings propose that changes in the abovementioned protein levels may not be relevant for performance in the spatial memory task used in aged rats.
+|keywords=* Aging
-|keywords=* Tehran Lipid and Glucose Study (TLGS)
+* DNA methylation
-* anti-müllerian hormone (AMH)
+* Doublecortin
-* menopause
+* Hippocampus
-* reproductive aging
+* IGF-1R
-|full-text-url=https://sci-hub.do/10.1210/clinem/dgaa083
+* mGluR5
+|full-text-url=https://sci-hub.do/10.1007/s00726-020-02834-3
 }}
-{{medline-entry
+==DKC1==
-|title=Antimullerian Hormone and Impending Menopause in Late Reproductive Age: The Study of Women's Health Across the Nation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31965189
-|keywords=* aging
-* female reproductive endocrinology
-* gonadotropins
-* inhibin/activin/follistatin/AMH
-* menopause
-* ovaries
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7067546
-}}
 {{medline-entry
-|title=Basal characterization and in vitro differentiation of putative stem cells derived from the adult mouse ovary.
+|title=Successful liver transplantation in short telomere syndromes without bone marrow failure due to [[DKC1]] mutation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31900800
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32166868
+|abstract=Short telomere syndromes are a heterogenous spectrum of disorders leading to premature cellular aging. These may involve bone marrow failure, adult-onset idiopathic pulmonary fibrosis, and liver disease, and classical entities such as dyskeratosis congenita. We report a patient who presented with common variable immunodeficiency at 3 years of age and autoimmune cytopenias at 8 years of age. He was found to have short telomeres, and genetic testing confirmed a hemizygous mutation NM_001363.4: c.-142C > G in [[DKC1]] gene. He subsequently developed cirrhosis with severe portal hypertension and hepatopulmonary syndrome, prompting liver transplantation at 11 years of age. He remains well 10 years after transplant with no progression of bone marrow failure or progressive lung disease. In conclusion, short telomere syndromes should be considered as a potential cause of pediatric liver disease of unknown etiology, and in severe cases, isolated liver transplantation may be both appropriate and successful.
-|mesh-terms=* Aging
+|keywords=* DKC1
-* Animals
+* cell death: senescence
-* Anti-Mullerian Hormone
+* cirrhosis
-* Antigens, Ly
+* hepatopulmonary syndrome
-* Cell Differentiation
+* liver transplantation
-* Cell Shape
+* short telomere syndromes
-* Female
+|full-text-url=https://sci-hub.do/10.1111/petr.13695
-* Lewis X Antigen
-* Membrane Proteins
-* Mice, Inbred C57BL
-* Ovary
-* Stem Cells
-|keywords=* BMP-4
-* Multipotent
-* Ovary
-* Retinoic acid
-* Stem cells
-|full-text-url=https://sci-hub.do/10.1007/s11626-019-00411-x
 }}
+==DMD==
 {{medline-entry
-|title=Serum anti-Müllerian hormone concentration and follicle density throughout reproductive life and in different diseases-implications in fertility preservation.
+|title=Aldehyde dehydrogenases contribute to skeletal muscle homeostasis in healthy, aging, and Duchenne muscular dystrophy patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31782794
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32157826
+|abstract=Aldehyde dehydrogenases (ALDHs) are key players in cell survival, protection, and differentiation via the metabolism and detoxification of aldehydes. ALDH activity is also a marker of stem cells. The skeletal muscle contains populations of ALDH-positive cells amenable to use in cell therapy, whose distribution, persistence in aging, and modifications in myopathic context have not been investigated yet. The Aldefluor® (ALDEF) reagent was used to assess the ALDH activity of muscle cell populations, whose phenotypic characterizations were deepened by flow cytometry. The nature of ALDH isoenzymes expressed by the muscle cell populations was identified in complementary ways by flow cytometry, immunohistology, and real-time PCR ex vivo and in vitro. These populations were compared in healthy, aging, or Duchenne muscular dystrophy ([[DMD]]) patients, healthy non-human primates, and Golden Retriever dogs (healthy vs. muscular dystrophic model, Golden retriever muscular dystrophy [GRMD]). ALDEF  cells persisted through muscle aging in humans and were equally represented in several anatomical localizations in healthy non-human primates. ALDEF  cells were increased in dystrophic individuals in humans (nine patients with [[DMD]] vs. five controls: 14.9 ± 1.63% vs. 3.6 ± 0.39%, P = 0.0002) and dogs (three GRMD dogs vs. three controls: 10.9 ± 2.54% vs. 3.7 ± 0.45%, P = 0.049). In [[DMD]] patients, such increase was due to the adipogenic ALDEF  /CD34  populations (11.74 ± 1.5 vs. 2.8 ± 0.4, P = 0.0003), while in GRMD dogs, it was due to the myogenic ALDEF  /CD34  cells (3.6 ± 0.6% vs. 1.03 ± 0.23%, P = 0.0165). Phenotypic characterization associated the ALDEF  /CD34  cells with CD9, CD36, CD49a, CD49c, CD49f, CD106, CD146, and CD184, some being associated with myogenic capacities. Cytological and histological analyses distinguished several ALDH isoenzymes (ALDH1A1, 1A2, 1A3, 1B1, 1L1, 2, 3A1, 3A2, 3B1, 3B2, 4A1, 7A1, 8A1, and 9A1) expressed by different cell populations in the skeletal muscle tissue belonging to multinucleated fibres, or myogenic, endothelial, interstitial, and neural lineages, designing them as potential new markers of cell type or of metabolic activity. Important modifications were noted in isoenzyme expression between healthy and [[DMD]] muscle tissues. The level of gene expression of some isoenzymes (ALDH1A1, 1A3, 1B1, 2, 3A2, 7A1, 8A1, and 9A1) suggested their specific involvement in muscle stability or regeneration in situ or in vitro. This study unveils the importance of the ALDH family of isoenzymes in the skeletal muscle physiology and homeostasis, suggesting their roles in tissue remodelling in the context of muscular dystrophies.
-|mesh-terms=* Adolescent
+|keywords=* Aging
-* Adult
+* Aldehyde dehydrogenase
-* Aging
+* Dog model
-* Anti-Mullerian Hormone
+* Duchenne muscular dystrophy
-* Child
+* Human
-* Child, Preschool
+* Myogenic
-* Female
+* Non-human primate
-* Fertility Preservation
+* Skeletal muscle
-* Humans
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432589
-* Ovarian Follicle
-* Retrospective Studies
-* Young Adult
-|keywords=* anti-Müllerian hormone
-* cancer
-* fertility preservation
-* ovarian reserve
-* ovarian tissue
-* primary follicle
-* primordial follicle
-|full-text-url=https://sci-hub.do/10.1093/humrep/dez215
 }}
 {{medline-entry
-|title=Associations Between Anti-Mullerian Hormone and Cardiometabolic Health in Reproductive Age Women Are Explained by Body Mass Index.
+|title=Life expectancy at birth in Duchenne muscular dystrophy: a systematic review and meta-analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31586179
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32107739
+|abstract=Several studies indicate that prognosis for survival in Duchenne muscular dystrophy ([[DMD]]) has improved in recent decades. However, published evidence is inconclusive and some estimates may be obsolete due to improvements in standards of care, in particular the routine use of mechanical ventilatory support in advanced stages of the disease. In this systematic review and meta-analysis (PROSPERO identifier: CRD42019121800), we searched MEDLINE (through PubMed), CINAHL, Embase, PsycINFO, and Web of Science for studies published from inception up until December 31, 2018, reporting results of life expectancy in [[DMD]]. We pooled median survival estimates from individual studies using the median of medians, and weighted median of medians, methods. Risk of bias was established with the Newcastle-Ottawa Scale. Results were stratified by ventilatory support and risk of bias. We identified 15 publications involving 2662 patients from 12 countries from all inhabited continents except Africa. Median life expectancy without ventilatory support ranged between 14.4 and 27.0 years (pooled median: 19.0 years, 95% CI 18.0-20.9; weighted pooled median: 19.4 years, 18.2-20.1). Median life expectancy with ventilatory support, introduced in most settings in the 1990s, ranged between 21.0 and 39.6 years (pooled median: 29.9 years, 26.5-30.8; weighted pooled median: 31.8 years, 29.3-36.2). Risk of bias had little impact on pooled results. In conclusion, median life expectancy at birth in [[DMD]] seems to have improved considerably during the last decades. With current standards of care, many patients with [[DMD]] can now expect to live into their fourth decade of life.
-|mesh-terms=* Adult
+|mesh-terms=* Female
-* Anti-Mullerian Hormone
-* Biomarkers
-* Body Mass Index
-* Cardiovascular Diseases
-* Case-Control Studies
-* Cross-Sectional Studies
-* Female
-* Follow-Up Studies
 * Humans
-* Incidence
+* Life Expectancy
-* Infertility, Female
+* Male
-* Polycystic Ovary Syndrome
+* Muscular Dystrophy, Duchenne
+* Parturition
+* Pregnancy
+* Prognosis
+* Quality of Life
+* Respiration, Artificial
+* Survival
+|keywords=* Mechanical ventilation
+* Mortality
 * Prognosis
-* United States
+* Survival
-|keywords=* anti-mullerian hormone (AMH)
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7387367
-* cardiometabolic health
-* cardiovascular risk
-* ovarian aging
-* ovarian reserve markers
-* reproductive aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7024739
 }}
+==DNAJB9==
 {{medline-entry
-|title=Relationships between antral follicle count, blood serum concentration of anti-Müllerian hormone and fertility in mares.
+|title=[[DNAJB9]] Inhibits p53-Dependent Oncogene-Induced Senescence and Induces Cell Transformation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31586925
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32264658
+|abstract=[i][[DNAJB9]][/i] is known to be a member of the molecular chaperone gene family, whose cellular function has not yet been fully characterized. Here, we investigated the cellular function of [[DNAJB9]] under strong mitogenic signals. We found that [[DNAJB9]] inhibits p53-dependent oncogene-induced senescence (OIS) and induces neoplastic transformation under oncogenic RAS activation in mouse primary fibroblasts. In addition, we observed that [[DNAJB9]] interacts physically with p53 under oncogenic RAS activation and that the p53-interacting region of [[DNAJB9]] is critical for the inhibition of p53-dependent OIS and induction of neoplastic transformation by [[DNAJB9]]. These results suggest that [[DNAJB9]] induces cell transformation under strong mitogenic signals, which is attributable to the inhibition of p53-dependent OIS by physical interactions with p53. This study might contribute to our understanding of the cellular function of [[DNAJB9]] and the molecular basis of cell transformation.
-|mesh-terms=* Aging
+|keywords=* DNAJB9
-* Animals
+* RAS
-* Anti-Mullerian Hormone
+* p53
-* Female
+* senescence
-* Fertility
+* transformation
-* Horses
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191047
-* Ovarian Follicle
+}}
-* Ovulation
+==DNMT3L==
-|keywords=* AMH
-* Anzahl Follikel
-* Ovar
-* Pferd
-* Ultraschall
-* compte folliculaire
-* conta dei follicoli
-* ecografia
-* equine
-* equini
-* follicle count
-* ovaia
-* ovaire
-* ovary
-* reproductive status
-* stato riproduttivo
-* ultrasonography
-* Reproduktionsstatus
-* échographie
-* équin
-* état reproducteur
-|full-text-url=https://sci-hub.do/10.17236/sat00225
-}}
-==AMT==
 {{medline-entry
-|title=A multi-method comparison of autobiographical memory impairments amongst younger and older adults.
+|title=Transient [[DNMT3L]] Expression Reinforces Chromatin Surveillance to Halt Senescence Progression in Mouse Embryonic Fibroblast.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32162531
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32195249
+|abstract=Global heterochromatin reduction, which is one of the hallmarks of senescent cells, is associated with reduced transposable element repression and increased risk of chromatin instability. To ensure genomic integrity, the irreparable cells in a population exit permanently from the cell cycle, and this process is termed "senescence." However, senescence only blocks the expansion of unwanted cells, and the aberrant chromatin of senescent cells remains unstable. Serendipitously, we found that the transient ectopic expression of a repressive epigenetic modulator, DNA methyltransferase 3-like ([[DNMT3L]]) was sufficient to delay the premature senescence progression of late-passage mouse embryonic fibroblasts (MEFs) associated with a tightened global chromatin structure. [[DNMT3L]] induces more repressive H3K9 methylation on endogenous retroviruses and downregulates the derepressed transposons in aging MEFs. In addition, we found that a pulse of ectopic [[DNMT3L]] resulted in the reestablishment of H3K27me3 on polycomb repressive complex 2 (PRC2)-target genes that were derepressed in old MEFs. We demonstrated that ectopic [[DNMT3L]] interacted with PRC2 in MEFs. Our data also suggested that ectopic [[DNMT3L]] might guide PRC2 to redress deregulated chromatin regions in cells undergoing senescence. This study might lead to an epigenetic reinforcement strategy for overcoming aging-associated epimutation and senescence.
+|keywords=* DNA methyltransferase 3-like (DNMT3L)
-|keywords=* Depression
+* chromatin surveillance
-* aging
+* epigenetics
-* episodic memory
+* polycomb repressive complex 2 (PRC2)
-* overgeneral
+* senescence
-* specificity
+* transposable element (TE)
-|full-text-url=https://sci-hub.do/10.1080/13607863.2020.1729338
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064442
 }}
-==ANGPTL2==
+==DOCK11==
 {{medline-entry
-|title=Circulating angiopoietin-like protein 2 levels and mortality risk in patients receiving maintenance hemodialysis: a prospective cohort study.
+|title=[Immunosenescence: The Forefront of Infection and Trophic Control].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31840173
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115558
+|abstract=Recently, aging is becoming an important social problem in many developed countries including Japan. It is socially and universally important to unveil the impact of aging and extend healthy life expectancy. Here we show our recent finding that dedicator of cytokinesis 11 ([[DOCK11]], also known as Zizimin2) may be involved in immunosenescence of B cells. [[DOCK11]] was identified as a guanine nucleotide exchange factor for a small GTPase called cell division cycle 42. Expression of [[DOCK11]] is restricted to lymphoid tissues, and becomes downregulated with age. Thus we examined the involvement of [[DOCK11]] in immunosenescence of B-1a B cells as an example. B-1a cells are the main source of antibodies at steady state, and function as the first line of defense against infection. Although [[DOCK11]] was expressed by B-1a cells, the expression levels declined with age. Furthermore, production of anti-pneumococcal immunoglobulin M antibodies was suppressed in aged mice, and was recovered by adoptive transfer with B-1a cells in a [[DOCK11]]-dependent manner. Thus [[DOCK11]] may be involved in immunosenescence of B-1a cells.
-|mesh-terms=* Aged
+|mesh-terms=* Aging
-* Angiopoietin-like Proteins
+* Animals
-* Biomarkers
+* B-Lymphocytes
-* C-Reactive Protein
+* Cytokinesis
-* Disease Progression
+* Gene Expression
-* Female
+* Guanine Nucleotide Exchange Factors
 * Humans
-* Kidney Diseases
+* Immunoglobulin M
-* Male
+* Immunosenescence
-* Middle Aged
+* Mice
-* Prognosis
+* Nutritional Status
-* Prospective Studies
+* Streptococcus pneumoniae
-* Renal Dialysis
+|keywords=* B-1a B cell
-* Risk Factors
+* dedicator of cytokinesis 11
-* Survival Rate
+* immunosenescence
-|keywords=* aging
+|full-text-url=https://sci-hub.do/10.1248/yakushi.19-00193-3
-* angiopoietin-like protein (ANGPTL) 2
-* chronic inflammation
-* hemodialysis
-* mortality risk
-|full-text-url=https://sci-hub.do/10.1093/ndt/gfz236
 }}
-==ANK3==
+==DPP4==
 {{medline-entry
-|title=Age-related atrophy of cortical thickness and genetic effect of [[ANK3]] gene in first episode MDD patients.
+|title=Dipeptidyl peptidase-4 inhibition improves endothelial senescence by activating AMPK/SIRT1/Nrf2 signaling pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32911427
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32251672
+|abstract=Dipeptidyl peptidase-4 ([[DPP4]]) is elevated in numerous cardiovascular pathological processes and [[DPP4]] inhibition is associated with reduced inflammation and oxidative stress. The aim of this study was to examine the role of [[DPP4]] in endothelial senescence. Sprague-Dawley rats (24 months) were orally administrated saxagliptin (10 mg·kg ·d ), a [[DPP4]] inhibitor, for 12 weeks in drinking water. Body weight, heart rate, blood glucose, and blood pressure were measured and vascular histological experiments were performed. In vitro studies were performed using H O -induced senescent human umbilical vein endothelial cells. Both in vivo and in vitro studies confirmed the elevation of [[DPP4]] in senescent vascular endothelium, and inhibition or knockdown of [[DPP4]] ameliorated endothelial senescence. In addition, [[DPP4]] inhibition or silencing reduced endothelial oxidative stress levels in aging vasculature and senescent endothelial cells. Moreover, [[DPP4]] inhibition or knockdown normalized the expression and phosphorylation of AMP-activated protein kinase-α (AMPKα) and sirtuin 1 (SIRT1) expression. Furthermore, the beneficial effects of [[DPP4]] inhibition or knockdown on endothelial cell senescence were at least partly dependent on SIRT1 and Nrf2 activation. In conclusion, our study demonstrated that [[DPP4]] inhibition or silencing ameliorated endothelial senescence both in vivo and in vitro by regulating AMPK/SIRT1/Nrf2. [[DPP4]] may be a new therapeutic target to combat endothelial senescence.
+|keywords=* Aging
-|keywords=* ANK3
+* Dipeptidyl peptidase-4
-* Aging
+* Endothelium
-* Cortical thickness
+* Oxidative stress
-* Major depressive disorder
+* Vascular
-* Neuroimage
+|full-text-url=https://sci-hub.do/10.1016/j.bcp.2020.113951
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7490581
 }}
-==AOX1==
+==DST==
 {{medline-entry
-|title=N1-Methylnicotinamide: An Anti-Ovarian Aging Hormetin?
+|title=Ancestral germen/soma distinction in microbes: Expanding the disposable soma theory of aging to all unicellular lineages.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32711159
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32268207
+|abstract=Life has persisted for about 3.5 billion years (Gy) despite fluctuating environmental pressures and the aging and mortality of individuals. The disposable soma theory ([[DST]]) notoriously contributes to explain this persistence for lineages with a clear soma/germen distinction. Beyond such lineages however, the phylogenetic scope of application of the [[DST]] is less obvious. Typically, the [[DST]] is not expected to explain the survival of microbial species that comprise single-celled organisms apparently lacking a germen/soma distinction. Here, we present an evolutionary argument that generalizes the explanatory scope of [[DST]] to the entire microbial world and provides a novel characterization of the deep molecular and evolutionary roots supporting this expanded disposable soma theory of aging. Specifically, we argue that the germen/soma distinction arose early in evolution and identify DNA semi-conservative replication as a critical process through which two forms of rejuvenation could have evolved in the first microbes. Our hypothesis has fundamental and practical implications. First, whereas unicellular organisms were long thought of as potentially immortal, we suggest instead that all unicellular individuals (prokaryotes or protists alike) are very likely to age, either replicatively or physiologically, or both. Second, our theory introduces a profound reconsideration of microbial individuality, whereby, all microbial individuals, as seen by natural selection, present an obligate transient germen/soma distinction during their life cycles. Third, our work promotes the study of cellular division in prokaryotes and in protist mitosis to illuminate the evolutionary origin of the soma and germen division, traditionally studied in animals. These ideas set the stage for progress in the evolutionary theory of aging from a heretofore overlooked microbial perspective.
+|mesh-terms=* Aging
-|keywords=* AMPK
+* Animals
-* MNAM
+* Biological Evolution
-* Ovarian Aging
+* DNA Replication
-* ROS
+* Humans
-|full-text-url=https://sci-hub.do/10.1016/j.arr.2020.101131
+* Phylogeny
+|keywords=* Aging
+* Asymmetric cell division
+* DNA replication
+* Disposable Soma Theory
+* Epigenetics
+* Evolution
+* Germen/Soma
+* Prokaryotes
+* Protists
+* Rejuvenation
+* Unicellular
+|full-text-url=https://sci-hub.do/10.1016/j.arr.2020.101064
 }}
-==AP2B1==
+==EGF==
 {{medline-entry
-|title=Circular RNA NF1-419 enhances autophagy to ameliorate senile dementia by binding Dynamin-1 and Adaptor protein 2 B1 in AD-like mice.
+|title=Insulin Signaling in Intestinal Stem and Progenitor Cells as an Important Determinant of Physiological and Metabolic Traits in [i]Drosophila[/i].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31860870
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32225024
+|abstract=The insulin-IGF-1 signaling (IIS) pathway is conserved throughout multicellular organisms and regulates many traits, including aging, reproduction, feeding, metabolism, stress resistance, and growth. Here, we present evidence of a survival-sustaining role for IIS in a subset of gut cells in [i]Drosophila melanogaster[/i], namely the intestinal stem cells (ISCs) and progenitor cells. Using RNAi to knockdown the insulin receptor, we found that inhibition of IIS in ISCs statistically shortened the lifespan of experimental flies compared with non-knockdown controls, and also shortened their survival under starvation or malnutrition conditions. These flies also showed decreased reproduction and feeding, and had lower amounts of glycogen and glucose in the body. In addition, increased expression was observed for the [i]Drosophila[/i] transcripts for the insulin-like peptides [i]dilp2[/i], [i]dilp5[/i], and [i]dilp6.[/i] This may reflect increased insulin signaling in peripheral tissues supported by up-regulation of the target of the brain insulin gene ([i]tobi[/i]). In contrast, activation of IIS (via knockdown of the insulin pathway inhibitor PTEN) in intestinal stem and progenitor cells decreased fly resistance to malnutrition, potentially by affecting adipokinetic hormone signaling. Finally, [i]Pten[/i] knockdown to enhance IIS also activated JAK-STAT signaling in gut tissue by up-regulation of [i]upd2[/i], [i]upd3[/i], and [i]soc36[/i] genes, as well as genes encoding the [[EGF]] receptor ligands [i]spitz[/i] and [i]vein[/i]. These results clearly demonstrate that manipulating insulin levels may be used to modulate various fly traits, which are important determinants of organismal survival.
-|mesh-terms=* Adaptor Protein Complex beta Subunits
+|keywords=* ISC
-* Aging
+* fruit fly
-* Alzheimer Disease
+* insulin signaling pathway
-* Animals
+* lifespan
-* Astrocytes
+* metabolism
-* Autophagy
+* midgut
-* Cellular Senescence
+* progenitor cells
-* Dynamin I
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7226132
-* Genes, Neurofibromatosis 1
-* Mice
-* RNA, Circular
-* Rats
-* Rats, Sprague-Dawley
-|keywords=* aging
-* astrocyte
-* autophagy
-* biological function
-* circular RNA
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6949063
 }}
-==APC==
+==EGFR==
 {{medline-entry
-|title=Differences between blacks and whites in well-being, beliefs, emotional states, behaviors and survival, 1978-2014.
+|title=Comparative effectiveness and cost-effectiveness of three first-line [[EGFR]]-tyrosine kinase inhibitors: Analysis of real-world data in a tertiary hospital in Taiwan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32925952
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32267879
+|abstract=Comparison of the effectiveness and cost-effectiveness of three first-line [[EGFR]]-tyrosine kinase inhibitors (TKIs) would improve patients' clinical benefits and save costs. Using real-world data, this study attempted to directly compare the effectiveness and cost-effectiveness of first-line afatinib, erlotinib, and gefitinib. During May 2011-December 2017, all patients with non-small cell lung cancer (NSCLC) visiting a tertiary center were invited to fill out the EuroQol five-dimension (EQ-5D) questionnaires and World Health Organization Quality of Life, brief version (WHOQOL-BREF), and received follow-ups for survival and direct medical costs. A total of 379 patients with [[EGFR]] mutation-positive advanced NSCLC under first-line TKIs were enrolled for analysis. After propensity score matching for the patients receiving afatinib (n = 48), erlotinib (n = 48), and gefitinib (n = 96), we conducted the study from the payers' perspective with a lifelong time horizon. Patients receiving afatinib had the worst lifetime psychometric scores, whereas the differences in quality-adjusted life expectancy (QALE) were modest. Considering 3 treatments together, afatinib was dominated by erlotinib. Erlotinib had an incremental cost-effectiveness of US$17,960/life year and US$12,782/QALY compared with gefitinib. Acceptability curves showed that erlotinib had 58.6% and 78.9% probabilities of being cost-effective given a threshold of 1 Taiwanese per capita GDP per life year and QALY, respectively. Erlotinib appeared to be cost-effective. Lifetime psychometric scores may provide additional information for effectiveness evaluation.
-|mesh-terms=* Adult
+|mesh-terms=* Afatinib
-* African Americans
 * Aged
-* Behavior
+* Carcinoma, Non-Small-Cell Lung
-* Cohort Studies
+* Cost-Benefit Analysis
-* Emotions
+* Erlotinib Hydrochloride
-* European Continental Ancestry Group
 * Female
-* Hispanic Americans
+* Gefitinib
 * Humans
-* Longevity
+* Life Expectancy
+* Lung Neoplasms
 * Male
-* Middle Aged
+* Propensity Score
-* Socioeconomic Factors
+* Protein Kinase Inhibitors
-* Survival Analysis
+* Quality of Life
-* United States
+* Survival Rate
+* Taiwan
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7489510
+* Tertiary Care Centers
+|keywords=#f
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7141611
 }}
 {{medline-entry
-|title=Wnt-induced, TRP53-mediated Cell Cycle Arrest of Precursors Underlies Interstitial Cell of Cajal Depletion During Aging.
+|title=An Optogenetic Method to Study Signal Transduction in Intestinal Stem Cell Homeostasis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32771388
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32201167
+|abstract=Homeostasis in adult organs involves replacement of cells from a stem cell pool maintained in specialized niches regulated by extracellular signals. This cell-to-cell communication employs signal transduction pathways allowing cells to respond with a variety of behaviors. To study these cellular behaviors, signaling must be perturbed within tissues in precise patterns, a technique recently made possible by the development of optogenetic tools. We developed tools to study signal transduction in vivo in an adult fly midgut stem cell model where signaling was regulated by the application of light. Activation was achieved by clustering of membrane receptors [[EGFR]] and Toll, while inactivation was achieved by clustering the downstream activators ERK/Rolled and NFκB/Dorsal in the cytoplasm, preventing nuclear translocation and transcriptional activation. We show that both pathways contribute to stem and transit amplifying cell numbers and affect the lifespan of adult flies. We further present new approaches to overcome overexpression phenotypes and novel methods for the integration of optogenetics into the already-established genetic toolkit of Drosophila.
+|mesh-terms=* Animals
-|keywords=* Compliance
+* Cell Communication
-* Senescence
+* Cell Proliferation
-* Stem Cell
+* Cells, Cultured
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7672319
+* Drosophila Proteins
+* Drosophila melanogaster
+* Gene Expression Regulation
+* Gene Regulatory Networks
+* Homeostasis
+* Intestinal Mucosa
+* Light
+* Longevity
+* Optogenetics
+* Signal Transduction
+* Stem Cells
+|keywords=* Drosophila
+* EGFR
+* Toll
+* optogenetics
+* stem cells
+|full-text-url=https://sci-hub.do/10.1016/j.jmb.2020.03.019
 }}
-{{medline-entry
+==EHF==
-|title=Burden of musculoskeletal disorders in Iran during 1990-2017: estimates from the Global Burden of Disease Study 2017.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32651719
-|mesh-terms=* Female
-* Global Burden of Disease
-* Global Health
-* Humans
-* Iran
-* Life Expectancy
-* Male
-* Musculoskeletal Diseases
-* Quality-Adjusted Life Years
-|keywords=* Burden
-* DALY
-* Decomposition
-* Global burden of diseases
-* Iran
-* Musculoskeletal diseases
-|full-text-url=https://sci-hub.do/10.1007/s11657-020-00767-8
-}}
 {{medline-entry
-|title=Fall-related mortality trends in older Japanese adults aged ≥65 years: a nationwide observational study.
+|title=Extended high frequency hearing and speech perception implications in adults and children.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31831549
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32111404
+|abstract=Extended high frequencies ([[EHF]]), above 8 kHz, represent a region of the human hearing spectrum that is generally ignored by clinicians and researchers alike. This article is a compilation of contributions that, together, make the case for an essential role of [[EHF]] in both normal hearing and auditory dysfunction. We start with the fundamentals of biological and acoustic determinism - humans have [[EHF]] hearing for a purpose, for example, the detection of prey, predators, and mates. [[EHF]] hearing may also provide a boost to speech perception in challenging conditions and its loss, conversely, might help explain difficulty with the same task. However, it could be that [[EHF]] are a marker for damage in the conventional frequency region that is more related to speech perception difficulties. Measurement of [[EHF]] hearing in concert with otoacoustic emissions could provide an early warning of age-related hearing loss. In early life, when [[EHF]] hearing sensitivity is optimal, we can use it for enhanced phonetic identification during language learning, but we are also susceptible to diseases that can prematurely damage it. [[EHF]] audiometry techniques and standardization are reviewed, providing evidence that they are reliable to measure and provide important information for early detection, monitoring and possible prevention of hearing loss in populations at-risk. To better understand the full contribution of [[EHF]] to human hearing, clinicians and researchers can contribute by including its measurement, along with measures of speech in noise and self-report of hearing difficulties and tinnitus in clinical evaluations and studies.
-|mesh-terms=* Accidental Falls
+|keywords=* Aging
-* Aged
+* Development
-* Aged, 80 and over
+* Extended high frequency audiometry
-* Female
+* Otitis media
-* Geriatrics
+* Ototoxicity
-* Health Policy
+* Speech in noise
-* Health Services Needs and Demand
+* Speech perception
-* Humans
+* Tinnitus
-* Japan
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431381
-* Male
-* Mortality
-* Public Health
-|keywords=* adult intensive & critical care
-* epidemiology
-* geriatric medicine
-* health & safety
-* health policy
-* public health
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6924807
 }}
-{{medline-entry
+==ERCC1==
-|title=Stroke Mortality Rates and Trends in Romania, 1994-2017.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31624036
-|mesh-terms=* Adult
-* Age Distribution
-* Aged
-* Aged, 80 and over
-* Cause of Death
-* Female
-* Humans
-* Life Expectancy
-* Male
-* Middle Aged
-* Prognosis
-* Registries
-* Risk Assessment
-* Risk Factors
-* Romania
-* Sex Distribution
-* Stroke
-* Time Factors
-|keywords=* Mortality
-* age-standardized mortality rates
-* life expectancy
-* stroke
-|full-text-url=https://sci-hub.do/10.1016/j.jstrokecerebrovasdis.2019.104431
-}}
 {{medline-entry
-|title=A new approach to quantifying the EEG during walking: Initial evidence of gait related potentials and their changes with aging and dual tasking.
+|title=Local endothelial DNA repair deficiency causes aging-resembling endothelial-specific dysfunction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31449852
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32202295
+|abstract=We previously identified genomic instability as a causative factor for vascular aging. In the present study, we determined which vascular aging outcomes are due to local endothelial DNA damage, which was accomplished by genetic removal of [[ERCC1]] (excision repair cross-complementation group 1) DNA repair in mice (EC-knockout (EC-KO) mice). EC-KO showed a progressive decrease in microvascular dilation of the skin, increased microvascular leakage in the kidney, decreased lung perfusion, and increased aortic stiffness compared with wild-type (WT). EC-KO showed expression of DNA damage and potential senescence marker p21 exclusively in the endothelium, as demonstrated in aorta. Also the kidney showed p21-positive cells. Vasodilator responses measured in organ baths were decreased in aorta, iliac and coronary artery EC-KO compared with WT, of which coronary artery was the earliest to be affected. Nitric oxide-mediated endothelium-dependent vasodilation was abolished in aorta and coronary artery, whereas endothelium-derived hyperpolarization and responses to exogenous nitric oxide (NO) were intact. EC-KO showed increased superoxide production compared with WT, as measured in lung tissue, rich in endothelial cells (ECs). Arterial systolic blood pressure (BP) was increased at 3 months, but normal at 5 months, at which age cardiac output (CO) was decreased. Since no further signs of cardiac dysfunction were detected, this decrease might be an adaptation to prevent an increase in BP. In summary, a selective DNA repair defect in the endothelium produces features of age-related endothelial dysfunction, largely attributed to loss of endothelium-derived NO. Increased superoxide generation might contribute to the observed changes affecting end organ perfusion, as demonstrated in kidney and lung.
-|mesh-terms=* Accelerometry
+|mesh-terms=* Age Factors
-* Adult
-* Aged
 * Aging
-* Electroencephalography
+* Animals
-* Evoked Potentials
+* Capillary Permeability
-* Exercise Test
+* Cellular Senescence
-* Female
+* Cyclin-Dependent Kinase Inhibitor p21
-* Gait
+* DNA Damage
-* Humans
+* DNA Repair
-* Male
+* DNA-Binding Proteins
-* Middle Aged
+* Endonucleases
-* Multitasking Behavior
+* Endothelial Cells
-* Reaction Time
+* Endothelium, Vascular
-* Walking
+* Mice, Inbred C57BL
-|keywords=* Dual task
+* Mice, Knockout
-* EEG
+* Nitric Oxide
-* Gait cycle
+* Nitric Oxide Synthase Type III
-* Gait related potentials (GRP)
+* Superoxides
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2019.110709
+* Vascular Stiffness
+* Vasodilation
+|keywords=* DNA damage
+* aging
+* endothelial dysfunction
+* endothelium-dependent dilation
+* nitric oxide
+|full-text-url=https://sci-hub.do/10.1042/CS20190124
 }}
-==APOC3==
+==F3==
 {{medline-entry
-|title=Positional Obstructive Sleep Apnea Syndrome in Elderly Patients.
+|title=Multigenerational exposure to TiO  nanoparticles in soil stimulates stress resistance and longevity of survived C. elegans via activating insulin/IGF-like signaling.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32050596
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32203849
+|abstract=With increasing release of nanoparticles (NPs) into the environment, soil organisms likely suffer from high dose and long duration of NPs contamination, while the effect of NPs across multiple generations in soil is rarely studied. Herein, we investigated how multigenerational exposure to different crystal forms (anatase, rutile, and their mixture) of TiO  NPs (nTiO ) affected the survival, behavior, physiological and biochemical traits, and lifespan of nematodes (C. elegans) in a paddy soil. The soil property changed very slightly after being spiked with nTiO , and the toxicities of three nTiO  forms were largely comparable. The nTiO  exposure adversely influenced the survival and locomotion of nematodes, and increased intracellular reactive oxygen species (ROS) generation. Interestingly, the toxic effect gradually attenuated and the lifespan of survived nematodes increased from the P0 to [[F3]] generation, which was ascribed to the survivor selection and stimulatory effect. The lethal effect and the increased oxidative stress may continuously screen out offspring possessing stronger anti-stress capabilities. Moreover, key genes (daf-2, age-1, and skn-1) in the insulin/IGF-like signaling (IIS) pathway actively responded to the nTiO  exposure, which further optimized the selective expression of downstream genes, increased the antioxidant enzyme activities and antioxidant contents, and thereby increased the stress resistance and longevity of survived nematodes across successive generations. Our findings highlight the crucial role of bio-responses in the progressively decreased toxicity of nTiO , and add new knowledge on the long-term impact of soil nTiO  contamination.
-|mesh-terms=* Adult
+|mesh-terms=* Animals
-* Aged
+* Caenorhabditis elegans
-* Humans
+* Caenorhabditis elegans Proteins
-* Middle Aged
+* Insulin
-* Polysomnography
+* Longevity
-* Posture
+* Nanoparticles
-* Prospective Studies
+* Oxidative Stress
-* Sleep Apnea, Obstructive
+* Soil
-* Supine Position
+* Titanium
-* Young Adult
+|keywords=* Insulin/IGF-like signaling
-|keywords=* aging effects
+* Longevity
-* obstructive sleep apnea
+* Multigenerational toxicity
-* polysomnography
+* Nanomaterial
-* positional sleep apnea
+* Soil nematode
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7042812
+|full-text-url=https://sci-hub.do/10.1016/j.envpol.2020.114376
 }}
-==APOE==
+==FAAH==
 {{medline-entry
-|title=Polygenic risk score of longevity predicts longer survival across an age-continuum.
+|title=Endocannabinoid genetic variation enhances vulnerability to THC reward in adolescent female mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33216869
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32095523
+|abstract=Adolescence represents a developmental period with the highest risk for initiating cannabis use. Little is known about whether genetic variation in the endocannabinoid system alters mesolimbic reward circuitry to produce vulnerability to the rewarding properties of the exogenous cannabinoid Δ -tetrahydrocannabinol (THC). Using a genetic knock-in mouse model ([[FAAH]] ) that biologically recapitulates the human polymorphism associated with problematic drug use, we find that in adolescent female mice, but not male mice, this [[FAAH]] polymorphism enhances the mesolimbic dopamine circuitry projecting from the ventral tegmental area (VTA) to the nucleus accumbens (NAc) and alters cannabinoid receptor 1 (CB R) levels at inhibitory and excitatory terminals in the VTA. These developmental changes collectively increase vulnerability of adolescent female [[FAAH]]  mice to THC preference that persists into adulthood. Together, these findings suggest that this endocannabinoid genetic variant is a contributing factor for increased susceptibility to cannabis dependence in adolescent females.
+|mesh-terms=* Aging
-|keywords=* centenarians
+* Amidohydrolases
-* cognitive health
+* Animals
-* genetics
+* Axons
-* healthy aging
+* Choice Behavior
-* longevity
+* Dronabinol
-|full-text-url=https://sci-hub.do/10.1093/gerona/glaa289
+* Endocannabinoids
-}}
+* Female
-{{medline-entry
+* Genetic Variation
-|title=Association Between [[APOE]] Alleles and Change of Neuropsychological Tests in the Long Life Family Study.
+* Male
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33216038
+* Mice, Inbred C57BL
+* Nerve Net
+* Nucleus Accumbens
+* Polymorphism, Single Nucleotide
+* Receptor, Cannabinoid, CB1
+* Reward
+* Tyrosine 3-Monooxygenase
+* Ventral Tegmental Area
+|keywords=#f
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7015690
+}}
+==FAS==
-|keywords=* APOE
-* cognition
-* longevity
-* longitudinal studies
-|full-text-url=https://sci-hub.do/10.3233/JAD-201113
-}}
 {{medline-entry
-|title=The [[APOE]] gene cluster responds to air pollution factors in mice with coordinated expression of genes that differs by age in humans.
+|title=Inhibition of USP7 activity selectively eliminates senescent cells in part via restoration of p53 activity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33215813
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32064756
+|abstract=The accumulation of senescent cells (SnCs) is a causal factor of various age-related diseases as well as some of the side effects of chemotherapy. Pharmacological elimination of SnCs (senolysis) has the potential to be developed into novel therapeutic strategies to treat these diseases and pathological conditions. Here we show that ubiquitin-specific peptidase 7 (USP7) is a novel target for senolysis because inhibition of USP7 with an inhibitor or genetic depletion of USP7 by RNA interference induces apoptosis selectively in SnCs. The senolytic activity of USP7 inhibitors is likely attributable in part to the promotion of the human homolog of mouse double minute 2 (MDM2) ubiquitination and degradation by the ubiquitin-proteasome system. This degradation increases the levels of p53, which in turn induces the pro-apoptotic proteins PUMA, NOXA, and [[FAS]] and inhibits the interaction of BCL-XL and BAK to selectively induce apoptosis in SnCs. Further, we show that treatment with a USP7 inhibitor can effectively eliminate SnCs and suppress the senescence-associated secretory phenotype (SASP) induced by doxorubicin in mice. These findings suggest that small molecule USP7 inhibitors are novel senolytics that can be exploited to reduce chemotherapy-induced toxicities and treat age-related diseases.
+|keywords=* MDM2
+* Senescence
+* USP7
+* apoptosis
+* p53
+* senolytics
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059172
+}}
+==FES==
-|keywords=* Alzheimer's disease
-* aging
-* air pollution
-* apolipoprotein E
-* chromosome 19q13
-|full-text-url=https://sci-hub.do/10.1002/alz.12230
-}}
 {{medline-entry
-|title=Homozygosity in the [i][[APOE]][/i] 3 Polymorphism Is Associated With Less Depression and Higher Serum Low-Density Lipoprotein in Chinese Elderly Schizophrenics.
+|title=A Single Question as a Screening Tool to Assess Fear of Falling in Young-Old Community-Dwelling Persons.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33178131
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32165062
+|abstract=Fear of falling (FOF) is common in older persons and related to negative outcomes. This study aimed to investigate the relationship between 2 FOF measures: the Falls Efficacy Scale-International ([[FES]]-I) and the single question on FOF and activity restriction (SQ-FAR). Factors associated with disagreement between the 2 measures were further examined. Cross-sectional study. Participants (N = 1359) were community-dwelling persons aged 65 to 70 years who were enrolled in the Lausanne cohort 65+. Data included demographic, functional, cognitive, affective, and health status. FOF was measured with [[FES]]-I and the 3-level SQ-FAR (no FOF, FOF without activity restriction (AR, FOF with AR). [[FES]]-I concern about falling was categorized as low (score 16-19), moderate (score 20-27), and high (score 28-64). Weighted agreement between the [[FES]]-I and the SQ-FAR was 87.8% (Kappa = 0.57). Using the [[FES]]-I as gold standard, the performance of SQ-FAR was good (specificity 86%; sensitivity 74%, negative predicting value 89%, positive predicting value 69%). Among participants with moderate/high FOF according to [[FES]]-I, male sex (P = .011) and the absence of previous falls (P < .001) were associated with disagreement between the 2 tools. Among participants with low FOF, female sex (P = .005), falls history (P < .001), and pre-frailty/frailty status (P = .050) were associated with disagreement. The SQ-FAR has a moderate agreement with [[FES]]-I and might be used as a screening tool. The results also may help design a step-by-step strategy to evaluate and address FOF in the clinical setting.
+|keywords=* FES-I
-|keywords=* APOE E3
+* elderly
-* Chinese
+* fear of falling
-* aging
+* healthy aging
-* depressive symptom
+* older adults
-* schizophrenia
+|full-text-url=https://sci-hub.do/10.1016/j.jamda.2020.01.101
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7593819
 }}
-{{medline-entry
+==FEV==
-|title=Effect of apolipoprotein E polymorphism on cognition and brain in the Cambridge Centre for Ageing and Neuroscience cohort.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33088920
-|keywords=* Cognition
-* ageing
-* apolipoprotein E
-* brain
-* lifespan
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7545750
-}}
 {{medline-entry
-|title=Cardiovascular risk factors and [[APOE]]-ε4 status affect memory functioning in aging via changes to temporal stem diffusion.
+|title=Current Bronchodilator Responsiveness Criteria Underestimate Asthma in Older Adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33070365
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32071132
+|abstract=Asthma is common in older adults and is confirmed by demonstration of variable expiratory air-flow limitations, typically evaluated by spirometric assessment of bronchodilator responsiveness. However, many patients with clinically suspected asthma and documented air-flow obstruction do not exhibit a post-bronchodilator response that meets or exceeds current established guidelines. We investigated if extending the time from bronchodilator administration to assessment of bronchodilator response increases the yield of spirometry for the diagnosis of asthma in older adults. This was a cross-sectional study. The subjects were non-smokers, ≥ 60 y old, and with suspected asthma. Subjects were characterized as (1) those with a positive bronchodilator response on the 30-min post-bronchodilator spirometry, (2) those with a positive bronchodilator response on the 60-min post-bronchodilator spirometry, and (3) those without a positive bronchodilator response but with a positive methacholine challenge test. Factors associated with a late response to bronchodilator were evaluated by using bivariate analysis and by multivariate analysis by using a logistic regression model. This study enrolled 165 subjects. Of these, 81 (49.1%) had a positive bronchodilator response on 30-min post-bronchodilator spirometry; 25 (15.2%) had a positive bronchodilator response on the 1-h post-bronchodilator spirometry; and 59 (35.8%) had no positive bronchodilator response but had a positive methacholine challenge test. On multivariable regression analysis, those with a higher baseline percentage of predicted [[FEV]] , higher scores on a standard asthma control test, and wheezing and/or cough after exercise were more likely to either have a late bronchodilator response or no bronchodilator response. Our study showed that a late positive response to bronchodilator use was more common than previously presumed in older subjects with suspected asthma. Pulmonary function testing laboratories should consider routinely reassessing spirometry at 1 h after bronchodilator use if the earlier assessment did not reveal a significant response.
+|keywords=* aging
-|keywords=* APOE
+* albuterol
-* BMI
+* asthma
-* RRID:SCR_001398
+* bronchodilator effect
-* RRID:SCR_002403
+* lung diseases
-* RRID:SCR_002823
+* older adult
-* RRID:SCR_002865
+* spirometry
-* RRID:SCR_007037
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7538007
-* aging
-* diffusion tensor imaging
-* hypertension
-* memory
-* path modeling
-|full-text-url=https://sci-hub.do/10.1002/jnr.24734
 }}
-{{medline-entry
+==FGF19==
-|title=[[APOE]] [i]ε[/i]4 and resting-state functional connectivity in racially/ethnically diverse older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32999914
-|keywords=* APOE ε4 differences
-* brain aging
-* dementia
-* neuroimaging
-* racial/ethnic differences
-* resting‐state functional connectivity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7508460
-}}
 {{medline-entry
-|title=Predictors of Olfactory Decline in Aging: A Longitudinal Population-Based Study.
+|title=Bile acid receptor agonists in primary biliary cholangitis: Regulation of the cholangiocyte secretome and downstream T cell differentiation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32886741
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32123836
+|abstract=Primary biliary cholangitis (PBC) is a chronic autoimmune liver disease. Approximately 30% of patients do not respond to therapy with ursodeoxycholic acid (UDCA). Previous studies have implicated increased senescence of cholangiocytes in patients who do not respond to UDCA. This may increase the release of cytokines which drive pathogenic T cell polarization. As FXR agonists are beneficial in treating UDCA non-responsive patients, the current study was designed to model the interactions between cholangiocytes and CD4+ T cells to investigate potential immunomodulatory mechanisms of bile acid receptor agonists. Human cholangiocytes were co-cultured with CD4+ T cells to model the biliary stress response. Senescent cholangiocytes were able to polarize T cells toward a Th17 phenotype and suppressed expression of FoxP3 ([i]P[/i] = 0.0043). Whilst FXR and TGR5 receptor agonists were unable directly to alter cholangiocyte cytokine expression, [[FGF19]] was capable of significantly reducing IL-6 release ([i]P[/i] = 0.044). Bile acid receptor expression was assessed in PBC patients with well-characterized responsiveness to UDCA therapy. A reduction in FXR staining was observed in both cholangiocytes and hepatocytes in PBC patients without adequate response to UDCA. Increased IL-6 expression by senescent cholangiocytes represents a potential mechanism by which biliary damage in PBC could contribute to excessive inflammation.
+|keywords=* FGF19
+* FXR
+* TGR5
+* autoimmunity
+* senescence
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996327
+}}
+==FGFR1==
-|keywords=*  Cognitive aging
-* Epidemiology
-* Olfactory
-* Olfactory impairment
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7662159
-}}
 {{medline-entry
-|title=When Culture Influences Genes: Positive Age Beliefs Amplify the Cognitive-Aging Benefit of [[APOE]] ε2.
+|title=Satellite cell-specific ablation of Cdon impairs integrin activation, FGF signalling, and muscle regeneration.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32835364
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32103583
+|abstract=Perturbation in cell adhesion and growth factor signalling in satellite cells results in decreased muscle regenerative capacity. Cdon (also called Cdo) is a component of cell adhesion complexes implicated in myogenic differentiation, but its role in muscle regeneration remains to be determined. We generated inducible satellite cell-specific Cdon ablation in mice by utilizing a conditional Cdon allele and Pax7   . To induce Cdon ablation, mice were intraperitoneally injected with tamoxifen (tmx). Using cardiotoxin-induced muscle injury, the effect of Cdon depletion on satellite cell function was examined by histochemistry, immunostaining, and 5-ethynyl-2'-deoxyuridine (EdU) incorporation assay. Isolated myofibers or myoblasts were utilized to determine stem cell function and senescence. To determine pathways related to Cdon deletion, injured muscles were subjected to RNA sequencing analysis. Satellite cell-specific Cdon ablation causes impaired muscle regeneration with fibrosis, likely attributable to decreased proliferation, and senescence, of satellite cells. Cultured Cdon-depleted myofibers exhibited 32 ± 9.6% of EdU-positive satellite cells compared with 58 ± 4.4% satellite cells in control myofibers (P < 0.05). About 32.5 ± 3.7% Cdon-ablated myoblasts were positive for senescence-associated β-galactosidase (SA-β-gal) while only 3.6 ± 0.5% of control satellite cells were positive (P < 0.001). Transcriptome analysis of muscles at post-injury Day 4 revealed alterations in genes related to mitogen-activated protein kinase signalling (P < 8.29 e  ) and extracellular matrix (P < 2.65 e  ). Consistent with this, Cdon-depleted tibialis anterior muscles had reduced phosphorylated extracellular signal-regulated kinase (p-ERK) protein levels and expression of ERK targets, such as Fos (0.23-fold) and Egr1 (0.31-fold), relative to mock-treated control muscles (P < 0.001). Cdon-depleted myoblasts exhibited impaired ERK activation in response to basic fibroblast growth factor. Cdon ablation resulted in decreased and/or mislocalized integrin β1 activation in satellite cells (weak or mislocalized integrin1 in tmx = 38.7 ± 1.9%, mock = 21.5 ± 6%, P < 0.05), previously linked with reduced fibroblast growth factor (FGF) responsiveness in aged satellite cells. In mechanistic studies, Cdon interacted with and regulated cell surface localization of [[FGFR1]] and FGFR4, likely contributing to FGF responsiveness of satellite cells. Satellite cells from a progeria model, Zmpste24  myofibers, showed decreased Cdon levels (Cdon-positive cells in Zmpste24  = 63.3 ± 11%, wild type = 90 ± 7.7%, P < 0.05) and integrin β1 activation (weak or mislocalized integrin β1 in Zmpste24  = 64 ± 6.9%, wild type = 17.4 ± 5.9%, P < 0.01). Cdon deficiency in satellite cells causes impaired proliferation of satellite cells and muscle regeneration via aberrant integrin and FGFR signalling.
+|keywords=* Cdon
+* Cellular senescence
+* FGFR
+* Growth factor signalling
+* Muscle regeneration
+* Satellite cell
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432598
+}}
+==FH==
-|keywords=*
-          APOE
-* Age beliefs
-* Cognition
-* Gene
-* Health and Retirement Study
-* Self-perceptions of aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7489069
-}}
 {{medline-entry
-|title=Age and the association between apolipoprotein E genotype and Alzheimer disease: A cerebrospinal fluid biomarker-based case-control study.
+|title=Macroscopic hematuria as a risk factor for hypertension in ageing people with hemophilia and a family history of hypertension.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32817639
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32118768
+|abstract=Ageing people with hemophilia (PWH) have a higher prevalence of hypertension than the general population. This study aimed to determine whether macroscopic hematuria was associated with hypertension in PWH in a post hoc analysis using data from a cross-sectional study conducted by the ADVANCE Working Group (the H3 study), which included PWH ≥ 40 years of age. Data from 16 contributing centers, located in 13 European countries and Israel, were analyzed using logistic regression models. Of 532 recruited PWH in the H3 study, 117 had hypertension and a positive family history of hypertension (hypertension [[FH]]+), 75 had hypertension and a negative family history of hypertension (hypertension [[FH]]-), 290 had no diagnosis of hypertension, and the remaining 50 had missing hypertension data. Logistic regressions showed that macroscopic hematuria was associated with hypertension [[FH]]+, both in the univariate (OR = 1.84 [1.17-2.90], P = .01) and in the multivariate model (OR = 1.80 [1.03-3.16], P = .04). Macroscopic hematuria was not associated with hypertension [[FH]]-. Moreover, in a multivariate logistic regression the odds of hypertension [[FH]]+ were increased with the number of macroscopic hematuria episodes. The association between macroscopic hematuria and hypertension was significant for PWH with a family history of hypertension.
 |mesh-terms=* Adult
 * Aged
 * Aged, 80 and over
 * Aging
-* Alzheimer Disease
+* Cross-Sectional Studies
-* Apolipoprotein E4
-* Biomarkers
-* Case-Control Studies
-* Cohort Studies
 * Female
-* Genotype
+* Hematuria
+* Hemophilia A
 * Humans
+* Hypertension
+* Israel
+* Logistic Models
 * Male
 * Middle Aged
+* Risk Factors
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7446786
+|keywords=#f
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7478422
 }}
-{{medline-entry
+==FOS==
-|title=Estimating the potential for dementia prevention through modifiable risk factors elimination in the real-world setting: a population-based study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32767997
-|keywords=* Aging
-* Alzheimer’s disease
-* Dementia
-* Dementia prevention
-* Modifiable risk factors
-* Population attributable fraction
-* Public health
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7414752
-}}
 {{medline-entry
-|title=Machine learning-based estimation of cognitive performance using regional brain MRI markers: the Northern Manhattan Study.
+|title=Muscle atrophy-related myotube-derived exosomal microRNA in neuronal dysfunction: Targeting both coding and long noncoding RNAs.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32740887
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32233025
+|abstract=In mammals, microRNAs can be actively secreted from cells to blood. miR-29b-3p has been shown to play a pivotal role in muscle atrophy, but its role in intercellular communication is largely unknown. Here, we showed that miR-29b-3p was upregulated in normal and premature aging mouse muscle and plasma. miR-29b-3p was also upregulated in the blood of aging individuals, and circulating levels of miR-29b-3p were negatively correlated with relative appendicular skeletal muscle. Consistently, miR-29b-3p was observed in exosomes isolated from long-term differentiated atrophic C2C12 cells. When C2C12-derived miR-29b-3p-containing exosomes were uptaken by neuronal SH-SY5Y cells, increased miR-29b-3p levels in recipient cells were observed. Moreover, miR-29b-3p overexpression led to downregulation of neuronal-related genes and inhibition of neuronal differentiation. Interestingly, we identified HIF1α-AS2 as a novel c-[[FOS]] targeting lncRNA that is induced by miR-29b-3p through down-modulation of c-[[FOS]] and is required for miR-29b-3p-mediated neuronal differentiation inhibition. Our results suggest that atrophy-associated circulating miR-29b-3p may mediate distal communication between muscle cells and neurons.
+|keywords=* HIF-1α-AS2
-|keywords=* Biomarkers
+* aging
-* Brain aging
+* lncRNAs
-* Cognitive aging
+* miR-29b-3p
-* Machine learning
+* muscle atrophy
-|full-text-url=https://sci-hub.do/10.1007/s11682-020-00325-3
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7253071
 }}
-{{medline-entry
+==FOSL2==
-|title=Effects of an [[APOE]] Promoter Polymorphism on Fronto-Parietal Functional Connectivity During Nondemented Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32694990
-|keywords=* APOE promoter
-* aging
-* brain connectome
-* fronto-parietal network
-* working memory
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7338603
-}}
 {{medline-entry
-|title=The relationship of parental longevity with the aging brain-results from UK Biobank.
+|title=LncRNA GUARDIN suppresses cellular senescence through a LRP130-PGC1α-FOXO4-p21-dependent signaling axis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32671621
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32149459
+|abstract=The long noncoding RNA GUARDIN functions to protect genome stability. Inhibiting GUARDIN expression can alter cell fate decisions toward senescence or apoptosis, but the underlying molecular signals are unknown. Here, we show that GUARDIN is an essential component of a transcriptional repressor complex involving LRP130 and PGC1α. GUARDIN acts as a scaffold to stabilize LRP130/PGC1α heterodimers and their occupancy at the FOXO4 promotor. Destabilizing this complex by silencing of GUARDIN, LRP130, or PGC1α leads to increased expression of FOXO4 and upregulation of its target gene p21, thereby driving cells into senescence. We also found that GUARDIN expression was induced by rapamycin, an agent that suppresses cell senescence. FOS-like antigen 2 ([[FOSL2]]) acts as a transcriptional repressor of GUARDIN, and lower [[FOSL2]] levels in response to rapamycin correlate with increased levels of GUARDIN. Together, these results demonstrate that GUARDIN inhibits p21-dependent senescence through a LRP130-PGC1α-FOXO4 signaling axis, and moreover, GUARDIN contributes to the anti-aging activities of rapamycin.
+|keywords=*
+GUARDIN
-|keywords=* Aging
+* LRP130-PGC1α
-* Brain structure
+* cellular senescence
-* DTI
+* lncRNAs
-* MRI
+* p21
-* Neuroimaging
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7132339
-* Parental longevity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7525531
 }}
+==FSHR==
 {{medline-entry
-|title=Alzheimer's Patient Microglia Exhibit Enhanced Aging and Unique Transcriptional Activation.
+|title=[[FSHR]] ablation induces depression-like behaviors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32610143
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32203083
+|abstract=Alteration in reproductive hormones profile is associated with the increasing risk of menopausal depression in women. Serum follicle-stimulating hormone (FSH) level is changed during the menopause transition, while the effect of FSH on menopausal depression has remained undefined. In this study we investigated whether or how FSH affected menopausal depression in postmenopausal (ovariectomized) [[FSHR]] knockout mice (Fshr ). We found that Fshr  mice displayed aggravated depression-like behaviors, accompanied by severe oxidative stress in the whole brain, resulted from significantly reduced glutamate cysteine ligase modifier subunit (GCLm) in glutathione synthesis and glucose-6-phosphate dehydrogenase (G6PD) in NADP/NADPH transition. Importantly, administration of ROS scavenger N-acetyl cysteine (NAC, 150 mg · kg  · d , i.p. for 12 weeks) attenuated the depression-like behaviors of Fshr  mice. Consistent with these in vivo experiment results, we found that pretreatment with FSH (50, 100 ng/mL) dose-dependently increased protein levels of GCLm and G6PD, and decreased the ROS production in N2a mouse neuroblastoma cells. These findings demonstrate that FSH signaling is involved in pathogenesis of menopausal depression, and likely to maintain the redox-optimized ROS balance in neurons.
+|keywords=* FSH
-|keywords=* Alzheimer’s disease
+* ROS
 * aging
-* microglia
+* antioxidants
-* neurodegenerative diseases
+* depression
-* neuroinflammation
+* metabolism
-* transcriptomics
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7468367
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7422733
 }}
+==GAP43==
 {{medline-entry
-|title=Relationships Between Plasma Lipids Species, Gender, Risk Factors, and Alzheimer's Disease.
+|title=HDAC inhibition leads to age-dependent opposite regenerative effect upon PTEN deletion in rubrospinal axons after SCI.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32474467
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32171589
+|abstract=Epigenetic changes associated with aging have been linked to functional and cognitive deficits in the adult CNS. Histone acetylation is involved in the control of the transcription of plasticity and regeneration-associated genes. The intrinsic axon growth capacity in the CNS is negatively regulated by phosphatase and tensin homolog (Pten). Inhibition of Pten is an effective method to stimulate axon growth following an injury to the optic nerve, corticospinal tract (CST), and rubrospinal tract (RST). Our laboratory has previously demonstrated that the deletion of Pten in aged animals diminishes the regenerative capacity in rubrospinal neurons. We hypothesize that changes in the chromatin structure might contribute to this age-associated decline. Here, we assessed whether Trichostatin A (TSA), a histone deacetylases (HDACs) inhibitor, reverses the decline in regeneration in aged Pten  mice. We demonstrate that HDAC inhibition induces changes in the expression of [[GAP43]] in both young and aged Pten  mice. The regenerative capacity of the RST did not improve significantly in young mice, neither their motor function on the horizontal ladder or cylinder test after TSA treatment for 7 days. Interestingly, TSA treatment in the aged mice worsened their motor function deficits, suggesting that the systemic treatment with TSA might have an overall adverse effect on motor recovery after SCI in aged animals.
+|mesh-terms=* Aging
-|keywords=* APOEɛ4
+* Animals
-* Aging
+* Axons
-* Alzheimer’s disease
+* GAP-43 Protein
-* gender
+* Gene Deletion
-* lipid
+* Gene Expression
-species
+* Histone Deacetylase Inhibitors
+* Histone Deacetylases
+* Hydroxamic Acids
+* Mice, Transgenic
+* Motor Activity
+* Nerve Regeneration
+* PTEN Phosphohydrolase
+* Recovery of Function
+* Spinal Cord
+* Spinal Cord Injuries
+|keywords=* Aging
+* Epigenetics
+* Histone deacetylase
+* Pten
+* Regeneration
+* Spinal cord injury
+|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.02.006
+}}
+==GC==
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7369125
-}}
 {{medline-entry
-|title=Effects of sex, age, and apolipoprotein E genotype on hippocampal parenchymal fraction in cognitively normal older adults.
+|title=Physicochemical characterization of a polysaccharide from Agrocybe aegirita and its anti-ageing activity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32416384
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32172871
+|abstract=The aim of the present study is to characterize the structure of a novel natural polysaccharide from Agrocybe aegirita (AAPS) and evaluate its anti-aging activity. The MALLS and [[GC]]-MS analysis indicated that the AAPS with molecular weights of 1.81 × 10  Da was mainly composed by rhamnose, fucose, mannose, and glucose in a molar ratio of 2.90:10.25:3.70:38.27. The FT-IR and NMR analysis showed that the backbone of AAPS was α-L-Rhap-(1→6)-β-D-Glcp-(1→2)-α-L-Fucp-(1→6)-α-D-Glcp-(1→5)-α-L-Araf-(1→4)-β-D-GlcpA-(1→5)-α-L-Araf-(1→6)-α-D-Manp-(1→6)-α-D-Manp-(1→2)-α-L-Fucp-(1→6)-β-D-Glap-(1→2)-α-L-Rhap-(1→6)-β-D-Galp-(1→, which linked with two side chains α-L-Fucp-(1→6)-β-D-Glcp-(1→6)-β-D-Manp-(1→ and α-D-Xylp-(1→2)-α-L-Fucp-(1→5) -α-D-Araf-(1→6)-β-D-Galp-(1→ at O  at H-4-arabinose and the terminal Galp residues, respectively. The MRC-5 cells induced by H O  were used to explore the anti-ageing effect and its underlying mechanism of AAPS. It showed a potent anti-ageing activity, representing by the increased cell viability and β-Gal viability, prevented G1-phase cell-cycle arrest, and decreased mitochondrial membrane potential. The polysaccharides extracted from A. aegirita might be applied in functional food as anti-ageing ingredient.
-|mesh-terms=* Age Factors
+|mesh-terms=* Aging
-* Aged
+* Agrocybe
-* Aged, 80 and over
+* Antioxidants
-* Apolipoproteins E
+* Carbohydrate Sequence
-* Biomarkers
+* Cell Line
-* Cognition
+* Chemical Phenomena
-* Databases, Factual
+* G1 Phase Cell Cycle Checkpoints
-* Female
-* Genotype
-* Hippocampus
 * Humans
-* Linear Models
+* Membrane Potential, Mitochondrial
+* Mitochondria
+* Polysaccharides
+|keywords=* Agrocybe aegirita polysaccharide
+* Anti-ageing
+* Cell cycle
+* Mitochondrial membrane potential
+* Structure
+|full-text-url=https://sci-hub.do/10.1016/j.carbpol.2020.116056
+}}
+{{medline-entry
+|title=Structural characteristics, antioxidant properties and antiaging activities of galactan produced by Mentha haplocalyx Briq.
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32070549
+|abstract=An antioxidant-active polysaccharide (WMP) with a molecular weight of 26.91 kDa was isolated from Mentha haplocalyx Briq by water extraction, ethanol precipitation and gel filtration. According to HPLC, methylation, [[GC]]-MS, and 1D/2D nuclear magnetic resonance spectroscopy, WMP is a heteropolysaccharide composed of Gal (84.2 %), Glc (9.8 %), Man (2.8 %) and Ara (3.2 %) with (1→6)-α-d-Galp and (1→4, 6)-α-d-Galp residues in the backbone and (1→6)-α-d-Galp and (1→6)-α-d-Glcp residues in the branch. The branch point was located at C-4 of (1→4, 6)-α-d-Galp residue with a branching degree of 19.71 %. WMP showed remarkably high scavenging ability for 1, 1-diphenyl-2-picrylhydrazyl (DPPH) and hydroxyl radicals, ferrous ion chelating activity and ferric reducing powder in vitro. In vivo result showed that WMP oral administration substantially increased the activities of antioxidant enzymes, including SOD, GSH-Px and CAT, and decreased MDA levels in the serum and liver of d-Gal-induced aging mice. Therefore, WMP can be an effective natural antioxidant.
+|mesh-terms=* Aging
+* Animals
+* Antioxidants
+* Biphenyl Compounds
+* Carbohydrate Conformation
+* Galactans
 * Male
-* Middle Aged
+* Mentha
-* Neuroimaging
+* Mice
-* Organ Size
+* Mice, Inbred Strains
-* Parenchymal Tissue
+* Particle Size
-* Reference Values
+* Picrates
-* Sex Factors
+* Surface Properties
-|keywords=* Alzheimer’s disease
+|keywords=* Anti-aging activity
-* Apolipoprotein E ϵ4
+* Antioxidant activity
-* Atrophy
+* Mentha haplocalyx Briq
-* Brain
+* Polysaccharides
-* Healthy aging
+|full-text-url=https://sci-hub.do/10.1016/j.carbpol.2020.115936
-* Hippocampal parenchymal fraction
-* Hippocampal volumetric integrity
-* Hippocampus
-* MRI
-* Mild cognitive impairment
-* Neurodegeneration
-* Sex
-|full-text-url=https://sci-hub.do/10.1016/j.pscychresns.2020.111107
 }}
+==GDF11==
 {{medline-entry
-|title=Cognitive Health of Nonagenarians in Southern Italy: A Descriptive Analysis from a Cross-Sectional, Home-Based Pilot Study of Exceptional Longevity (Cilento Initiative on Aging Outcomes Or CIAO).
+|title=Targeted Approach to Distinguish and Determine Absolute Levels of GDF8 and [[GDF11]] in Mouse Serum.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32380778
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32104967
+|abstract=Growth differentiation factor 11 ([[GDF11]]) is a TGF-β superfamily circulating factor that regulates cardiomyocyte size in rodents, sharing 90% amino acid sequence identity in the active domains with myostatin (GDF8)-the major determinant of skeletal muscle mass. Conflicting data on age-related changes in circulating levels have been reported mainly due to the lack of specific detection methods. More recently, liquid chromatography tandem mass spectrometry (LC-MS/MS) based assay showed that the circulating levels of [[GDF11]] do not change significantly throughout human lifespan, but GDF8 levels decrease with aging in men. Here a novel detection method is demonstrated based on parallel reaction monitoring LC-MS/MS assay combined with immunoprecipitation to reliably distinguish [[GDF11]] and GDF8 as well as determine their endogenous levels in mouse serum. The data indicate that both [[GDF11]] and GDF8 circulating levels significantly decline with aging in female mice.
+|keywords=* GDF11
+* aging
+* immunoprecipitation
+* myostatin/GDF8
+* serum
+* targeted-quantitative proteomics
+|full-text-url=https://sci-hub.do/10.1002/pmic.201900104
+}}
+==GFAP==
-|keywords=* Cilento Region
-* cognitive health
-* lifestyle
-* longevity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7279440
-}}
 {{medline-entry
-|title=Apolipoprotein E and Health in Older Men: The Concord Health and Ageing in Men Project.
+|title=Meta-analysis of human prefrontal cortex reveals activation of [[GFAP]] and decline of synaptic transmission in the aging brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32342099
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32138778
+|abstract=Despite ongoing research efforts, mechanisms of brain aging are still enigmatic and need to be elucidated for a better understanding of age-associated cognitive decline. The aim of this study is to investigate aging in the prefrontal cortex region of human brain in a meta-analysis of transcriptome datasets. We analyzed 591 gene expression datasets pertaining to female and male human prefrontal cortex biopsies of distinct ages. We used hierarchical clustering and principal component analysis (PCA) to determine the influence of sex and age on global transcriptome levels. In sex-specific analysis we identified genes correlating with age and differentially expressed between groups of young, middle-aged and aged. Pathways and gene ontologies (GOs) over-represented in the resulting gene sets were calculated. Potential causal relationships between genes and between GOs were explored employing the Granger test of gene expression time series over the range of ages. The most outstanding results were the age-related decline of synaptic transmission and activated expression of glial fibrillary acidic protein ([[GFAP]]) in both sexes. We found an antagonistic relationship between calcium/calmodulin dependent protein kinase IV (CAMK4) and [[GFAP]] which may include regulatory mechanisms involving cAMP responsive element binding protein (CREB) and mitogen-activated protein kinase (MAPK, alias ERK). Common to both sexes was a decline in synaptic transmission, neurogenesis and an increased base-level of inflammatory and immune-related processes. Furthermore, we detected differences in dendritic spine morphogenesis, catecholamine signaling and cellular responses to external stimuli, particularly to metal (Zinc and cadmium) ions which were higher in female brains.
 |keywords=* Aging
-* Alzheimer’s disease
+* Meta-analysis
-* Apolipoprotein E
+* Prefrontal cortex
-* Cognition
+* Sex-specific
-* Cognitive frailty
+* Transcriptome
-* Frailty
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059712
-* Male
-|full-text-url=https://sci-hub.do/10.1093/gerona/glaa105
 }}
+==GHRH==
 {{medline-entry
-|title=CSF amyloid is a consistent predictor of white matter hyperintensities across the disease course from aging to Alzheimer's disease.
+|title=Transcriptomic and metabolomic profiling of long-lived growth hormone releasing hormone knock-out mice: evidence for altered mitochondrial function and amino acid metabolism.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32305782
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32091406
+|abstract=Numerous genetic manipulations that extend lifespan in mice have been discovered over the past two decades, the most robust of which has arguably been the down regulation of growth hormone (GH) signaling. However, while decreased GH signaling has been associated with improved health and lifespan, many of the underlying physiological changes and molecular mechanisms associated with GH signaling have yet to be elucidated. To this end, we have completed the first transcriptomic and metabolomic study on long-lived growth hormone releasing hormone knockout ([[GHRH]]-KO) and wild-type mice in brown adipose tissue (transcriptomics) and blood serum (metabolomics). We find that [[GHRH]]-KO mice have increased transcript levels of mitochondrial and amino acid genes with decreased levels of extracellular matrix genes. Concurrently, mitochondrial metabolites are differentially regulated in [[GHRH]]-KO. Furthermore, we find a strong signal of genotype-by-sex interactions, suggesting the sexes have differing physiological responses to GH deficiency. Overall, our results point towards a strong influence of mitochondrial metabolism in [[GHRH]]-KO mice which potentially is tightly intertwined with their extended lifespan phenotype.
-|mesh-terms=* Aged
+|keywords=* aging
-* Aged, 80 and over
+* growth hormone
-* Aging
+* metabolite
-* Alzheimer Disease
+* mouse
-* Amyloid beta-Peptides
+* transcriptomics
-* Biomarkers
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066919
-* Cerebrovascular Disorders
-* Cognitive Dysfunction
-* Female
-* Humans
-* Magnetic Resonance Imaging
-* Male
-* Peptide Fragments
-* White Matter
-* tau Proteins
-|keywords=* Alzheimer's disease
-* Amyloid
-* Cerebrospinal fluid
-* Tau
-* Vascular disease
-* White matter hyperintensities
-|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.03.008
 }}
+==GREM1==
 {{medline-entry
-|title=Association of Cardiovascular Risk Factors with Cerebral Perfusion in Whites and African Americans.
+|title=[[GREM1]] inhibits osteogenic differentiation, senescence and BMP transcription of adipose-derived stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32310160
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32151168
+|abstract=: Adipose-derived stem cells (ADSCs) are ideal for cell-based therapies to support bone regeneration. It is vital to understand the critical genes and molecular mechanisms involved in the functional regulation of ADSCs for enhancing bone regeneration. In the present study, we investigated the Gremlin 1 ([[GREM1]]) effect on ADSCs osteogenic differentiation and senescence. : The [i]in vitro[/i] ADSCs osteogenic differentiation potential was evaluated by determining alkaline phosphatase (ALP) activity, mineralization ability, and the expression of osteogenic markers. Cell senescence is determined by SA-β-gal staining, telomerase assay, and the expression of aging markers. : [[GREM1]] overexpression in ADSCs reduced ALP activity and mineralization, inhibited the expression of osteogenic related genes [i]OCN, OPN, DSPP, DMP1[/i], and [i]BSP[/i], and key transcription factors, [i]RUNX2[/i] and [i]OSX[/i]. [[GREM1]] knockdown in ADSCs enhanced ALP activity and mineralization, promoted the expression of [i]OCN, OPN, DSPP, DMP1, BSP, RUNX2[/i], and [i]OSX[/i]. [[GREM1]] overexpression in ADSCs reduced the percent SA-β-Gal positive cells, [i]P16[/i] and [i]P53[/i] expressions, and increased telomerase activity. [[GREM1]] knockdown in ADSCs increased the percentage of SA-β-Gal positive cells, [i]P16[/i] and [i]P53[/i] expressions, and reduced telomerase activity. Furthermore, [[GREM1]] reduced the mRNA expression levels of BMP2, BMP6, and BMP7. : In summary, our findings suggested that [[GREM1]] inhibited ADSCs senescence and osteogenic differentiation and antagonized BMP transcription.
+|keywords=* BMP
+* GREM1
+* adipose-derived stem cells (ADSCs)
+* osteogenic differentiation
+* senescence
+|full-text-url=https://sci-hub.do/10.1080/03008207.2020.1736054
+}}
+==GRID1==
-|keywords=* Aging
+{{medline-entry
-* Alzheimer’s disease
+|title=Gene discovery for high-density lipoprotein cholesterol level change over time in prospective family studies.
-* blood pressure
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109663
-* cerebrovascular circulation
+|abstract=Several genes are known to contribute to the levels and metabolism of HDL-C, however, their protective effects in cardiovascular disease (CVD), healthy aging, and longevity are complex and poorly understood. It is also unclear if these genes predict longitudinal HDL-C change. We aimed to identify loci influencing HDL-C change. We performed a genome-wide association study (GWAS) with harmonized HDL-C and imputed genotype in three family-based studies recruited for exceptional survival (Long Life Family Study), from community-based (Framingham Heart Study) and enriched for CVD (Family Heart Study). In 7738 individuals with at least 2 visits, we employed a growth curve model to estimate the random linear trajectory parameter of age-sex-adjusted HDL-C for each person. GWAS was performed using a linear regression model on HDL-C change accounting for kinship correlations, population structure, and differences among studies. We identified a novel association for HDL-C with [[GRID1]] (p = 5.43 × 10 ), which encodes a glutamate receptor channel subunit involved in synaptic plasticity. Seven suggestive novel loci (p < 1.0 × 10 ; MBOAT2, LINC01876-NR4A2, NTNG2, CYSLTR2, SYNE2, CTXND1-LINC01314, and CYYR1) and a known lipid gene (ABCA10) showed associations with HDL-C change. Two additional sex-specific suggestive loci were identified in women (DCLK2 and KCNJ2). Several of these genetic variants are associated with lipid-related conditions influencing cardiovascular and metabolic health, have predictive regulatory function, and are involved in lipid-related pathways. Modeling longitudinal HDL-C in prospective studies, with differences in healthy aging, longevity and CVD risk, contributed to gene discovery and provided insights into mechanisms of HDL-C regulation.
-* neuroimaging
-* obesity
+|keywords=* GWAS
-|full-text-url=https://sci-hub.do/10.3233/JAD-190360
+* HDL-C metabolism
+* Healthy aging
+* Longevity
+* Longitudinal HDL-C change
+|full-text-url=https://sci-hub.do/10.1016/j.atherosclerosis.2020.02.005
 }}
+==GRK2==
 {{medline-entry
-|title=Alzheimer's Risk Factors Age, [[APOE]] Genotype, and Sex Drive Distinct Molecular Pathways.
+|title=Loss of dynamic regulation of G protein-coupled receptor kinase 2 by nitric oxide leads to cardiovascular dysfunction with aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32199103
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32216616
+|abstract=Nitric oxide (NO) and [i]S[/i]-nitrosothiol (SNO) are considered cardio- and vasoprotective substances. We now understand that one mechanism in which NO/SNOs provide cardiovascular protection is through their direct inhibition of cardiac G protein-coupled receptor (GPCR) kinase 2 ([[GRK2]]) activity via [i]S[/i]-nitrosylation of [[GRK2]] at cysteine 340 (C340). This maintains GPCR homeostasis, including β-adrenergic receptors, through curbing receptor [[GRK2]]-mediated desensitization. Previously, we have developed a knockin mouse ([[GRK2]]-C340S) where endogenous [[GRK2]] is resistant to dynamic [i]S[/i]-nitrosylation, which led to increased [[GRK2]] desensitizing activity. This unchecked regulation of cardiac [[GRK2]] activity resulted in significantly more myocardial damage after ischemic injury that was resistant to NO-mediated cardioprotection. Although young adult [[GRK2]]-C340S mice show no overt phenotype, we now report that as these mice age, they develop significant cardiovascular dysfunction due to the loss of SNO-mediated [[GRK2]] regulation. This pathological phenotype is apparent as early as 12 mo of age and includes reduced cardiac function, increased cardiac perivascular fibrosis, and maladaptive cardiac hypertrophy, which are common maladies found in patients with cardiovascular disease (CVD). There are also vascular reactivity and aortic abnormalities present in these mice. Therefore, our data demonstrate that a chronic and global increase in [[GRK2]] activity is sufficient to cause cardiovascular remodeling and dysfunction, likely due to [[GRK2]]'s desensitizing effects in several tissues. Because [[GRK2]] levels have been reported to be elevated in elderly CVD patients, [[GRK2]]-C340 mice can give insight into the aged-molecular landscape leading to CVD.  Research on G protein-coupled receptor kinase 2 ([[GRK2]]) in the setting of cardiovascular aging is largely unknown despite its strong established functions in cardiovascular physiology and pathophysiology. This study uses a mouse model of chronic [[GRK2]] overactivity to further investigate the consequences of long-term [[GRK2]] on cardiac function and structure. We report for the first time that chronic [[GRK2]] overactivity was able to cause cardiac dysfunction and remodeling independent of surgical intervention, highlighting the importance of GRK activity in aged-related heart disease.
-|mesh-terms=* Adaptor Proteins, Signal Transducing
+|mesh-terms=* Aging
-* Age Factors
-* Aging
-* Alzheimer Disease
 * Animals
-* Apolipoprotein E2
-* Apolipoprotein E3
-* Apolipoprotein E4
-* Apolipoproteins E
-* Brain
 * Female
-* Gene Expression
+* G Protein-Coupled Inwardly-Rectifying Potassium Channels
-* Gene Expression Profiling
+* Heart
-* Gene Regulatory Networks
+* Heart Diseases
-* Genotype
+* Homeostasis
-* Humans
 * Male
-* Membrane Glycoproteins
-* Membrane Proteins
-* Metabolome
 * Mice
-* Mice, Transgenic
+* Mutation
-* Protective Factors
+* Myocardium
-* Receptors, Immunologic
+* Nitric Oxide
-* Risk Factors
+|keywords=* S-nitrosylation
-* Serpins
+* cardiac hypertrophy
-* Sex Factors
+* heart disease
-* Unfolded Protein Response
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7346533
-|keywords=* APOE
-* Alzheimer’s disease
-* Serpina3
-* age
-* extracellular vesicles
-* inflammation
-* lipid metabolism
-* metabolomics
-* sex
-* transcriptomics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388065
 }}
+==GRM3==
 {{medline-entry
-|title=Less agreeable, better preserved? A PET amyloid and MRI study in a community-based cohort.
+|title=Profiling gene expression in the human dentate gyrus granule cell layer reveals insights into schizophrenia and its genetic risk.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32169357
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32203495
+|abstract=Specific cell populations may have unique contributions to schizophrenia but may be missed in studies of homogenate tissue. Here laser capture microdissection followed by RNA sequencing (LCM-seq) was used to transcriptomically profile the granule cell layer of the dentate gyrus (DG-GCL) in human hippocampus and contrast these data to those obtained from bulk hippocampal homogenate. We identified widespread cell-type-enriched aging and genetic effects in the DG-GCL that were either absent or directionally discordant in bulk hippocampus data. Of the ~9 million expression quantitative trait loci identified in the DG-GCL, 15% were not detected in bulk hippocampus, including 15 schizophrenia risk variants. We created transcriptome-wide association study genetic weights from the DG-GCL, which identified many schizophrenia-associated genetic signals not found in transcriptome-wide association studies from bulk hippocampus, including [[GRM3]] and CACNA1C. These results highlight the improved biological resolution provided by targeted sampling strategies like LCM and complement homogenate and single-nucleus approaches in human brain.
-|mesh-terms=* Aged
+|mesh-terms=* Adolescent
+* Adult
+* Aged
 * Aged, 80 and over
-* Amyloidogenic Proteins
+* Aging
-* Apolipoproteins E
+* Bipolar Disorder
-* Brain
+* Dentate Gyrus
-* Cognition
+* Depressive Disorder, Major
-* Cohort Studies
 * Female
-* Follow-Up Studies
+* Gene Expression Profiling
+* Genetic Predisposition to Disease
+* Genome-Wide Association Study
 * Humans
-* Magnetic Resonance Imaging
 * Male
-* Neuroimaging
+* Middle Aged
-* Organ Size
+* Neurons
-* Personality
+* Quantitative Trait Loci
-* Positron-Emission Tomography
+* Schizophrenia
-|keywords=* Amyloid load
+* Transcriptome
-* Cognitive aging
+* Young Adult
-* Cohort studies
+|keywords=#f
-* Personality
+|full-text-url=https://sci-hub.do/10.1038/s41593-020-0604-z
-* Structural MRI
-|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.02.004
 }}
+==GUK1==
 {{medline-entry
-|title=Physical Activity as Moderator of the Association Between [[APOE]] and Cognitive Decline in Older Adults: Results from Three Longitudinal Cohort Studies.
+|title=Characterization of the impact of GMP/GDP synthesis inhibition on replicative lifespan extension in yeast.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32110803
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32232569
+|abstract=Slowing down aging-associated accumulation of molecular damage or its prevention represents a promising therapeutic paradigm to combat aging-related disease and death. While several chemical compounds extend lifespan in model organisms, their mechanism of action is often unknown, reducing their therapeutic potential. Using a systematic approach, here we characterize the impact of the GMP pathway on yeast lifespan and elucidate GMP synthesis inhibition as a lifespan extension mechanism. We further discover that proteasome activation extends lifespan in part through the GMP pathway. GMP synthesis inhibition exerts its lifespan extension effect independently of the canonical nutrient-sensing pathway regulating lifespan. Exposing longitudinally aging yeast cells to GMP pathway inhibition in an age-dependent manner, we demonstrate that the lifespan extension is facilitated by slowing, rather than reversing, the aging process in cells. Using a [[GUK1]] mutant with lower GMP-to-GDP conversion activity, we observe lifespan extension, suggesting that reduced GDP level by itself can also extend yeast lifespan. These findings elucidate the involvement of nucleotide metabolism in the aging process. The existence of clinically-approved GMP pathway inhibitors elicits the potential of a new class of therapeutics for aging-related disorders.
+|keywords=* Aging
+* GDP
+* GMP
+* Mycophenolic acid
+* Proteasome
+* Replicative lifespan
+* Yeast
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7367712
+}}
+==H2AX==
-|keywords=* Gene–environment interaction
-* InCHIANTI
-* Longitudinal Aging Study Amsterdam
-* Rotterdam Study
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7518558
-}}
 {{medline-entry
-|title=Longitudinal Maintenance of Cognitive Health in Centenarians in the 100-plus Study.
+|title=Guanine Deaminase Stimulates Ultraviolet-induced Keratinocyte Senescence in Seborrhoeic Keratosis via Guanine Metabolites.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32101309
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32215662
+|abstract=DNA damage and oxidative stress play a critical role in photoageing. Seborrhoeic keratosis (SK) affects sunlight-exposed sites in aged individuals. This study examined the mechanism of photoageing in SK. The guanine deaminase gene, which is involved in purine metabolism, was upregulated with uric acid levels and p21 in SK. Guanine deaminase was detectable in keratinocytes. Repeated exposure to ultraviolet (UV) increased levels of guanine deaminase, together with DNA damage, such as γ-[[H2AX]] and cyclobutane pyrimidine dimer formation, generation of reactive oxygen species, and keratinocyte senescence, which were reversed by guanine deaminase knockdown. However, guanine deaminase overexpression and H2O2 formed γ-[[H2AX]], but not cyclobutane pyrimidine dimer. Loss-of-function guanine deaminase mutants reduced the metabolic end-product uric acid, which was increased by exposure to exogenous xanthine. Repeated exposure to UV increased levels of uric acid. Exogenous uric acid increased cellular senescence, reactive oxygen species, and γ-[[H2AX]], similar to guanine deaminase. Overall, guanine deaminase upregulation increased UV-induced keratinocyte senescence in SK, via uric acid mediated by reactive oxygen species followed by DNA damage.
-|mesh-terms=* Aged, 80 and over
+|keywords=*  DNA damage
-* Aging
+*  UV-induced keratinocyte senescence
-* Apolipoprotein E4
+*  guanine deaminase
-* Cognition
+*  reactive oxygen species
-* Female
+*  uric acid
-* Humans
+* seborrhoeic keratosis
-* Longitudinal Studies
+|full-text-url=https://sci-hub.do/10.2340/00015555-3473
-* Male
+}}
-* Mental Status and Dementia Tests
+==HCN1==
-* Prospective Studies
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7137688
-}}
 {{medline-entry
-|title=Interaction of [[APOE]], cerebral blood flow, and cortical thickness in the entorhinal cortex predicts memory decline.
+|title=Protein expression changes of [[HCN1]] and HCN2 in hippocampal subregions of gerbils during the normal aging process.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32048144
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32128096
+|abstract=Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels play essential roles in various hippocampal functions, including regulation of long-term potentiation, synaptic plasticity, and hippocampal-dependent cognitive process. The objective of this study was to investigate age-related changes in [[HCN1]] and HCN2 protein expressions in gerbil hippocampus at various ages. In this study, the protein expressions of [[HCN1]] and HCN2 were compared in the hippocampus at the ages of 1, 3, 12, and 24 months using Western blot analysis and immunohistochemistry. Immunoreactivity of both [[HCN1]] and HCN2 was shown primarily in cells of the pyramidal cell layer in the hippocampus proper and in cells of the granule cell layer in the dentate gyrus. [[HCN1]] and HCN2 protein expression levels and immunoreactivity were significantly increased at three months (3 M) of age compared with those at 1 M of age. After that, both [[HCN1]] and HCN2 expression levels in the hippocampus were gradually decreased with age. Our results show that the normal aging process affects the expression levels of [[HCN1]] and HCN2 in hippocampal cells in gerbils. There are marked reductions in [[HCN1]] and HCN2 expressions in the aged hippocampus compared to the young hippocampus. Such reductions might be related to aging in the hippocampus.
+|keywords=* Aging
+* Dentate gyrus
+* Granule cells
+* HCN channel
+* Hippocampus proper
+* Pyramidal cells
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7038419
+}}
+==HDC==
-|keywords=* APOE ε4
-* Aging
-* Cerebral blood flow
-* Cognitive decline
-* Cortical thickness
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7165062
-}}
 {{medline-entry
-|title=Determinants of mesial temporal lobe volume loss in older individuals with preserved cognition: a longitudinal PET amyloid study.
+|title=Induced pluripotency and spontaneous reversal of cellular aging in supercentenarian donor cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32057528
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115145
+|abstract=Supercentenarians (≥110-year-old, SC) are a uniquely informative population not only because they surpass centenarians in age, but because they appear to age more slowly with fewer incidences of chronic age-related disease than centenarians. We reprogramed donor B-lymphoblastoid cell lines (LCL) derived from a 114-year-old (SC), a 43-year-old healthy disease-free control ([[HDC]]) and an 8-year-old with a rapid aging disease (Hutchinson-Gilford progeria syndrome (HGPS)) and compared SC-iPSC to [[HDC]]-iPSC and HGPS-iPSCs. Reprogramming to pluripotency was confirmed by pluripotency marker expression and differentiation to 3 germ-layers. Each iPSC clone differentiated efficiently to mesenchymal progenitor cells (MPC) as determined by surface marker expression and RNAseq analysis. We identified supercentenarian and HGPS associated gene expression patterns in the differentiated MPC lines that were not evident in the parental iPSC lines. Importantly, telomere length resetting occurred in iPSC from all donors albeit at a lower incidence in supercentenarian iPSCs. These data indicate the potential to use reprogramming to reset both developmental state and cellular age in the "oldest of the old." We anticipate that supercentenarian iPSC and their differentiated derivatives will be valuable tools for studying the underlying mechanisms of extreme longevity and disease resistance.
-|mesh-terms=* Aged
+|mesh-terms=* Adult
 * Aged, 80 and over
-* Aging
+* Cell Differentiation
-* Alleles
+* Cell Line
-* Amyloidogenic Proteins
+* Cellular Reprogramming
-* Apolipoprotein E4
+* Cellular Senescence
-* Cognitive Reserve
+* Child
-* Female
+* Clone Cells
-* Follow-Up Studies
+* Gene Expression Regulation
-* Genotype
 * Humans
-* Longitudinal Studies
+* Induced Pluripotent Stem Cells
-* Male
+* Mesenchymal Stem Cells
-* Neuropsychological Tests
+* Telomere Homeostasis
-* Organ Size
+* Tissue Donors
-* Positron-Emission Tomography
+* Transcriptome
-* Sex Factors
+|keywords=* Aging
-* Temporal Lobe
+* Longevity
-|keywords=* APOE
+* Reprogramming
-* Amyloid load
+* Supercentenarian
-* Cognitive changes
+* Telomere
-* Mesial temporal lobe
+* iPSC
-* Normal aging
+|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2020.02.092
-* Structural MRI
-|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2019.12.002
 }}
+==HGF==
 {{medline-entry
-|title=Long-term exposure to ambient air pollution, [[APOE]]-ε4 status, and cognitive decline in a cohort of older adults in northern Manhattan.
+|title=Phenytoin sodium-ameliorated gingival fibroblast aging is associated with autophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31926436
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32281104
+|abstract=Human gingival fibrolasts aging is an important cause of periodontal disease. Phenytoin sodium (phenytoin) has a side effect of gingival hyperplasia and an effect on the autophagy progress. This study investigated whether the effect of phenytoin on aging gingival fibroblast is related to the autophagy pathway. The aging model of gingival fibroblast cell line [[HGF]]-1 was induced by hydrogen peroxide (H  O  ), and the treatment of phenytoin and 3-methyladenine (3-MA) was performed simultaneously. Cell viability, cell cycle, and intracellular calcium ion were measured by flow cytometry. Changes in expression of basic fibroblast growth factor (bFGF), P16  , P21  , and bFGF, P16  , P21  , LC3II, p62, and Beclin were tested by using reverse transcription polymerase chain reaction, western blot, and immunofluorescence staining. The results showed that aging [[HGF]]-1 proliferation was inhibited by H  O  , gene, protein expression of bFGF, P16  , and P21  were decreased, autophagy-related proteins LC3II, p62, and Becline were decreased, and the proportion of G0/G1 phase and intracellular calcium ion of cell cycle was increased. Phenytoin treatment could recovery above changes, but the effect of phenytoin could be blocked by 3-MA. We propose that phenytoin alleviates the aging of gingival fibroblasts induced by H  O  . This condition is related to the enhancement of autophagy pathway.
-|mesh-terms=* Aged
+|keywords=* aging
-* Air Pollutants
+* autophagy
-* Air Pollution
+* gingival fibroblast
-* Apolipoprotein E4
+* phenytoin sodium
-* Apolipoproteins E
+|full-text-url=https://sci-hub.do/10.1111/jre.12750
-* Cognitive Dysfunction
-* Female
-* Genotype
-* Humans
-* Male
-* Prospective Studies
-* Washington
-|keywords=* APOE-ε4 allele
-* Aging
-* Air pollution
-* Cognitive decline
-* Cognitive risk factors
-* Epidemiology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7024003
 }}
 {{medline-entry
-|title=Evidence in support of chromosomal sex influencing plasma based metabolome vs [[APOE]] genotype influencing brain metabolome profile in humanized [[APOE]] male and female mice.
+|title=Impaired integrin α  /β  -mediated hepatocyte growth factor release by stellate cells of the aged liver.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31917799
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32157808
+|abstract=Hepatic blood flow and sinusoidal endothelial fenestration decrease during aging. Consequently, fluid mechanical forces are reduced in the space of Disse where hepatic stellate cells (HSC) have their niche. We provide evidence that integrin α  /β  is an important mechanosensor in HSC involved in shear stress-induced release of hepatocyte growth factor ([[HGF]]), an essential inductor of liver regeneration which is impaired during aging. The expression of the integrin subunits α  and β  decreases in liver and HSC from aged rats. CRISPR/Cas9-mediated integrin α  and β  knockouts in isolated HSC lead to lowered [[HGF]] release and impaired cellular adhesion. Fluid mechanical forces increase integrin α  and laminin gene expression whereas integrin β  remains unaffected. In the aged liver, laminin β2 and γ1 protein chains as components of laminin-521 are lowered. The integrin α  knockout in HSC reduces laminin expression via mechanosensory mechanisms. Culture of HSC on nanostructured surfaces functionalized with laminin-521 enhances Hgf expression in HSC, demonstrating that these ECM proteins are critically involved in HSC function. During aging, HSC acquire a senescence-associated secretory phenotype and lower their growth factor expression essential for tissue repair. Our findings suggest that impaired mechanosensing via integrin α  /β  in HSC contributes to age-related reduction of ECM and [[HGF]] release that could affect liver regeneration.
-|mesh-terms=* Age of Onset
+|keywords=* aging
-* Aging
+* hepatic stellate cells
-* Alzheimer Disease
+* integrins
-* Amyloid beta-Peptides
+* laminins
-* Animals
+* mechanobiology
-* Apolipoprotein E4
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189994
-* Apolipoproteins E
+}}
-* Brain
+==HMGA2==
-* Disease Models, Animal
-* Female
-* Genotype
-* Humans
-* Magnetic Resonance Imaging
-* Male
-* Metabolome
-* Mice
-* Mice, Transgenic
-* Sex Characteristics
-* Sex Chromosomes
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6952084
-}}
 {{medline-entry
-|title=[[APOE]] region molecular signatures of Alzheimer's disease across races/ethnicities.
+|title=4D Genome Rewiring during Oncogene-Induced and Replicative Senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31813627
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32220303
+|abstract=To understand the role of the extensive senescence-associated 3D genome reorganization, we generated genome-wide chromatin interaction maps, epigenome, replication-timing, whole-genome bisulfite sequencing, and gene expression profiles from cells entering replicative senescence (RS) or upon oncogene-induced senescence (OIS). We identify senescence-associated heterochromatin domains (SAHDs). Differential intra- versus inter-SAHD interactions lead to the formation of senescence-associated heterochromatin foci (SAHFs) in OIS but not in RS. This OIS-specific configuration brings active genes located in genomic regions adjacent to SAHDs in close spatial proximity and favors their expression. We also identify DNMT1 as a factor that induces SAHFs by promoting [[HMGA2]] expression. Upon DNMT1 depletion, OIS cells transition to a 3D genome conformation akin to that of cells in replicative senescence. These data show how multi-omics and imaging can identify critical features of RS and OIS and discover determinants of acute senescence and SAHF formation.
-|mesh-terms=* Alleles
+|mesh-terms=* Cells, Cultured
-* Alzheimer Disease
+* Cellular Senescence
-* Apolipoproteins E
+* Chromatin Assembly and Disassembly
-* Continental Population Groups
+* DNA (Cytosine-5-)-Methyltransferase 1
-* Haplotypes
+* DNA Methylation
-* Heterozygote
+* Fibroblasts
-* Homozygote
+* Genome, Human
+* Heterochromatin
 * Humans
-* Linkage Disequilibrium
+* In Situ Hybridization, Fluorescence
-* Polymorphism, Single Nucleotide
+* Oncogenes
-* Risk Factors
+|keywords=* 3D genome architecture
-|keywords=* APOE polymorphism
+* DNMT1
-* Aging
+* Hi-C
-* Alzheimer's disease
+* chromatin compartments
-* Health span
+* gene regulation
-* Life span
+* oncogene-induced senescence
-* Neurodegenerative disorders
+* replicative senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064423
+* senescence
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7208559
 }}
 {{medline-entry
-|title=Varying Effects of [[APOE]] Alleles on Extreme Longevity in European Ethnicities.
+|title=The protective effects of [[HMGA2]] in the senescence process of bone marrow-derived mesenchymal stromal cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31724059
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32068957
+|abstract=Bone marrow-derived mesenchymal stromal cells (MSCs) have been wildly applied to cell-based strategies for tissue engineering and regenerative medicine; however, they have to undergo the senescence process and thus appeared to be less therapeutic effective. [[HMGA2]], a protein belonged to high mobility group A (HMGA) family, exhibits an inverse expression level related to embryonic development and acts as a developmental regulator in stem cell self-renewal progression. Therefore, we performed senescence-associated β-galactosidase (SA-β-gal) staining, transwell assay, to examine the changes of MSCs in different stages and then over-expressed [[HMGA2]] in MSCs by lentivirus transfection. We found the percentage of SA-β-gal staining positive cells in MSCs from 24-month-old Sprague-Dawley (SD) rats (O-MSCs) was significantly higher compared with MSCs from 2-week-old SD rats (Y-MSCs), and the expression levels of P21 and P53, two senescence-related molecules, were also significantly up-regulated in O-MSCs than in Y-MSCs. In contrast, the [[HMGA2]] expression level in O-MSCs was dramatically down-regulated in contrast to Y-MSCs. In additional, the migration ability in O-MSCs was significantly attenuated than in Y-MSCs. After successfully over-expressed [[HMGA2]] in O-MSCs, the percentage of SA-β-gal staining positive cells and the expression levels of P21 and P53 were reduced, and the migration ability was improved compared with O-MSCs without treatment. Further, mRNA sequencing analysis revealed that overexpression of [[HMGA2]] changed the expression of genes related to cell proliferation and senescence, such as Lyz2, Pf4, Rgs2, and Mstn. Knockdown of Rgs2 in [[HMGA2]] overexpression O-MSCs could antagonize the protective effect of [[HMGA2]] in the senescence process of O-MSCs.
-|mesh-terms=* Aged, 80 and over
+|keywords=* bone marrow derived mesenchymal stromal cells (MSCs)
-* Alleles
+* high-mobility group AT-hook 2 (HMGA2)
-* Apolipoproteins E
+* regulator of G protein signaling 2 (Rgs2)
-* Ethnic Groups
+* senescence
-* Europe
+|full-text-url=https://sci-hub.do/10.1002/term.3023
-* European Continental Ancestry Group
-* Female
-* Humans
-* Longevity
-* Male
-|keywords=* APOE
-* Bioinformatics
-* Human genetics
-* Longevity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7330482
 }}
+==HP==
 {{medline-entry
-|title=Prospective Evaluation of Cognitive Health and Related Factors in Elderly at Risk for Developing Alzheimer's Dementia: A Longitudinal Cohort Study.
+|title=Beta Human Papillomavirus 8E6 Attenuates LATS Phosphorylation after Failed Cytokinesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31686098
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32238586
+|abstract=Beta genus human papillomaviruses (β-[[HP]]Vs) cause cutaneous squamous cell carcinomas (cSCCs) in a subset of immunocompromised patients. However, β-[[HP]]Vs are not necessary for tumor maintenance in the general population. Instead, they may destabilize the genome in the early stages of cancer development. Supporting this idea, β-[[HP]]V's 8E6 protein attenuates p53 accumulation after failed cytokinesis. This paper offers mechanistic insight into how β-[[HP]]V E6 causes this change in cell signaling. An [i]in silico[/i] screen and characterization of HCT 116 cells lacking p300 suggested that the histone acetyltransferase is a negative regulator of Hippo pathway ([[HP]]) gene expression. [[HP]] activation restricts growth in response to stimuli, including failed cytokinesis. Loss of p300 resulted in increased [[HP]] gene expression, including proproliferative genes associated with [[HP]] inactivation. β-[[HP]]V 8E6 expression recapitulates some of these phenotypes. We used a chemical inhibitor of cytokinesis (dihydrocytochalasin B [H2CB]) to induce failed cytokinesis. This system allowed us to show that β-[[HP]]V 8E6 reduced activation of large tumor suppressor kinase (LATS), an [[HP]] kinase. LATS is required for p53 accumulation following failed cytokinesis. These phenotypes were dependent on β-[[HP]]V 8E6 destabilizing p300 and did not completely attenuate the [[HP]]. It did not alter H2CB-induced nuclear exclusion of the transcription factor YAP. β-[[HP]]V 8E6 also did not decrease [[HP]] activation in cells grown to a high density. Although our group and others have previously described inhibition of DNA repair, to the best of our knowledge, this marks the first time that a β-[[HP]]V E6 protein has been shown to hinder [[HP]] signaling.  β-[[HP]]Vs contribute to cSCC development in immunocompromised populations. However, it is unclear if these common cutaneous viruses are tumorigenic in the general population. Thus, a more thorough investigation of β-[[HP]]V biology is warranted. If β-[[HP]]V infections do promote cSCCs, they are hypothesized to destabilize the cellular genome. [i]In vitro[/i] data support this idea by demonstrating the ability of the β-[[HP]]V E6 protein to disrupt DNA repair signaling events following UV exposure. We show that β-[[HP]]V E6 more broadly impairs cellular signaling, indicating that the viral protein dysregulates the [[HP]]. The [[HP]] protects genome fidelity by regulating cell growth and apoptosis in response to a myriad of deleterious stimuli, including failed cytokinesis. After failed cytokinesis, β-[[HP]]V 8E6 attenuates phosphorylation of the [[HP]] kinase (LATS). This decreases some, but not all, [[HP]] signaling events. Notably, β-[[HP]]V 8E6 does not limit senescence associated with failed cytokinesis.
-|mesh-terms=* Aged
+|mesh-terms=* Apoptosis
-* Aged, 80 and over
+* Cell Cycle Proteins
-* Alzheimer Disease
+* Cell Line, Tumor
-* Anxiety
+* Cell Proliferation
-* Apolipoprotein E4
+* Cell Survival
-* Cognition
+* Cytochalasin B
-* Cognitive Dysfunction
+* Cytokinesis
-* Cohort Studies
+* DNA Repair
-* Depression
+* E1A-Associated p300 Protein
-* Efficiency
+* Gene Expression Regulation
-* Female
+* HCT116 Cells
-* Healthy Volunteers
+* Host-Pathogen Interactions
 * Humans
-* Longitudinal Studies
+* Keratinocytes
-* Male
+* Oncogene Proteins, Viral
-* Mental Status and Dementia Tests
+* Osteoblasts
-* Middle Aged
+* Papillomaviridae
-* Neuropsychological Tests
+* Phenotype
-* Prospective Studies
+* Phosphorylation
-* Risk Factors
+* Primary Cell Culture
-* Sleep
+* Protein-Serine-Threonine Kinases
-* United Kingdom
+* Signal Transduction
-* Work
+* Transcription Factors
-|keywords=* Alzheimer Disease
+* Tumor Suppressor Protein p53
-* CHARIOT
+|keywords=* Hippo signaling pathway
-* aging registry
+* apoptosis
-* cognitive health
+* cancer
-* pre-clinical
+* cytokinesis
-|full-text-url=https://sci-hub.do/10.14283/jpad.2019.31
+* human papillomavirus
+* senescence
+* skin cancer
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7307087
 }}
+==HPSE==
 {{medline-entry
-|title=Association of Cardiovascular and Alzheimer's Disease Risk Factors with Intracranial Arterial Blood Flow in Whites and African Americans.
+|title=Distribution of heparan sulfate correlated with the expression of heparanase-1 and matrix metalloproteinase-9 in an ovariectomized rats skin.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31658057
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32159248
+|abstract=There are few studies on heparan sulfate (HS) in the skin, during aging, when estrogen is suppressed. The enzyme heparanase-1 ([[HPSE]]-1), has its 17β-estrogen-regulated expression in pathological conditions such as cancer and chronic inflammatory diseases. [[HPSE]]-1 is correlated with the matrix metalloproteinase-9 (MMP-9), an endopeptidase that also undergoes estrogen action. We investigated the distribution of HS, expression [[HPSE]]-1 and MMP-9 in the skin of adult rats at different ages and in the age-matched ovariectomized rats to evaluate the influence of low estrogen on the distribution of HS. Thirty female Wistar rats were used. Rats underwent to a sham surgery (ctr, n = 15) or to a bilateral ovariectomy (ovx, n = 15) and were euthanized after 45, 75, and 90 days after ovariectomy. Morphological, morphometric, biochemical, and reverse transcriptase polymerase chain reaction (RT-PCR) methodologies were used. A significant decrease (P < 0.001) in total skin thickness was observed in the ctr and ovx animals, being higher in the older animals. The thickness of the epidermis and dermis decreased; however, the proportion in the total skin remained similar comparing ctr and ovx. An increase of HS with increasing age and ovariectomy was observed. The expression of the [[HPSE]]-1 and MMP-9 enzymes decreased, being higher in old animals. A correlation between the increase of HS and the decrease of the [[HPSE]]-1 was demonstrated in both groups. Overall, these data suggested that estrogen acts in the regulation of the expression of the [[HPSE]]-1, not only in pathological states, as already established, but also in aging.
-|mesh-terms=* African Americans
+|keywords=* aging
-* Aged
+* estrogen
-* Alzheimer Disease
+* extracellular matrix
-* Biomarkers
+* heparan sulfate
-* Blood Flow Velocity
+* heparanase-1
-* Cardiovascular Diseases
+* matrix metalloproteinase-9
-* Cerebrovascular Circulation
+|full-text-url=https://sci-hub.do/10.1002/cbin.11339
-* European Continental Ancestry Group
-* Female
-* Humans
-* Male
-* Middle Aged
-* Risk Factors
-|keywords=* African Americans
-* Alzheimer’s disease
-* Apolipoprotein E4
-* aging
-* cerebrovascular circulation
-* glucose
-* metabolic syndrome
-* neuroimaging
-* risk factors
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7081660
 }}
+==HR==
 {{medline-entry
-|title=Is Ongoing Anticholinergic Burden Associated With Greater Cognitive Decline and Dementia Severity in Mild to Moderate Alzheimer's Disease?
+|title=Physical activity trajectories, mortality, hospitalization, and disability in the Toledo Study of Healthy Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31613323
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32163233
+|abstract=Physical activity (PA) is a recognized contributor to healthy aging. However, the majority of studies exploring its associations with adverse outcomes in cohorts of older adults use single-time PA estimates, which do not consider its dynamic nature. The aim of the present study is to explore the presence of different PA trajectories in the Toledo Study of Healthy Aging and their association with adverse outcomes. Our hypothesis is that prospectively maintaining or increasing PA is associated with a reduced risk of adverse outcomes. We used data from 1679 participants enrolled in the Toledo Study of Healthy Aging. Trajectories based on the Physical Activity Scale for the Elderly were identified using group-based trajectory modelling. Cox and logistic regression were used to investigate associations between PA trajectories and mortality and hospitalization, and incident and worsening disability, respectively. Mortality was ascertained by linkage to the Spanish National Death Index; disability was evaluated through the Katz Index; and hospitalization was defined as the first admission to Toledo Hospital. Models were adjusted by age, sex, smoking, Charlson Index, education, cognitive impairment, polypharmacy, and Katz Index at Wave 2. We found four PA-decreasing and one PA-increasing trajectories: high PA-consistent (n = 566), moderate PA-mildly decreasing (n = 392), low PA-increasing (n = 237), moderate PA-consistent (n = 191), and low PA-decreasing (n = 293). Belonging to the high PA-consistent trajectory group was associated with reduced risks of mortality as compared with the low PA-decreasing group [hazard ratio ([[HR]]) 1.68; 95% confidence interval (CI) = 1.21-2.31] and hospitalization compared with the low PA-increasing and low PA-decreasing trajectory groups ([[HR]] 1.24; 95% CI = 1.004-1.54 and [[HR]] 1.25; 95% CI = 1.01-1.55, respectively) and with lower rates of incident [odds ratio (OR) 3.14; 95% CI = 1.59-6.19] and worsening disability (OR 2.16; 95% CI = 1.35-3.45) in relation to the low PA-decreasing trajectory group and at follow-up. Increasing PA during late life (low PA-increasing group) was associated with lower incident disability rates (OR 0.38; 95% CI = 0.19-0.82) compared with decreasing PA (low PA-decreasing group), despite similar baseline PA. Our results suggest that sustaining higher PA levels during aging might lead to healthy aging, characterized by a reduction in adverse outcomes. Our study supports the need for enhancing PA participation among older populations, with the goal of reducing personal and economic burden in a worldwide aging population.
-|keywords=* Alzheimers
+|keywords=* Adverse outcomes
-* Cognitive aging
+* Healthy aging
-* Drug related
+* Mortality
-* Medication
+* Older adults
-|full-text-url=https://sci-hub.do/10.1093/gerona/glz244
+* Physical activity
+* Trajectories
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432572
 }}
 {{medline-entry
-|title=Multicenter Alzheimer's and Parkinson's disease immune biomarker verification study.
+|title=U-Shaped Association of Plasma Testosterone, and no Association of Plasma Estradiol, with Incidence of Fractures in Men.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31630996
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32155267
+|abstract=Whether androgens, distinct from estrogen, maintain bone health during male aging has implications for understanding osteoporosis. We assessed associations of different sex hormones with incidence of any bone fracture or hip fracture in older men. Analysis of 3307 community-dwelling men aged 76.8 ± 3.5 years, median follow-up period of 10.6 years. Plasma testosterone (T), dihydrotestosterone (DHT), and estradiol (E2) assayed by mass spectrometry, sex hormone-binding globulin (SHBG), and luteinizing hormone (LH) using immunoassay. Incident fractures determined via data linkage. We analyzed probability of fracture and performed Cox regression adjusted for age, medical comorbidities, and frailty. Incident fractures occurred in 330 men, including 144 hip fractures. Probability plots suggested nonlinear relationships between hormones and risk of any fracture and hip fracture, with higher risk at lower and higher plasma T, lower E2, higher SHBG, and higher LH. In fully adjusted models, there was a U-shaped association of plasma T with incidence of any fracture (Quartile 2 [Q2] versus Q1: fully adjusted hazard ratio [[[HR]]] = 0.69, 95% confidence interval [CI] 0.51-0.94, P = .020; Q3: [[HR]] 0.59, 95% CI 0.42-0.83, P = .002) and hip fracture (Q2 versus Q1: [[HR]] 0.60, 95% CI 0.37-0.93, P = .043; Q3: [[HR]] 0.52, 95% CI 0.31-0.88, P = .015). DHT, E2, and LH were not associated with fracture. Higher SHBG was associated with hip fracture (Q4 versus Q1: [[HR]] 1.76, 95% CI 1.05-2.96, P = .033). Midrange plasma T was associated with lower incidence of any fracture and hip fracture, and higher SHBG with increased risk of hip fracture. Circulating androgen rather than estrogen represents a biomarker for hormone effects on bone driving fracture risk.
-|mesh-terms=* Age Factors
+|keywords=* estradiol
-* Aged
+* fracture
-* Aged, 80 and over
+* male aging
-* Alzheimer Disease
+* osteoporosis
-* Amyloid
+* sex hormone-binding globulin
-* Biomarkers
+* testosterone
-* Cohort Studies
+|full-text-url=https://sci-hub.do/10.1210/clinem/dgaa115
-* Europe
-* Female
-* Humans
-* Inflammation
-* Male
-* Middle Aged
-* Parkinson Disease
-* Sex Factors
-* tau Proteins
-|keywords=* Aging
-* Alzheimer's disease
-* Amyloid
-* Biomarker
-* Cerebrospinal fluid
-* Inflammation
-* Mild cognitive impairment
-* Multicenter
-* Parkinson's disease
-* Tau
-|full-text-url=https://sci-hub.do/10.1016/j.jalz.2019.07.018
 }}
 {{medline-entry
-|title=Prospective Memory: Age related change is influenced by [[APOE]] genotype.
+|title=Pregnancy-Related Bone Mineral and Microarchitecture Changes in Women Aged 30 to 45 Years.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31578124
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32119748
+|abstract=At birth, the neonatal skeleton contains 20 to 30 g calcium (Ca). It is hypothesized maternal bone mineral may be mobilized to support fetal skeletal development, although evidence of pregnancy-induced mineral mobilization is limited. We recruited healthy pregnant (n = 53) and non-pregnant non-lactating (NPNL; n = 37) women aged 30 to 45 years (mean age 35.4 ± 3.8 years) and obtained peripheral quantitative computed tomography (pQCT) and high-resolution pQCT ([[HR]]-pQCT) scans from the tibia and radius at 14 to 16 and 34 to 36 weeks of pregnancy, with a similar scan interval for NPNL. Multiple linear regression models were used to assess group differences in change between baseline and follow-up; differences are expressed as standard deviation scores (SDS) ± SEM. Decreases in volumetric bone mineral density (vBMD) outcomes were found in both groups; however, pregnancy-related decreases for pQCT total and trabecular vBMD were -0.65 ± 0.22 SDS and -0.50 ± 0.23 SDS greater (p < .05). [[HR]]-pQCT total and cortical vBMD decreased compared with NPNL by -0.49 ± 0.24 SDS and -0.67 ± 0.23 SDS, respectively; trabecular vBMD decreased in both groups to a similar magnitude. Pregnancy-related changes in bone microarchitecture significantly exceeded NPNL change for trabecular number (0.47 ± 0.23 SDS), trabecular separation (-0.54 ± 0.24 SDS), cortical thickness (-1.01 ± 0.21 SDS), and cortical perimeter (0.78 ± 0.23 SDS). At the proximal radius, cortical vBMD and endosteal circumference increased by 0.50 ± 0.23 SDS and 0.46 ± 0.23 SDS, respectively, compared with NPNL, whereas cortical thickness decreased -0.50 ± 0.22 SDS. Pregnancy-related decreases in total and compartment-specific vBMD exceed age-related change at the distal tibia. Changes at the radius were only evident with pQCT at the cortical-rich proximal site and suggest endosteal resorption. Although the magnitude of these pregnancy-related changes in the appendicular skeleton are small, if they reflect global changes across the skeleton at large, they may contribute substantially to the Ca requirements of the fetus. © 2020 Crown copyright. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR). This article is published with the permission of the Controller of HMSO and the Queen's Printer for Scotland.
+|keywords=* AGING
+* ANALYSIS/QUANTITATION OF BONE
+* BONE QCT/μCT
+* EPIDEMIOLOGY
+* GENERAL POPULATION STUDIES
+|full-text-url=https://sci-hub.do/10.1002/jbmr.3998
+}}
+==HRAS==
-|keywords=*  APOE
-* Alzheimer’s disease
-* aging
-* mid-adulthood
-* prospective memory
-|full-text-url=https://sci-hub.do/10.1080/13825585.2019.1671305
-}}
 {{medline-entry
-|title=Education Moderates the Relation Between [[APOE]] ɛ4 and Memory in Nondemented Non-Hispanic Black Older Adults.
+|title=How do combinations of unhealthy behaviors relate to attitudinal factors and subjective health among the adult population in the Netherlands?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31594222
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32245376
+|abstract=Health behaviours like smoking, nutrition, alcohol consumption and physical activity (SNAP) are often studied separately, while combinations can be particularly harmful. This study aims to contribute to a better understanding of lifestyle choices by studying the prevalence of (combinations of) unhealthy SNAP behaviours in relation to attitudinal factors (time orientation, risk attitude) and subjective health (self-rated health, life expectancy) among the adult Dutch population. In total 1006 respondents, representative of the Dutch adult population (18-75 years) in terms of sex, age, and education, were drawn from a panel in 2016. They completed an online questionnaire. Groups comparisons and logistic regression analyses (crude and adjusted) were applied to analyse (combinations of) SNAP behaviours in relation to time orientation (using the Consideration of Future Consequences scale comprising Immediate (CFC-I) and Future (CFC-F) scales) and risk attitude (Health-Risk Attitude Scale; [[HRAS]]-6), as well as subjective health (visual analogue scale and subjective life expectancy). In the analyses, 989 respondents (51% men, average 52 years, 22% low, 48% middle, and 30% high educated) were included. About 8% of respondents engaged in four unhealthy SNAP behaviours and 18% in none. Self-rated health varied from 5.5 to 7.6 in these groups, whilst subjective life expectancy ranged between 73.7 and 85.5 years. Logistic regression analyses, adjusted for socio-demographic variables, showed that smoking, excessive drinking and combining two or more unhealthy SNAP behaviours were significantly associated with CFC-I scores, which increased the odds by 30%, 18% and 19%, respectively. Only physical inactivity was significantly associated with CFC-F scores, which increased the odds by 20%. Three out of the four SNAP behaviours were significantly associated with [[HRAS]]-6, which increased the odds between 6% and 12%. An unhealthy diet, excessive drinking, and physical inactivity were significantly associated with SRH, which decreased the odds by 11%. Only smoking was significantly associated with subjective life expectancy, which decreased the odds by 3%. Our findings suggest that attitudinal factors and subjective health are relevant in the context of understanding unhealthy SNAP behaviours and their clustering. This emphasizes the relevance of a holistic approach to health prevention rather than focusing on a single unhealthy SNAP behaviour.
 |mesh-terms=* Adult
-* African Americans
+* Alcohol Drinking
-* Aged
+* Attitude to Health
-* Aged, 80 and over
+* Cluster Analysis
-* Aging
+* Diagnostic Self Evaluation
-* Alzheimer Disease
+* Diet, Healthy
-* Apolipoprotein E4
+* Exercise
-* Cognitive Reserve
-* Educational Status
-* Executive Function
 * Female
+* Health Risk Behaviors
 * Humans
+* Life Expectancy
+* Life Style
+* Logistic Models
 * Male
-* Memory
-* Memory, Episodic
-* Memory, Short-Term
 * Middle Aged
-* Neuropsychological Tests
+* Netherlands
-* Sex Characteristics
+* Prevalence
-|keywords=* APOE
+* Sedentary Behavior
-* African American
+* Smoking
-* Alzheimer’s disease
+* Surveys and Questionnaires
-* cognitive reserve
+* Young Adult
-* educational attainment
+|keywords=* Clustering risk attitude
-* episodic memory
+* Health behaviours
-* genetic risk
+* Subjective health
-* neuropsychological evaluation
+* Time orientation
-|full-text-url=https://sci-hub.do/10.3233/JAD-190415
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7126128
 }}
+==IHH==
 {{medline-entry
-|title=Apolipoprotein E ε4 allele effects on longitudinal cognitive trajectories are sex and age dependent.
+|title=Indian Hedgehog regulates senescence in bone marrow-derived mesenchymal stem cell through modulation of ROS/mTOR/4EBP1, p70S6K1/2 pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31561966
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32235006
+|abstract=Premature senescence of bone marrow-derived mesenchymal stem cells (BMSC) remains a major concern for their application clinically. Hedgehog signaling has been reported to regulate aging-associated markers and MSC skewed differentiation. Indian Hedgehog ([[IHH]]) is a ligand of Hedgehog intracellular pathway considered as an inducer in chondrogenesis of human BMSC. However, the role of [[IHH]] in the aging of BMSC is still unclear. This study explored the role [[IHH]] in the senescence of BMSC obtained from human samples and senescent mice. Isolated BMSC were transfected with [[IHH]] siRNA or incubated with exogenous [[IHH]] protein and the mechanisms of aging and differentiation investigated. Moreover, the interactions between [[IHH]], and mammalian target of rapamycin (mTOR) and reactive oxygen species (ROS) were evaluated using the corresponding inhibitors and antioxidants. BMSC transfected with [[IHH]] siRNA showed characteristics of senescence-associated features including increased senescence-associated β-galactosidase activity (SA-β-gal), induction of cell cycle inhibitors (p53/p16), development of senescence-associated secretory phenotype (SASP), activation of ROS and mTOR pathways as well as the promotion of skewed differentiation. Interestingly, BMSC treatment with [[IHH]] protein reversed the senescence markers and corrected biased differentiation. Moreover, [[IHH]] shortage-induced senescence signs were compromised after mTOR and ROS inhibition. Our findings presented anti-aging activity for [[IHH]] in BMSC through down-regulation of ROS/mTOR pathways. This discovery might contribute to increasing the therapeutic, immunomodulatory and regenerative potency of BMSC and introduce a novel remedy in the management of aging-related diseases.
-|mesh-terms=* Age Factors
+|keywords=* Indian hedgehog
-* Aged
+* aging
-* Alleles
+* differentiation
-* Apolipoprotein E4
+* mammalian target of rapamycin
-* Cognition Disorders
+* mesenchymal stem cell
-* European Continental Ancestry Group
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185126
-* Executive Function
-* Female
-* Humans
-* Longitudinal Studies
-* Male
-* Memory
-* Neuropsychological Tests
-* Sex Factors
-|keywords=* Aging
-* Alzheimer's disease
-* Apolipoprotein E ε4
-* Cognitive decline
-* Sex
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7561018
 }}
+==IL15==
 {{medline-entry
-|title=Interactive effect of age and [[APOE]]-ε4 allele load on white matter myelin content in cognitively normal middle-aged subjects.
+|title=Moderate physical activity associated with a higher naïve/memory T-cell ratio in healthy old individuals: potential role of [[IL15]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31520917
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32221610
+|abstract=ageing is accompanied by impairments in immune responses due to remodelling of the immune system (immunesenescence). Additionally, a decline in habitual physical activity has been reported in older adults. We have recently published that specific features of immunesenescence, such as thymic involution and naïve/memory T-cell ratio, are prevented by maintenance of a high level of physical activity. This study compares immune ageing between sedentary and physically active older adults. a cross-sectional study recruited 211 healthy older adults (60-79 years) and assessed their physical activity levels using an actigraph. We compared T- and B-cell immune parameters between relatively sedentary (n = 25) taking 2,000-4,500 steps/day and more physically active older adults (n = 25) taking 10,500-15,000 steps/day. we found a higher frequency of naïve CD4 (P = 0.01) and CD8 (P = 0.02) and a lower frequency of memory CD4 cells (P = 0.01) and CD8 (P = 0.04) T cells in the physically active group compared with the sedentary group. Elevated serum IL7 (P = 0.03) and [[IL15]] (P = 0.003), cytokines that play an essential role in T-cell survival, were seen in the physically active group. Interestingly, a positive association was observed between [[IL15]] levels and peripheral CD4 naïve T-cell frequency (P = 0.023). we conclude that a moderate level of physical activity may be required to give a very broad suppression of immune ageing, though 10,500-15,000 steps/day has a beneficial effect on the naïve T-cell pool.
-|mesh-terms=* Age Factors
+|keywords=* T cells
-* Aged
+* ageing
-* Aging
+* immune senescence
-* Apolipoprotein E4
+* older people
-* Female
+* physical activity
-* Humans
+|full-text-url=https://sci-hub.do/10.1093/ageing/afaa035
-* Magnetic Resonance Imaging
-* Male
-* Middle Aged
-* Myelin Sheath
-* White Matter
-|keywords=* Aging
-* Alzheimer
-* Apolipoprotein E
-* Cognitively normal subjects
-* Myelination
-* T1w/T2w ratio
-* White matter integrity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6742967
 }}
+==IMPACT==
 {{medline-entry
-|title=[[APOE]] modifies the interaction of entorhinal cerebral blood flow and cortical thickness on memory function in cognitively normal older adults.
+|title=Using Video Telehealth to Deliver Patient-Centered Collaborative Care: The G-[[IMPACT]] Pilot.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31493534
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32228299
+|abstract=: This pilot project aimed to explore a new model of healthcare delivery to older adult medically complex Veterans by combining telehealth technology with an interdisciplinary medical team operating in real time. : The Geriatric-Interdisciplinary Mobile Patient Access Team (G-[[IMPACT]]) was comprised of a field team including a nurse practitioner and technology assistant who visited enrolled patients in their homes using synchronous video to link to a suite of geriatric specialists in a video-enabled room at a Veterans Affairs hospital. Clinicians interacted with patients, caregivers, and each other to develop mutually agreed upon treatment plans that were then immediately implemented in the field. : 11 total visits were conducted with 9 Veteran patients aged 55-91 (mean = 75.3 years). Both patients and clinicians reported a high level of satisfaction across multiple metrics, including visit quality, and positive indirect indicators of effectiveness were apparent from qualitative data. : Nurse practitioner facilitated video visits allowed geriatric patients to meet with multiple specialists simultaneously with both high patient satisfaction and increased real-time care coordination. : This project identified challenges and opportunities afforded by this type of real-time telehealth care delivery and can inform the development of future interdisciplinary mobile medical teams.
-|mesh-terms=* Aged
+|keywords=* Telehealth
-* Aged, 80 and over
+* aging
-* Apolipoproteins E
+* care coordination
-* Cerebral Cortex
+* home care
-* Cerebrovascular Circulation
+* interdisciplinary
-* Entorhinal Cortex
+* medicine
-* Female
+* older adult
-* Genotype
+* video
-* Humans
+|full-text-url=https://sci-hub.do/10.1080/07317115.2020.1738000
-* Linear Models
-* Male
-* Memory
-* Middle Aged
-|keywords=* APOE ε4
-* Aging
-* Alzheimer’s disease
-* Cerebral blood flow
-* Cognitive decline
-* Cortical thickness
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6819270
 }}
+==IQGAP1==
 {{medline-entry
-|title=When time's arrow doesn't bend: [[APOE]]-ε4 influences episodic memory before old age.
+|title=Hyaluronan-binding protein 1 (HABP1) overexpression triggers induction of senescence in fibroblasts cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31473197
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32068317
+|abstract=Hyaluronan-binding protein 1 (HABP1), a multi-compartmental, multi-functional protein has a wide range of functions, which can be attributed to its ability to associate with a variety of cellular ligands. Earlier we have reported that HABP1 overexpression in rat normal fibroblasts (F-HABP07) shows chronic generation of reactive oxygen species (ROS), induction of autophagy, and apoptosis. However, a significant proportion of cells remained viable after the majority went through apoptosis from 60 to 72 h. In this study, an attempt has been made to delineate the cellular events in the declined population of surviving cells. It has been elucidated here that, these cells at later time points of growth, that is, 72 and 84 h, not only appeared to shrink but also are devoid of autophagic vacuoles and displayed polyploidy. F-HABP07 cells exhibited an altered cytoskeletal structure from their parental cell line F111, assumed to be caused upon inhibition of actin polymerization and decrease in IQ motif-containing GTPase activating protein 1 ([[IQGAP1]]), a key protein associated with maintenance of cytoskeletal integrity. Enhanced expression and nuclear localization of AKT observed in F-HABP07 cells appears to be contributing toward the maintenance of high ROS levels in these cells and also potentially modulating the [[IQGAP1]] activity. These observations, in fact have been considered to result in sustained DNA damage, which then leads to increased expression of p53 and activation of p21 and carry out the cellular events responsible for senescence. Subsequent assessment of the presence of positive β-gal staining and enhanced expression of p16  in F-HABP07, confirmed that HABP1 overexpressing fibroblasts undergo senescence.
-|mesh-terms=* Adult
+|keywords=* F-HABP07
-* Alleles
+* HABP1
-* Alzheimer Disease
+* IQGAP1
-* Apolipoprotein E4
+* senescence
-* Cognition
+|full-text-url=https://sci-hub.do/10.1002/cbin.11326
-* Cognitive Aging
-* Female
-* Genotype
-* Humans
-* Linear Models
-* Male
-* Memory
-* Memory, Episodic
-* Middle Aged
-* Young Adult
-|keywords=* Alzheimer's diseas
-* Apolipoprotein E
-* Cognition
-* Episodic memory
-* Semantic memory
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6817416
 }}
-{{medline-entry
+==JAK1==
-|title=Cognitive-Motor Integration Performance Is Affected by Sex, [[APOE]] Status, and Family History of Dementia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31424400
-|mesh-terms=* Aged
-* Apolipoproteins E
-* Cognition
-* Cognitive Dysfunction
-* Cross-Sectional Studies
-* Dementia
-* Female
-* Humans
-* Male
-* Medical History Taking
-* Middle Aged
-* Photic Stimulation
-* Psychomotor Performance
-* Sex Characteristics
-* Surveys and Questionnaires
-|keywords=* Aging
-* alzheimer’s disease
-* apolipoprotein E4
-* dementia risk
-* geriatric
-assessment
-* motor skills
-* movement
-* visuomotor integration
-|full-text-url=https://sci-hub.do/10.3233/JAD-190403
-}}
 {{medline-entry
-|title=Associations among amyloid status, age, and longitudinal regional brain atrophy in cognitively unimpaired older adults.
+|title=Irradiation-induced senescence of bone marrow mesenchymal stem cells aggravates osteogenic differentiation dysfunction via paracrine signaling.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31437719
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32233952
+|abstract=The role of cellular senescence induced by radiation in bone loss has attracted much attention. As one of the common complications of anticancer radiotherapy, irradiation-induced bone deterioration is common and clinically significant, but the pathological mechanism has not been elucidated. This study was performed to explore the cellular senescence and senescence-associated secretory phenotype (SASP) induction of bone marrow-derived mesenchymal stem cells (BMSCs) by irradiation and its role in osteogenic differentiation dysfunction. It was observed that irradiated BMSCs lost typical fibroblast-like morphology, exhibited suppressed viability and differentiation potential accompanied with senescence phenotypes, including an increase in senescence-associated β-galactosidase (SA-β-gal) staining-positive cells, and upregulated senescence-related genes [i]p53/p21[/i], whereas no changes happened to [i]p16[/i]. Additionally, DNA damage γ-H2AX foci, G0/G1 phase of cell cycle arrest, and cellular and mitochondrial reactive oxygen species (ROS) increased in an irradiation dose-dependent manner. Meanwhile, the [[JAK1]]/STAT3 pathway was activated and accompanied by an increase in SASP secretion, such as IL-6, IL-8, and matrix metalloproteinase-9 (MMP9), whereas 0.8 μM [[JAK1]] inhibitor (JAKi) treatment effectively inhibited the JAK pathway and SASP production. Furthermore, conditioned medium (CM) from irradiation-induced senescent (IRIS) BMSCs exhibited a markedly reduced ability in osteogenic differentiation and marker gene expression of osteoblasts, whereas CM with JAKi intervention may effectively improve these deterioration effects. In conclusion, irradiation could provoke BMSC senescence and SASP secretion and further aggravate osteogenic differentiation dysfunction via paracrine signaling, whereas SASP targeting may be a possible intervention strategy for alleviating irradiation-induced bone loss.
-|mesh-terms=* Aged
+|mesh-terms=* Bone Resorption
-* Aged, 80 and over
+* Cell Cycle Checkpoints
-* Aging
+* Cell Differentiation
-* Amyloid beta-Peptides
+* Cell Proliferation
-* Atrophy
+* Cellular Senescence
-* Brain
+* DNA Damage
-* Cognition
+* Gene Expression Regulation, Developmental
-* Cognitive Dysfunction
+* Histones
-* Databases, Factual
-* Female
 * Humans
-* Longitudinal Studies
+* Janus Kinase 1
-* Male
+* Mesenchymal Stem Cells
-* Middle Aged
+* Mitochondria
-|keywords=* Aging
+* Osteogenesis
-* Alzheimer's disease
+* Paracrine Communication
-* Amyloid-β
+* Radiation
-* Brain atrophy
+* Reactive Oxygen Species
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7198229
+* STAT3 Transcription Factor
+* Signal Transduction
+|keywords=* SASP
+* bone marrow mesenchymal stem cells
+* cellular senescence
+* irradiation
+* osteogenic differentiation
+|full-text-url=https://sci-hub.do/10.1152/ajpcell.00520.2019
 }}
+==KDM2B==
 {{medline-entry
-|title=Cognitive function and neuropathological outcomes: a forward-looking approach.
+|title=Identification of Structural Elements of the Lysine Specific Demethylase 2B CxxC Domain Associated with Replicative Senescence Bypass in Primary Mouse Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31435771
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32270414
+|abstract=Lysine specific demethylase 2B, [[KDM2B]], regulates genes that participate in cellular development, morphogenesis, differentiation and metabolism as a component of the polycomb repressive complex 1 (PRC1). The CxxC finger of [[KDM2B]] is responsible for the DNA binding capacity of this epigenetic regulator, acting as a sampling mechanism across chromatin for gene repression OBJECTIVES: The molecular determinants of the CxxC-DNA interaction remain largely unknown, revealing a significant knowledge gap to be explored. Our goal was to elucidate the key residues of the CxxC domain that contribute to its function as well as to further elaborate on the significance of this domain in the [[KDM2B]] role METHODS: By using electrophoresis mobility swift assay, we identified structural elements of CxxC domain that participate in the DNA recognition. We created mouse embryonic fibroblasts overexpressing different truncated and point-mutated mouse [[KDM2B]] variants to examine the contribution of the [[KDM2B]] domains in replicative senescence bypass RESULTS: In this study, we show that only the CxxC finger is essential for the ability of m[[KDM2B]] to bypass replicative senescence in primary cells by ink4A-Arf-ink4B locus repression, and that this is mediated by specific interactions of residues R585, K608 and K616 with non-methylated CpG containing DNA CONCLUSIONS: These results provide new structural insights into the molecular interactions of CxxC and could serve as a stepping-stone for developing domain-specific inhibitors for [[KDM2B]].
-|mesh-terms=* Aged
+|keywords=* Lysine demethylase
-* Aged, 80 and over
+* Non-methylated CpG
-* Aging
+* Oncogene
-* Alzheimer Disease
+* Polycomb repressive complex
-* Cognitive Dysfunction
+* Replicative senescence
-* Female
+* Zn-finger
-* Humans
+|full-text-url=https://sci-hub.do/10.1007/s10930-020-09895-z
-* Male
-* Middle Aged
-|keywords=* Alzheimer’s disease
-* Cognition
-* Multi-state model
-* Neuropathology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6851487
 }}
+==KIT==
 {{medline-entry
-|title=[[APOE]] gene-dependent BOLD responses to a breath-hold across the adult lifespan.
+|title=Prediction of ovarian aging using ovarian expression of BMP15, GDF9, and C-[[KIT]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31408838
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32223330
+|abstract=Ovarian aging is becoming a more important issue in terms of fertility preservation and infertility treatment. Serum anti-Mullerian hormone (AMH) level and antral follicle count (AFC) are being practically used as markers of ovarian aging as well as ovarian reserve in human. However, these factors have some drawbacks in assessing ovarian aging and reserve. Therefore, the identification of ovarian expressions of BMP15, GDF9, and C-[[KIT]] according to female could be applied as a potent predictor of ovarian aging. This work provides new information on the development of diagnosis and treatment strategy of age-related fertility decline and premature ovarian insufficiency.
-|mesh-terms=* Adult
+|keywords=* BMP15
-* Aged
+* C-KIT
-* Aging
+* GDF9
-* Apolipoprotein E3
+* Ovarian aging
-* Apolipoprotein E4
+* biomarkers
-* Apolipoproteins E
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7221484
-* Breath Holding
-* Cerebrovascular Circulation
-* Cross-Over Studies
-* Double-Blind Method
-* Female
-* Genotype
-* Hemodynamics
-* Humans
-* Longevity
-* Magnetic Resonance Imaging
-* Male
-* Middle Aged
-* Nitrates
-|keywords=* Ageing
-* Alzheimer's disease
-* Apolipoprotein E
-* BOLD fMRI
-* Breath-hold
-* Cerebrovascular reactivity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6699560
 }}
-==APP==
+==KRAS==
 {{medline-entry
-|title=Pre-symptomatic Caspase-1 inhibitor delays cognitive decline in a mouse model of Alzheimer disease and aging.
+|title=Senescence-Induced Vascular Remodeling Creates Therapeutic Vulnerabilities in Pancreas Cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32917871
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32234521
+|abstract=[[KRAS]] mutant pancreatic ductal adenocarcinoma (PDAC) is characterized by a desmoplastic response that promotes hypovascularity, immunosuppression, and resistance to chemo- and immunotherapies. We show that a combination of MEK and CDK4/6 inhibitors that target [[KRAS]]-directed oncogenic signaling can suppress PDAC proliferation through induction of retinoblastoma (RB) protein-mediated senescence. In preclinical mouse models of PDAC, this senescence-inducing therapy produces a senescence-associated secretory phenotype (SASP) that includes pro-angiogenic factors that promote tumor vascularization, which in turn enhances drug delivery and efficacy of cytotoxic gemcitabine chemotherapy. In addition, SASP-mediated endothelial cell activation stimulates the accumulation of CD8  T cells into otherwise immunologically "cold" tumors, sensitizing tumors to PD-1 checkpoint blockade. Therefore, in PDAC models, therapy-induced senescence can establish emergent susceptibilities to otherwise ineffective chemo- and immunotherapies through SASP-dependent effects on the tumor vasculature and immune system.
 |mesh-terms=* Aging
-* Alzheimer Disease
-* Amyloid beta-Peptides
 * Animals
-* Behavior, Animal
+* CD8-Positive T-Lymphocytes
-* Cognitive Dysfunction
+* Carcinoma, Pancreatic Ductal
-* Cytokines
+* Cell Line, Tumor
-* Dipeptides
+* Cell Proliferation
-* Disease Models, Animal
+* Cyclin-Dependent Kinase 4
-* Encephalitis
+* Cyclin-Dependent Kinase 6
+* Gene Expression Regulation, Neoplastic
+* Genes, ras
+* Humans
+* Immunotherapy
+* MAP Kinase Signaling System
+* Mice
+* Pancreatic Neoplasms
+* Retinoblastoma Protein
+* Signal Transduction
+* Tumor Microenvironment
+* Vascular Remodeling
+|keywords=* T cells
+* chemotherapy resistance
+* endothelial cell activation
+* immunotherapy
+* pancreatic cancer
+* senescence
+* senescence-associated secretory phenotype
+* targeted therapy
+* tumor microenvironment
+* vascular biology
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7278897
+}}
+==LBP==
+{{medline-entry
+|title=Aging-related liver degeneration is associated with increased bacterial endotoxin and lipopolysaccharide binding protein levels.
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32090603
+|abstract=Aging is a risk factor in the development of many diseases, including liver-related diseases. The two aims of the present study were [i]1[/i]) to determine how aging affects liver health in mice in the absence of any interventions and [i]2[/i]) if degenerations observed in relation to blood endotoxin levels are critical in aging-associated liver degeneration. Endotoxin levels and markers of liver damage, mitochondrial dysfunction, insulin resistance, and apoptosis as well as the Toll-like receptor 4 (Tlr-4) signaling cascade were studied in liver tissue and blood, respectively, of 3- and 24-mo-old male C57BL/6J mice. In a second set of experiments, 3- to 4-mo-old and 14-mo-old female lipopolysaccharide-binding protein ([[LBP]])  mice and littermates fed standard chow, markers of liver damage, insulin resistance, and mitochondrial dysfunction were assessed. Plasma activity of aspartate aminotransferase and histological signs of hepatic inflammation and fibrosis were significantly higher in old C57BL/6J mice than in young animals. The number of neutrophils, CD8α-positive cells, and mRNA expression of markers of apoptosis were also significantly higher in livers of old C57BL/6J mice compared with young animals, being also associated with a significant induction of hepatic Tlr-4 and [[LBP]] expression as well as higher endotoxin levels in peripheral blood. Compared with age-matched littermates, [[LBP]]  mice display less signs of senescence in liver. Taken together, our data suggest that, despite being fed standard chow, old mice developed liver inflammation and beginning fibrosis and that bacterial endotoxin may play a critical role herein.  Old age in mice is associated with marked signs of liver degeneration, hepatic inflammation, and fibrosis. Aging-associated liver degeneration is associated with elevated bacterial endotoxin levels and an induction of lipopolysaccharide-binding protein ([[LBP]]) and Toll-like receptor 4-dependent signaling cascades in liver tissue. Furthermore, in old aged [[LBP]]  mice, markers of senescence seem to be lessened, supporting the hypothesis that bacterial endotoxin levels might be critical in aging-associated decline of liver.
+|mesh-terms=* Acute-Phase Proteins
+* Aging
+* Animals
+* Apoptosis
+* Biomarkers
+* Carrier Proteins
+* Endotoxins
 * Female
-* Humans
+* Gene Expression Regulation
+* Glucose
 * Inflammation
+* Insulin Receptor Substrate Proteins
+* Liver
+* Liver Cirrhosis
+* Malate Dehydrogenase
 * Male
-* Memory Disorders
+* Membrane Glycoproteins
 * Mice
 * Mice, Inbred C57BL
-* Mice, Transgenic
+* Mice, Knockout
-* Serpins
+* RNA, Messenger
-* Spatial Memory
+* Receptor, Insulin
-* Viral Proteins
+* Toll-Like Receptor 4
-* para-Aminobenzoates
+|keywords=* Tlr-4 signaling
+* aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7486940
+* bacterial endotoxin
+* lipopolysaccharide binding protein
+* liver degeneration
+|full-text-url=https://sci-hub.do/10.1152/ajpgi.00345.2018
 }}
+==LBR==
 {{medline-entry
-|title=Regorafenib Regulates AD Pathology, Neuroinflammation, and Dendritic Spinogenesis in Cells and a Mouse Model of AD.
+|title=The impact of age beyond ploidy: outcome data from 8175 euploid single embryo transfers.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32660121
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32173784
+|abstract=The rate of embryonic aneuploidy increases with increasing female age and is the primary cause of lower pregnancy and live birth rates ([[LBR]]) in older reproductive age women. This retrospective cohort study evaluates single euploid embryo transfers to determine whether an age-related decline in reproductive efficiency persists. A total of 8175 non-donor single embryo transfers (SET) after pre-implantation testing for aneuploidy (PGT-A) and cryopreservation were included. These were divided into five groups by patient age: < 35 years old (n = 3789 embryos transferred), 35-37 (n = 2200), 38-40 (n = 1624), 41-42 (n = 319), and > 42 (n = 243). Implantation rate (IR), clinical pregnancy rate (CPR), and [[LBR]] were calculated for each group as a percentage of embryos transferred and compared. CPR was also analyzed as a percentage of implanted pregnancies, and [[LBR]] as a percentage of clinical pregnancies, to determine when age has the greatest impact. These results were then adjusted for confounding variables via a multivariate logistic regression model. Implantation rates negatively correlated with age. After adjusting for confounders, women 38 years or older had a significantly lower IR than those under 35 (OR 0.85, 95%CI 0.73-0.99 for 38-40 years old; 0.69, 0.53-0.91 for 41-42, and 0.69, 0.51-0.94 for > 42). These differences are also apparent in CPR and [[LBR]]. The rates of progression to clinical pregnancy and live birth did not differ significantly by age group. Other factors observed to affect IR independently were anti-Müllerian hormone (AMH), day of embryo transfer, and embryo morphology. While selection of euploid embryos may be effective in overcoming a significant proportion of the age-related decline in reproductive efficiency, a decrease in IR, CPR, and [[LBR]] persists even when analyzing only euploid embryo transfers. The observed impact of aging is, therefore, independent of ploidy, as well as of other variables that affect reproductive efficiency. These results indicate that factors other than aneuploidy contribute to reproductive senescence.
+|keywords=* Aneuploidy
-|keywords=* aging
+* Pregestational genetic testing
-* amyloid beta
+* Reproductive aging
-* dendritic spine
+* Single embryo transfer
-* neuroinflammation
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7125286
-* regorafenib
-* tau
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7408082
 }}
 {{medline-entry
-|title=An agnostic reevaluation of the amyloid cascade hypothesis of Alzheimer's disease pathogenesis: The role of [[APP]] homeostasis.
+|title=The role of lamin B receptor in the regulation of senescence-associated secretory phenotype (SASP).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32588983
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32126237
+|abstract=Cellular senescence is a phenomenon of irreversible growth arrest of mammalian somatic cells. Senescent cells increase the production of secretory proteins such as inflammatory cytokines, a phenomenon termed senescence-associated secretory phenotype (SASP). SASP is known to have profound effects on organismal health and aging; however, the molecular mechanisms of SASP are not precisely understood. In our previous studies, we have shown that senescent cells show decreased function of lamin B receptor ([[LBR]]), a nuclear membrane protein that regulates heterochromatin organization. Here we examined the implication of [[LBR]] in the regulation of SASP because senescent cells show altered heterochromatin organization, which would affect gene expression. We found that knock-down of [[LBR]] up-regulated the expression of the SASP factors such as IL-6, IL-8, and MMP1 in HeLa cells, even though cellular senescence was not induced by [[LBR]] knock-down. Conversely, enforced expression of [[LBR]] suppressed their up-regulated expression in senescent cells induced by excess thymidine. Further, our gene expression profile analysis also showed that many secretory proteins were up-regulated by [[LBR]] knock-down. We then analyzed the regulatory mechanisms of the expression of SASP factors by [[LBR]], and found that the promoters of these SASP factors associated with [[LBR]] in normally growing cells, but dissociated from it in senescent cells. Additionally, we found that enforced expression of [[LBR]] decreased the generation of cytoplasmic DNA, which could be involved in SASP, in senescent cells. These findings suggested that [[LBR]] would play crucial roles in the regulation of SASP.
+|keywords=* Gene expression
+* LBR
+* SAHF
+* SASP
+* Senescence
+|full-text-url=https://sci-hub.do/10.1016/j.yexcr.2020.111927
+}}
+==LMNA==
-|keywords=* aging
-* amyloid hypothesis
-* amyloid precursor protein homeostasis
-* late onset Alzheimer's disease
-* young onset Alzheimer's disease
-|full-text-url=https://sci-hub.do/10.1002/alz.12124
-}}
 {{medline-entry
-|title=Transcriptomic profiling of microglia and astrocytes throughout aging.
+|title=The JAK1/2 inhibitor ruxolitinib delays premature aging phenotypes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32238175
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32196928
+|abstract=Hutchinson-Gilford progeria syndrome (HGPS) is caused by an [[LMNA]] mutation that results in the production of the abnormal progerin protein. Children with HGPS display phenotypes of premature aging and have an average lifespan of 13 years. We found earlier that the targeting of the transmembrane protein PLA2R1 overcomes senescence and improves phenotypes in a mouse model of progeria. PLA2R1 is regulating the JAK/STAT signaling, but we do not yet know whether targeting this pathway directly would influence cellular and in vivo progeria phenotypes. Here, we show that JAK1/2 inhibition with ruxolitinib rescues progerin-induced cell cycle arrest, cellular senescence, and misshapen nuclei in human normal fibroblasts expressing progerin. Moreover, ruxolitinib administration reduces several premature aging phenotypes: bone fractures, bone mineral content, grip strength, and a trend to increase survival in a mouse model of progeria. Thus, we propose that ruxolitinib, an FDA-approved drug, should be further evaluated as a drug candidate in HGPS therapy.
+|keywords=* JAK/STAT pathway
+* cellular senescence
+* progeria
+* ruxolitinib
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189991
+}}
+==LOX==
-|keywords=* Aging
-* Alzheimer’s disease (AD)
-* Astrocyte
-* Microglia
-* RNA-seq
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7115095
-}}
 {{medline-entry
-|title=Platelets in Amyloidogenic Mice Are Activated and Invade the Brain.
+|title=12-[[LOX]] catalyzes the oxidation of 2-arachidonoyl-lysolipids in platelets generating eicosanoid-lysolipids that are attenuated by iPLA γ knockout.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32194368
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32161117
+|abstract=The canonical pathway of eicosanoid production in most mammalian cells is initiated by phospholipase A -mediated release of arachidonic acid, followed by its enzymatic oxidation resulting in a vast array of eicosanoid products. However, recent work has demonstrated that the major phospholipase in mitochondria, iPLA γ (patatin-like phospholipase domain containing 8 (PNPLA8)), possesses [i]sn[/i]-1 specificity, with polyunsaturated fatty acids at the [i]sn[/i]-2 position generating polyunsaturated [i]sn[/i]-2-acyl lysophospholipids. Through strategic chemical derivatization, chiral chromatographic separation, and multistage tandem MS, here we first demonstrate that human platelet-type 12-lipoxygenase (12-[[LOX]]) can directly catalyze the regioselective and stereospecific oxidation of 2-arachidonoyl-lysophosphatidylcholine (2-AA-LPC) and 2-arachidonoyl-lysophosphatidylethanolamine (2-AA-LPE). Next, we identified these two eicosanoid-lysophospholipids in murine myocardium and in isolated platelets. Moreover, we observed robust increases in 2-AA-LPC, 2-AA-LPE, and their downstream 12-[[LOX]] oxidation products, 12([i]S[/i])-HETE-LPC and 12([i]S[/i])-HETE-LPE, in calcium ionophore (A23187)-stimulated murine platelets. Mechanistically, genetic ablation of iPLA γ markedly decreased the calcium-stimulated production of 2-AA-LPC, 2-AA-LPE, and 12-HETE-lysophospholipids in mouse platelets. Importantly, a potent and selective 12-[[LOX]] inhibitor, ML355, significantly inhibited the production of 12-HETE-LPC and 12-HETE-LPE in activated platelets. Furthermore, we found that aging is accompanied by significant changes in 12-HETE-LPC in murine serum that were also markedly attenuated by iPLA γ genetic ablation. Collectively, these results identify previously unknown iPLA γ-initiated signaling pathways mediated by direct 12-[[LOX]] oxidation of 2-AA-LPC and 2-AA-LPE. This oxidation generates previously unrecognized eicosanoid-lysophospholipids that may serve as biomarkers for age-related diseases and could potentially be used as targets in therapeutic interventions.
+|keywords=* 2-arachidonoyl-lysophospholipids
-|keywords=* Alzheimer’s disease
 * aging
-* astrocytes
+* calcium
-* platelets
+* eicosanoid
-* vascular pathology
+* iPLA2γ
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7063083
+* lysophospholipid
+* myocardium
+* platelet
+* platelet-type 12-lipoxygenase (12-LOX)
+* polyunsaturated fatty acids (PUFAs)
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7170522
 }}
+==LPA==
 {{medline-entry
-|title=CHIP modulates [[APP]]-induced autophagy-dependent pathological symptoms in Drosophila.
+|title=Does sedentary time increase in older adults in the days following participation in intense exercise?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31777182
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32130714
+|abstract=Older adults have the highest sedentary time across all age groups, and only a small portion is meeting the minimum recommendations for weekly physical activity. Little research to date has looked at how changes in one of these behaviours influences the other. To assess changes in 24-h movement behaviours (sedentary time, light intensity physical activity ([[LPA]]), moderate-vigorous PA (MVPA) and sleep) over three consecutive days, following acute bouts of exercise of varying intensity in older adults. Participants (n = 28, 69.7 ± 6.5 years) completed a maximal exercise test and the following exercise protocols in random order: moderate continuous exercise (MOD), high-intensity interval exercise (HI) and sprint interval exercise (SPRT). A thigh-worn device (ActivPAL™) was used to measure movement behaviours at baseline and the 3 days following each exercise session. Repeated measures analysis of variance indicated that compared to baseline, participants decreased MVPA in the 3 days following all exercise sessions and decreased [[LPA]] following HI and SPRT (p < 0.05). Over half of the sample had clinically meaningful increases in sedentary time (30 min/day) in the days following exercise participation. Older adults who compensate for exercise participation by reducing physical activity and increasing sedentary time in subsequent days may require behavioural counseling to ensure that incidental and recreational physical activities are not reduced. It appears that older adults compensate for acute exercise by decreasing MVPA and [[LPA]], and increasing sedentary time in the days following exercise. Future research is needed to determine whether compensation persists with regular engagement.
-|mesh-terms=* Alzheimer Disease
+|mesh-terms=* Accelerometry
-* Amyloid beta-Protein Precursor
+* Aged
-* Animals
+* Exercise
-* Aspartic Acid Endopeptidases
+* Exercise Test
-* Autophagy
+* Humans
-* Brain
+* Sedentary Behavior
-* Cognitive Dysfunction
+* Sleep
-* Disease Models, Animal
+|keywords=* Aging
-* Dopaminergic Neurons
+* Compensation
-* Down-Regulation
+* High intensity
-* Drosophila
+* Movement behaviours
-* Drosophila Proteins
+|full-text-url=https://sci-hub.do/10.1007/s40520-020-01502-6
-* Eye
-* Learning Disabilities
-* Locomotion
-* Longevity
-* Nuclear Proteins
-* Presenilins
-* RNA Interference
-* Wings, Animal
-|keywords=*
-CHIP
-* APP
-* Alzheimer’s disease
-* Aβ
-* autophagy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996943
 }}
 {{medline-entry
-|title=Studies on [[APP]] metabolism related to age-associated mitochondrial dysfunction in [[APP]]/PS1 transgenic mice.
+|title=Association of Long-term Exposure to Elevated Lipoprotein(a) Levels With Parental Life Span, Chronic Disease-Free Survival, and Mortality Risk: A Mendelian Randomization Analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31744937
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32108890
+|abstract=Elevated lipoprotein(a) (Lp[a]) levels are associated with atherosclerotic cardiovascular diseases. The association between high Lp(a) levels and human longevity phenotypes is, however, controversial. To examine whether genetically determined Lp(a) levels are associated with parental life span and chronic disease-free survival (health span) and the association between Lp(a) levels and long-term, all-cause mortality risk. In this genetic association study, cross-sectional mendelian randomization (UK Biobank [2006-2010] and LifeGen Consortium) and prospective analyses (European Prospective Investigation Into Cancer and Nutrition (EPIC)-Norfolk [1993-1997, with patients followed up to 2016]) were conducted using individual-level data on 139 362 participants. The association between a weighted genetic risk score of 26 independent single-nucleotide polymorphisms at the [[LPA]] locus on parental life span using individual participant data from the UK Biobank, as well as with summary statistics of a genome-wide association study of more than 1 million life spans (UK Biobank and LifeGen), were examined. The association between these single-nucleotide polymorphisms and the age at the end of the health span was tested using summary statistics of a previous genome-wide association study in the UK Biobank. The association between Lp(a) levels and all-cause mortality in the EPIC-Norfolk study was also investigated. Data were analyzed from December 2018 to December 2019. Genetically determined and measured Lp(a) levels. Parental life span, health span, and all-cause mortality. In 139 362 white British participants (mean [SD] age, 62.8 [3.9] years; 52% women) from the UK Biobank, increases in the genetic risk score (weighted for a 50-mg/dL increase in Lp[a] levels) were inversely associated with a high parental life span (odds ratio, 0.92; 95% CI, 0.89-0.94; P = 2.7 × 10-8). Using the Egger-mendelian randomization method, a negative association between [[LPA]] single-nucleotide polymorphisms and parental life span (mean [SD] Egger-mendelian randomization slope, -0.0019 [0.0002]; P = 2.22 × 10-18) and health span (-0.0019 [0.0003]; P = 3.00 × 10-13) was noted. In 18 720 participants from EPIC-Norfolk (5686 cases), the mortality risk for those with Lp(a) levels equal to or above the 95th percentile was equivalent to being 1.5 years older in chronologic age (β coefficient [SE], 0.194 [0.064]). The results of this study suggest a potential causal effect of absolute Lp(a) levels on human longevity as defined by parental life span, health span, and all-cause mortality. The results also provide a rationale for trials of Lp(a)-lowering therapy in individuals with high Lp(a) levels.
-|mesh-terms=* Adenosine Triphosphate
-* Aging
-* Alzheimer Disease
-* Amyloid beta-Protein Precursor
-* Animals
-* Blood Platelets
-* Disease Models, Animal
-* Hippocampus
-* Mice
-* Mice, Inbred C57BL
-* Mice, Transgenic
-* Mitochondria
-* Presenilin-1
-|keywords=* APP/PS1 mice
-* Amyloid-beta
-* adenosine 5’-triphosphate
-* mitochondria dysfunction
-* platelets
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6914425
-}}
-{{medline-entry
-|title=Intermittent Hypoxia-Hyperoxia Training Improves Cognitive Function and Decreases Circulating Biomarkers of Alzheimer's Disease in Patients with Mild Cognitive Impairment: A Pilot Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31671598
 |mesh-terms=* Aged
-* Alzheimer Disease
-* Biomarkers
 * Case-Control Studies
-* Cognition
+* Cross-Sectional Studies
-* Cognitive Dysfunction
 * Female
 * Humans
-* Hyperoxia
+* Lipoprotein(a)
-* Hypoxia
+* Longevity
 * Male
+* Mendelian Randomization Analysis
 * Middle Aged
-* Pilot Projects
+* Parents
-* Respiratory Therapy
+* Phenotype
-* Treatment Outcome
+* Prospective Studies
-|keywords=* Alzheimer’s disease
+* Risk Factors
-* adaptation
+|keywords=#f
-* aging
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7049087
-* amyloid beta
-* biomarker
-* cognitive function
-* hyperoxia
-* intermittent hypoxia
-* platelets
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6862463
 }}
+==LPO==
 {{medline-entry
-|title=The Implication of Androgens in the Presence of Protein Kinase C to Repair Alzheimer’s Disease-Induced Cognitive Dysfunction
+|title=[Features of the changes in lipid peroxidation and activity of Na+/K+-ATPase in the brain of the aged rats in the conditions of two-vessel cerebral ischemia/reperfusion.]
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31677609
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32160433
+|abstract=The success of preclinical neuroprotection studies depends on the model used in animal research. The methodological approaches developed on young animals and widely used for modeling cerebral ischemia/reperfusion injury may not be so effective or not suitable for its modeling on senescent animals, which usage is recommended for preclinical trials. The aim of this study was to investigate the age-related features on the effect of brain reperfusion with different duration (1 and 3 h) after 2-vessel forebrain ischemia on the level of lipid peroxidation ([[LPO]]) products and on the activity of Na+/K+-ATPase in the cerebral cortex of rats aged 22-24 months. We found a later accumulation of [[LPO]] products (3 h instead of 1 h after blood recirculation), specifically triene conjugates and Schiff bases, and a decrease in the activity of Na+/K+-ATPase in the cerebral cortex of aged rats compared to young animals. The data obtained reveal the difference in the molecular and physiological mechanisms of the development of disorders in the brain during ischemia/reperfusion in aged and young animals. The revealed differences in these mechanisms should be consider in developing and testing compounds, which will be further used for the treatment of elderly patients with stroke and ischemic brain damage.
-|mesh-terms=* Adult
+|mesh-terms=* Aging
-* Aged
+* Animals
-* Aged, 80 and over
+* Brain Ischemia
-* Aging
+* Disease Models, Animal
-* Alzheimer Disease
+* Lipid Peroxidation
-* Amyloid Precursor Protein Secretases
+* Rats
-* Amyloid beta-Peptides
+* Reperfusion Injury
-* Androgens
+* Sodium-Potassium-Exchanging ATPase
-* Aspartic Acid Endopeptidases
+|keywords=* Na+/K+-ATPase
-* Cognition
+* aging
-* Cognitive Dysfunction
+* brain
-* Cyclic AMP Response Element-Binding Protein
+* lipid peroxidation
-* Female
+* oxidative stress
-* Hippocampus
+* stroke
-* Humans
-* Learning
-* MAP Kinase Signaling System
-* Male
-* Middle Aged
-* Neoplasm Proteins
-* Phosphorylation
-* Protein Kinase C
-* Receptors for Activated C Kinase
-* tau Proteins
-|keywords=* Androgens
-* Cognition
-* Hippocampus
-* Protein kinase C
-* Spatial memory
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6984714
 }}
+==LRP1==
 {{medline-entry
-|title=Modulation of Neural and Muscular Adaptation Processes During Resistance Training by Fish Protein Ingestions in Older Adults.
+|title=Drug Targeting of Plasminogen Activator Inhibitor-1 Inhibits Metabolic Dysfunction and Atherosclerosis in a Murine Model of Metabolic Syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31596471
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32268785
+|abstract=Enhanced expression of PAI-1 (plasminogen activator inhibitor-1) has been implicated in atherosclerosis formation in humans with obesity and metabolic syndrome. However, little is known about the effects of pharmacological targeting of PAI-1 on atherogenesis. This study examined the effects of pharmacological PAI-1 inhibition on atherosclerosis formation in a murine model of obesity and metabolic syndrome. Approach and Results: LDL receptor-deficient ([i]ldlr[/i] ) mice were fed a Western diet high in cholesterol, fat, and sucrose to induce obesity, metabolic dysfunction, and atherosclerosis. Western diet triggered significant upregulation of PAI-1 expression compared with normal diet controls. Addition of a pharmacological PAI-1 inhibitor (either PAI-039 or MDI-2268) to Western diet significantly inhibited obesity and atherosclerosis formation for up to 24 weeks without attenuating food consumption. Pharmacological PAI-1 inhibition significantly decreased macrophage accumulation and cell senescence in atherosclerotic plaques. Recombinant PAI-1 stimulated smooth muscle cell senescence, whereas a PAI-1 mutant defective in [[LRP1]] (LDL receptor-related protein 1) binding did not. The prosenescent effect of PAI-1 was blocked by PAI-039 and R2629, a specific anti-[[LRP1]] antibody. PAI-039 significantly decreased visceral adipose tissue inflammation, hyperglycemia, and hepatic triglyceride content without altering plasma lipid profiles. Pharmacological targeting of PAI-1 inhibits atherosclerosis in mice with obesity and metabolic syndrome, while inhibiting macrophage accumulation and cell senescence in atherosclerotic plaques, as well as obesity-associated metabolic dysfunction. PAI-1 induces senescence of smooth muscle cells in an [[LRP1]]-dependent manner. These results help to define the role of PAI-1 in atherosclerosis formation and suggest a new plasma-lipid-independent strategy for inhibiting atherogenesis.
+|mesh-terms=* Animals
-|keywords=* Aging
+* Atherosclerosis
-* Alaska pollack protein
+* Cellular Senescence
-* Motor unit identification
+* Diet, Western
-* Multichannel surface electromyography
+* Disease Models, Animal
-* Nutritional supplementation
+* Indoleacetic Acids
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7164534
+* Macrophages
+* Metabolic Syndrome
+* Mice
+* Mice, Knockout
+* Obesity
+* Plaque, Atherosclerotic
+* Plasminogen Activator Inhibitor 1
+* Receptors, LDL
+|keywords=* atherosclerosis
+* cellular senescence
+* fibrinolysis
+* metabolic syndrome
+* muscle, smooth
+* obesity
+* plasminogen activator inhibitor-1
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7255962
 }}
-{{medline-entry
+==LRP6==
-|title=Antipsychotic Polypharmacy in Older Adult Asian Patients With Schizophrenia: Research on Asian Psychotropic Prescription Pattern.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31480982
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Antipsychotic Agents
-* Asian Continental Ancestry Group
-* Female
-* Humans
-* Male
-* Middle Aged
-* Polypharmacy
-* Schizophrenia
-|keywords=* Asian
-* antipsychotic polypharmacy
-* older adult patients
-* schizophrenia
-|full-text-url=https://sci-hub.do/10.1177/0891988719862636
-}}
 {{medline-entry
-|title=A pleiotropic role for exosomes loaded with the amyloid β precursor protein carboxyl-terminal fragments in the brain of Down syndrome patients.
+|title=Low-density lipoprotein receptor-related protein 6-mediated signaling pathways and associated cardiovascular diseases: diagnostic and therapeutic opportunities.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31479861
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32076828
+|abstract=Low-density lipoprotein receptor-related protein 6 ([[LRP6]]) is a member of the low-density lipoprotein receptors (LDLRs) family and accumulating evidence points to the critical role of [[LRP6]] in cardiovascular health and homeostasis. In addition to presenting the well-appreciated roles in canonical signaling regulating blood pressure, blood glucose, lipid metabolism, atherosclerosis, cardiac valve disease, cardiac development, Alzheimer's disease and tumorigenesis, [[LRP6]] also inhibits non-canonical Wnt signals that promote arterial smooth muscle cell proliferation and vascular calcification. Noticeably, the role of [[LRP6]] is displayed in cardiometabolic disease, an increasingly important clinical burden with aging and obesity. The prospect for cardiovascular diseases treatment via targeting [[LRP6]]-mediated signaling pathways may improve central blood pressure and lipid metabolism, and reduce neointima formation and myocardial ischemia-reperfusion injury. Thus, a deep and comprehensive understanding of [[LRP6]] structure, function and signaling pathways will contribute to clinical diagnosis, therapy and new drug development for [[LRP6]]-related cardiovascular diseases.
-|mesh-terms=* Amyloid beta-Protein Precursor
+|mesh-terms=* Aging
-* Brain
+* Animals
-* Down Syndrome
+* Cardiovascular Diseases
-* Exosomes
 * Humans
-|keywords=* APP
+* Low Density Lipoprotein Receptor-Related Protein-6
-* APP-CTFs
+* Muscle, Smooth, Vascular
-* Aging
+* Myocytes, Smooth Muscle
-* Brain
+* Obesity
-* Down syndrome
-* Exosomes
-* Extracellular vesicles
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6960325
-}}
-==APPL1==
-{{medline-entry
-|title=Insulin and adipokine signaling and their cross-regulation in postmortem human brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31539648
-|mesh-terms=* Adipokines
-* Aging
-* Brain
-* Humans
-* Insulin
-* Leptin
-* Postmortem Changes
 * Signal Transduction
-|keywords=* Adipokine
+* Structure-Activity Relationship
-* Adiponectin receptors
+* Vascular Calcification
-* Alzheimer's disease–related dementias
+* Wnt Signaling Pathway
-* Leptin receptors
+|keywords=#f
-* Postmortem brain
+|full-text-url=https://sci-hub.do/10.1007/s00439-020-02124-8
-* Type 2 diabetes
-* insulin signaling
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6960343
 }}
-==AQP3==
+==LRRK2==
 {{medline-entry
-|title=Transbuccal platform for delivery of lipogenic actives to facial skin: Because fat matters.
+|title=Parkinson's disease-related Leucine-rich repeat kinase 2 modulates nuclear morphology and genomic stability in striatal projection neurons during aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32592290
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32075681
+|abstract=Multiple missense mutations in Leucine-rich repeat kinase 2 ([[LRRK2]]) are associated with familial forms of late onset Parkinson's disease (PD), the most common age-related movement disorder. The dysfunction of dopamine transmission contributes to PD-related motor symptoms. Interestingly, [[LRRK2]] is more abundant in the dopaminoceptive striatal spiny projection neurons (SPNs) compared to the dopamine-producing nigrostriatal dopaminergic neurons. Aging is the most important risk factor for PD and other neurodegenerative diseases. However, whether [[LRRK2]] modulates the aging of SPNs remains to be determined. We conducted RNA-sequencing (RNA-seq) analyses of striatal tissues isolated from Lrrk2 knockout (Lrrk2 ) and control (Lrrk2 ) mice at 2 and 12 months of age. We examined SPN nuclear DNA damage and epigenetic modifications; SPN nuclear, cell body and dendritic morphology; and the locomotion and motor skill learning of Lrrk2  and Lrrk2  mice from 2 to 24 months of age. Considering the strength of cell cultures for future mechanistic studies, we also performed preliminary studies in primary cultured SPNs derived from the Lrrk2  and Lrrk2  mice as well as the PD-related Lrrk2 G2019S and R1441C mutant mice. Lrrk2-deficiency accelerated nuclear hypertrophy and induced dendritic atrophy, soma hypertrophy and nuclear invagination in SPNs during aging. Additionally, increased nuclear DNA damage and abnormal histone methylations were also observed in aged Lrrk2  striatal neurons, together with alterations of molecular pathways involved in regulating neuronal excitability, genome stability and protein homeostasis. Furthermore, both the PD-related Lrrk2 G2019S mutant and [[LRRK2]] kinase inhibitors caused nuclear hypertrophy, while the Lrrk2 R1441C mutant and γ-Aminobutyric acid type A receptor (GABA-AR) inhibitors promoted nuclear invagination in the cultured SPNs. On the other hand, inhibition of neuron excitability prevented the formation of nuclear invagination in the cultured Lrrk2  and R1441C SPNs. Our findings support an important physiological function of [[LRRK2]] in maintaining nuclear structure integrity and genomic stability during the normal aging process, suggesting that PD-related [[LRRK2]] mutations may cause the deterioration of neuronal structures through accelerating the aging process.
+|keywords=* And aging
-|keywords=* adipocytes
+* Dendritic hypotrophy
-* aging
+* Excitability
-* cosmetics
+* G2019S
-* face
+* GABAA
-* fat pads
+* LRRK2
-* integument
+* Nuclear DNA damage
-* subcutis
+* Nuclear hypertrophy
-* wrinkles
+* Nuclear invagination
-|full-text-url=https://sci-hub.do/10.1002/term.3087
+* Parkinson’s disease
+* R1441C
+* Striatal spiny projection neuron
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031993
 }}
-==AR==
+==MBP==
 {{medline-entry
-|title=Mechanisms of Androgen Receptor Agonist- and Antagonist-Mediated Cellular Senescence in Prostate Cancer.
+|title=Demyelination associated with chronic arsenic exposure in Wistar rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32650419
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32171569
+|abstract=Inorganic arsenic is among the major contaminants of groundwater in the world. Worldwide population-based studies demonstrate that chronic arsenic exposure is associated with poor cognitive performance among children and adults, while research in animal models confirms learning and memory deficits after arsenic exposure. The aim of this study was to investigate the long-term effects of environmentally relevant arsenic exposure in the myelination process of the prefrontal cortex (PFC) and corpus callosum (CC). A longitudinal study with repeated follow-up assessments was performed in male Wistar rats exposed to 3 ppm sodium arsenite in drinking water. Animals received the treatment from gestation until 2, 4, 6, or 12 months of postnatal age. The levels of myelin basic protein ([[MBP]]) were evaluated by immunohistochemistry/histology and immunoblotting from the PFC and CC. As plausible alterations associated with demyelination, we considered mitochondrial mass (VDAC) and two axonal damage markers: amyloid precursor protein (APP) level and phosphorylated neurofilaments. To analyze the microstructure of the CC in vivo, we acquired diffusion-weighted images at the same ages, from which we derived metrics using the tensor model. Significantly decreased levels of [[MBP]] were found in both regions together with significant increases of mitochondrial mass and slight axonal damage at 12 months in the PFC. Ultrastructural imaging demonstrated arsenic-associated decreases of white matter volume, water diffusion anisotropy, and increases in radial diffusivity. This study indicates that arsenic exposure is associated with a significant and persistent negative impact on microstructural features of white matter tracts.
+|mesh-terms=* Aging
-|keywords=* PKB/Akt
+* Amyloid beta-Protein Precursor
-* Src
-* androgen receptor antagonist
-* antiandrogen
-* bipolar androgen therapy
-* cellular senescence
-* prostate cancer
-* supraphysiological androgen levels
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7408918
-}}
-{{medline-entry
-|title=Interleukin-23 Represses the Level of Cell Senescence Induced by the Androgen Receptor Antagonists Enzalutamide and Darolutamide in Castration-Resistant Prostate Cancer Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32562083
-|keywords=* Androgen receptor antagonists
-* Cellular senescence
-* Interleukin-23
-* Prostate cancer spheroids
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7335377
-}}
-{{medline-entry
-|title=A Landscape of Murine Long Non-Coding RNAs Reveals the Leading Transcriptome Alterations in Adipose Tissue during Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32460027
-|keywords=* adipocyte
-* adipose tissue
-* aging
-* lncRNA
-* long non-coding RNA
-* non-coding RNA
-* transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7603645
-}}
-{{medline-entry
-|title=Senolytic compounds control a distinct fate of androgen receptor agonist- and antagonist-induced cellular senescent LNCaP prostate cancer cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32351687
-|keywords=* Akt inhibitor
-* Antiandrogen
-* Bcl-2 family inhibitor
-* Bipolar androgen therapy
-* Cellular senescence
-* HSP90 inhibitor
-* Prostate cancer
-* Senolytic compounds
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7183592
-}}
-{{medline-entry
-|title=Role of gut microbiota in sex- and diet-dependent metabolic disorders that lead to early mortality of androgen receptor-deficient male mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32017595
-|mesh-terms=* Adipocytes
-* Adipose Tissue
 * Animals
-* Anti-Bacterial Agents
+* Arsenic Poisoning
-* Diet
+* Arsenites
-* Diet, High-Fat
+* Axons
-* Feces
+* Corpus Callosum
-* Female
+* Demyelinating Diseases
-* Gastrointestinal Microbiome
+* Diffusion Tensor Imaging
-* Lipid Metabolism
+* Drinking Water
-* Longevity
+* Immunohistochemistry
 * Male
-* Metabolic Diseases
+* Mitochondria
-* Mice
+* Myelin Basic Protein
-* Mice, Inbred C57BL
+* Neurofilament Proteins
-* Mice, Knockout
+* Prefrontal Cortex
-* Obesity
+* Rats
-* Receptors, Androgen
+* Rats, Wistar
-* Sex Characteristics
+* Sodium Compounds
-|keywords=* androgen-insensitive syndrome
+* White Matter
-* longevity
+|keywords=* Amyloid
-* metabolic syndrome
+* Anisotropy
-* testosterone
+* Arsenic
-* type 2 diabetes
+* Axonal damage
-|full-text-url=https://sci-hub.do/10.1152/ajpendo.00461.2019
+* DTI
+* Demyelination
+* Development
+* MRI
+* Microstructure
+* Mitochondria
+|full-text-url=https://sci-hub.do/10.1016/j.taap.2020.114955
 }}
 {{medline-entry
-|title=A jaboticaba extract prevents prostatic damage associated with aging and high-fat diet intake.
+|title=Natural killer cells as participants in pathogenesis of rat experimental autoimmune encephalomyelitis (EAE): lessons from research on rats with distinct age and strain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32003372
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32140045
+|abstract=Natural killer (NK) cells, influencing dendritic cell (DC)-mediated CD4+ lymphocyte priming in draining lymph nodes (dLNs) and controlling spinal cord (SC) infiltration with encephalitogenic CD4+T lymphocytes, modulate EAE (multiple sclerosis model). This study examined their putative contribution to age-related differences in EAE development in Dark Agouti (DA) (exhibiting age-related decrease in EAE susceptibility) and Albino Oxford (AO) (becoming susceptible to EAE with aging) rats. Aging increased NK cell number in dLNs from rats of both strains. In AO rats, but not in DA ones, it also increased the numbers of IFN-γ-producing NK cells (important for DC activation) and activated/matured DCs, thereby increasing activated/matured DC/conventional Foxp3-CD4+ cell ratio and activated CD25+Foxp3-CD4+ cell number. Aging in DA rats diminished activated/matured DC/conventional Foxp3-CD4+ cell ratio and activated Foxp3-CD4+ cell number. However, [[MBP]]-stimulated CD4+ cell proliferation did not differ in dLN cell cultures from young and aged AO rats (as more favorable activated/matured DC/Foxp3-CD4+ cell ratio was abrogated by lower intrinsic CD4+ cell proliferative capacity and a greater regulatory CD25+Foxp3+CD4+ lymphocyte frequency), but was lower in those from aged compared with young DA rats. At SC level, aging shifted Foxp3-CD4+/cytotoxic CX3CR1+ NK cell ratio towards the former in AO rats, so it was less favorable in aged AO rats exhibiting prolonged neurological deficit compared with their DA counterparts. The study showed strain and age differences in number of IFN-γ-producing NK cells in EAE rat dLNs, and suggested that their pathogenetic relevance depends on frequency and/or activity of other cells involved in CD4+ T cell (auto)immune response.
-|mesh-terms=* Aging
+|keywords=* EAE
-* Animals
+* NK cells
-* Cell Proliferation
+* aging
-* Diet, High-Fat
+* dendritic cells
-* Male
+* strain differences
-* Mice
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7050050
-* Myrtaceae
+}}
-* Plant Extracts
+==MDH1==
-* Prostate
+{{medline-entry
+|title=Oxidative Damage to the TCA Cycle Enzyme [[MDH1]] Dysregulates Bioenergetic Enzymatic Activity in the Aged Murine Brain.
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32175745
+|abstract=Aging can have profound effects on the mammalian brain leading to neurodegeneration and cognitive impairment. The brain has exceptionally high-energy requirements and is particularly susceptible to damage within its bioenergetic pathways. Here, we asked how the bioenergetic proteome of the murine brain changed with age and how this might affect brain function. Using label-free LC-MS/MS proteomics for the discovery phase and quantitative multiple reaction monitoring LC-MRM-MS/MS for the validation phase, we found dysregulated expression of multiple components of the tricarboxylic acid cycle, which is key for mitochondrial energy production, including SULA2, IDH1, IDH2, SDHB, PDHB, [[MDH1]], FH1, and NDUFS3, in old murine brains. We also saw that the oxidoreductases, thioredoxin and glutaredoxin, were significantly down-regulated in the old mouse brain and showed through MS that this correlated with the accumulation of trioxidation in the key metabolic enzyme [[MDH1]] at Cys137. 3D modeling of [[MDH1]] predicted that the damaged sites were located at the protein active zone, and enzymatic kinetic analysis confirmed that [[MDH1]] function was significantly reduced in the old mouse brain. These findings identify the tricarboxylic acid cycle as a key target of degenerative protein modifications with deleterious effects on the aging brain's bioenergetic function.
-|full-text-url=https://sci-hub.do/10.1039/c9fo02621e
+|keywords=* DPM
+* MRM
+* TCA cycle
+* aging
+* brain
+|full-text-url=https://sci-hub.do/10.1021/acs.jproteome.9b00861
 }}
+==MET==
 {{medline-entry
-|title=Identifying blood-specific age-related DNA methylation markers on the Illumina MethylationEPIC® BeadChip.
+|title=Leisure-time physical activity volume, intensity, and duration from mid- to late-life in U.S. subpopulations by race and sex. The Atherosclerosis Risk In Communities (ARIC) Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31546163
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32170049
+|abstract=Mitigating age-related disease and disability presents challenges. Physical activity (PA) may be influential for prolonging health and functioning, warranting characterization of its patterns over the life course in population-based data. With the availability of up to three self-reported assessments of past year leisure-time PA (LTPA) over multiple decades in 15,036 participants (26% African American; 55% women; mean baseline age=54; median follow-up=23 years) from the Atherosclerosis Risk in Communities (ARIC) Study sampled from four U.S. communities, race-sex-stratified trajectories of average weekly intensity (metabolic equivalent of task ([[MET]])), duration (hours), and energy expenditure or volume ([[MET]]-h) of LTPA were developed from age 45 to 90 using joint models to accommodate expected non-ignorable attrition. Declines in weekly LTPA intensity, duration, and volume from age 70 to 90 were observed in white women (2.9 to 1.2 [[MET]]; 2.5 to 0.6 h; 11.1 to 2.6 [[MET]]-h), white men (2.5 to 1.0 [[MET]]; 3.5 to 1.8 h; 15.5 to 6.4 [[MET]]-h), African American women (2.5 to 2.4 [[MET]]; 0.8 to 0.1 h; 6.7 to 6.0 [[MET]]-h), and African American men (2.3 to 1.4 [[MET]]; 1.5 to 0.6 h; 8.0 to 2.3 [[MET]]-h). These data reveal population-wide shifts towards less active lifestyles in older adulthood.
-|mesh-terms=* Adolescent
+|keywords=* exercise
-* Adult
+* healthy aging
-* Aged
+* physical activity
-* Aged, 80 and over
+* retirement
-* Aging
+* successful aging
-* Child
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7093185
-* Child, Preschool
-* Cohort Studies
-* CpG Islands
-* DNA Methylation
-* Forensic Genetics
-* Genetic Markers
-* Humans
-* Infant
-* Infant, Newborn
-* Linear Models
-* Middle Aged
-* Oligonucleotide Array Sequence Analysis
-* Young Adult
-|keywords=* Age
-* CpG sites
-* DNA methylation
-* Forensic age estimation
-* Forensic epigenetics
-* Illumina MethylationEPIC
-|full-text-url=https://sci-hub.do/10.1016/j.forsciint.2019.109944
 }}
-==ARC==
+==MMD==
 {{medline-entry
-|title=The Polymorphism rs2968 of [i]LSS[/i] Gene Confers Susceptibility to Age-Related Cataract.
+|title=Impact and Lessons From the Lifestyle Interventions and Independence for Elders (LIFE) Clinical Trials of Physical Activity to Prevent Mobility Disability.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32877255
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32105353
+|abstract=Walking independently is basic to human functioning. The Lifestyle Interventions and Independence for Elders (LIFE) studies were developed to assess whether initiating physical activity could prevent major mobility disability ([[MMD]]) in sedentary older adults. We review the development and selected findings of the LIFE studies from 2000 through 2019, including the planning phase, the LIFE-Pilot Study, and the LIFE Study. The planning phase and the LIFE-Pilot provided key information for the successful implementation of the LIFE Study. The LIFE Study, involving 1635 participants randomized at eight sites throughout the United States, showed that compared with health education, the physical activity program reduced the risk of the primary outcome of [[MMD]] (inability to walk 400 m: hazard ratio = 0.82; 95% confidence interval = 0.69-0.98; P = .03), and that the intervention was cost-effective. There were no significant effects on cognitive outcomes, cardiovascular events, or serious fall injuries. In addition, the LIFE studies provided relevant findings on a broad range of other outcomes, including health, frailty, behavioral outcomes, biomarkers, and imaging. To date, the LIFE studies have generated a legacy of 109 peer-reviewed publications, 19 ancillary studies, and 38 independently funded grants and clinical trials, and advanced the development of 59 early career scientists. Data and biological samples of the LIFE Study are now publicly available from a repository sponsored by the National Institute on Aging (https://agingresearchbiobank.nia.nih.gov). The LIFE studies generated a wealth of important scientific findings and accelerated research in geriatrics and gerontology, benefiting the research community, trainees, clinicians, policy makers, and the general public. J Am Geriatr Soc 68:872-881, 2020.
-|mesh-terms=* Aged
+|keywords=* aging
-* Aging
+* mobility disability
-* Alleles
+* multicenter trialphysical activity
-* Cataract
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7187344
-* Female
-* Gene Expression Regulation
-* Genetic Association Studies
-* Genetic Predisposition to Disease
-* Genotype
-* Haplotypes
-* Humans
-* Hydroxymethylglutaryl CoA Reductases
-* Intramolecular Transferases
-* Lens, Crystalline
-* Male
-* Middle Aged
-* Polymorphism, Single Nucleotide
-|keywords=* ARC
-* HMGCR
-* LSS
-* SNPs
-* lanosterol
-|full-text-url=https://sci-hub.do/10.1089/dna.2020.5872
 }}
-{{medline-entry
+==MOS==
-|title=Decreased Anti-Müllerian hormone and Anti-Müllerian hormone receptor type 2 in hypothalami of old Japanese Black cows.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32554955
-|keywords=* Müllerian inhibiting substance
-* female reproductive senescence
-* gonadotropin-releasing hormone neuron
-* preoptic area
-* ruminant
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7468072
-}}
 {{medline-entry
-|title=Resveratrol delay the cataract formation against naphthalene-induced experimental cataract in the albino rats.
+|title=Effect of mannan oligosaccharides on the microbiota and productivity parameters of Litopenaeus vannamei shrimp under intensive cultivation in Ecuador.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31746523
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32066764
+|abstract=The white leg Litopenaeus vannamei shrimp is of importance to the eastern Pacific fisheries and aquaculture industry but suffer from diseases such as the recently emerged early mortality syndrome. Many bacterial pathogens have been identified but the L. vannamei microbiota is still poorly known. Using a next-generation sequencing (NGS) approach, this work evaluated the impact of the inclusion in the diet of mannan oligosaccharide, ([[MOS]], 0.5% w/w), over the L. vannamei microbiota and production behavior of L. vannamei under intensive cultivation in Ecuador. The [[MOS]] supplementation lasted for 60 days, after which the shrimp in the ponds were harvested, and the production data were collected. [[MOS]] improved productivity outcomes by increasing shrimp survival by 30%. NGS revealed quantitative differences in the shrimp microbiota between [[MOS]] and control conditions. In the treatment with inclusion of dietary [[MOS]], the predominant phylum was Actinobacteria (28%); while the control group was dominated by the phylum Proteobacteria (30%). [[MOS]] has also been linked to an increased prevalence of Lactococcus- and Verrucomicrobiaceae-like bacteria. Furthermore, under the treatment of [[MOS]], the prevalence of potential opportunistic pathogens, like Vibrio, Aeromonas, Bergeyella and Shewanella, was negligible. This may be attributable to [[MOS]] blocking the adhesion of pathogens to the surfaces of the host tissues. Together, these findings point to the fact that the performance (survival) improvements of the dietary [[MOS]] may be linked to the impact on the microbiota, since bacterial lines with pathogenic potential towards shrimps were excluded in the gut.
-|mesh-terms=* Animals
+|mesh-terms=* Actinobacteria
-* Cataract
+* Aeromonas
-* Dose-Response Relationship, Drug
+* Animal Feed
-* Male
-* Naphthalenes
-* Rats
-* Rats, Sprague-Dawley
-* Resveratrol
-|keywords=* age-related cataracts
-* aging
-* oxidative stress
-* resveratrol
-|full-text-url=https://sci-hub.do/10.1002/jbt.22420
-}}
-==AREG==
-{{medline-entry
-|title=Targeting amphiregulin ([[AREG]]) derived from senescent stromal cells diminishes cancer resistance and averts programmed cell death 1 ligand (PD-L1)-mediated immunosuppression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31493351
-|mesh-terms=* Amphiregulin
 * Animals
-* Antineoplastic Agents
+* Aquaculture
-* B7-H1 Antigen
+* Bacterial Adhesion
-* Cells, Cultured
+* Ecuador
-* Cellular Senescence
+* Flavobacteriaceae
-* Drug Resistance, Neoplasm
+* Lactococcus
-* Humans
+* Longevity
-* Mice
+* Mannans
-* Mice, Inbred NOD
+* Microbiota
-* Mice, SCID
+* Oligosaccharides
-* Stromal Cells
+* Penaeidae
-* Tumor Microenvironment
+* Proteobacteria
-|keywords=* aging
+* Seafood
-* amphiregulin
+* Shewanella
-* cancer resistance
+* Verrucomicrobia
-* clinical biomarker
+* Vibrio
-* combinational treatment
+|keywords=#f
-* programmed cell death 1 ligand
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7026423
-* senescence-associated secretory phenotype
-* stroma
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826133
 }}
-==ARNT==
+==MPHOSPH6==
 {{medline-entry
-|title=Loss of [[ARNT]] in skeletal muscle limits muscle regeneration in aging.
+|title=Genome-wide Association Analysis in Humans Links Nucleotide Metabolism to Leukocyte Telomere Length.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33064329
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109421
+|abstract=Leukocyte telomere length (LTL) is a heritable biomarker of genomic aging. In this study, we perform a genome-wide meta-analysis of LTL by pooling densely genotyped and imputed association results across large-scale European-descent studies including up to 78,592 individuals. We identify 49 genomic regions at a false dicovery rate (FDR) < 0.05 threshold and prioritize genes at 31, with five highlighting nucleotide metabolism as an important regulator of LTL. We report six genome-wide significant loci in or near SENP7, MOB1B, CARMIL1, PRRC2A, TERF2, and RFWD3, and our results support recently identified PARP1, POT1, ATM, and [[MPHOSPH6]] loci. Phenome-wide analyses in >350,000 UK Biobank participants suggest that genetically shorter telomere length increases the risk of hypothyroidism and decreases the risk of thyroid cancer, lymphoma, and a range of proliferative conditions. Our results replicate previously reported associations with increased risk of coronary artery disease and lower risk for multiple cancer types. Our findings substantially expand current knowledge on genes that regulate LTL and their impact on human health and disease.
+|mesh-terms=* Genome-Wide Association Study
+* Humans
+* Leukocytes
+* Nucleotides
+* Telomere
+|keywords=* Mendelian randomisation
+* age-related disease
+* biological aging
+* telomere length
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7058826
+}}
+==MPI==
-|keywords=* aging
-* hypoxia signaling
-* muscle regeneration
-|full-text-url=https://sci-hub.do/10.1096/fj.202000761RR
-}}
 {{medline-entry
-|title=[Arylhydrocarbon receptor nuclear translocator ([[ARNT]]) in human skin during aging.]
+|title=Age-related decline of lymphatic drainage from the eye: A noninvasive in vivo photoacoustic tomography study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32593246
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32251650
+|abstract=We aim to determine whether lymphatic drainage from the eye changes with age. Using quantitative photoacoustic tomography, groups of young and older mice were studied in the live state. 10 CD-1 mice of 2-3 months (5M/5F) were studied in addition to 13 older mice of 12-13 months (6M/7F). In each of 23 mice, near-infrared tracer (a near-infrared dye, QC-1 conjugated with Bovine Serum Albumin) was injected into the right eye, and imaging of ipsilateral cervical lymph nodes was performed with laser pulses at 11 different wavelengths prior to and 20 min, 2, 4 and 6 h after injection. Mean pixel intensities ([[MPI]]s) of nodes were calculated at each imaging session. The areas under the curves (AUC) were calculated for both groups of mice and compared using the t-test. The slopes of [[MPI]] of each region of interest were compared using the linear mixed model before and after adjusting for sex, body weight and intraocular pressure of the right eye. The mean intraocular pressure of right eyes before injection was similar in older and younger groups (12.77 ± 2.01 mmHg and 12.90 ± 2.38 mmHg, respectively; p = 0.888). In each mouse, the photoacoustic signal was detected in the right cervical lymph nodes at the 2-h time point following tracer injection into the right eye. At the 4 and 6 h imaging times, a steady increase of tracer signal was observed. Areas under the curve in the right cervical nodes were decreased significantly in older mice compared to younger mice (p = 0.007). The slopes of [[MPI]] in the nodes were significantly decreased in old mice compared to young mice both before and after adjusting for sex, body weight and intraocular pressure of the right eye (p = 0.003). In conclusion, lymphatic drainage from the eye is significantly reduced in older eyes. This finding suggests that impaired lymphatic clearance of aqueous humor, proteins and antigens from the eye may contribute to age-related disease of the eye such as glaucoma and inflammatory eye disease.
-|mesh-terms=* Adolescent
+|keywords=* Age-related
-* Adult
-* Aged
-* Aged, 80 and over
 * Aging
-* Aryl Hydrocarbon Receptor Nuclear Translocator
+* Aqueous humor
-* Child
+* Drainage
-* Child, Preschool
+* Eye
-* Dermis
+* Glaucoma
-* Fetus
+* Imaging
-* Fibroblasts
+* In vivo
-* Humans
+* Lymph node
-* Infant
+* Lymphatic
-* Infant, Newborn
+* Mice
-* Skin
+* Photoacoustic tomography
-* Skin Aging
+* Uveoscleral
-* Young Adult
+|full-text-url=https://sci-hub.do/10.1016/j.exer.2020.108029
-|keywords=* ARNT
+}}
-* PCNA
+==MSC==
-* aging
-* fibroblasts
-* skin
-}}
 {{medline-entry
-|title=The E3 ubiquitin ligase STUB1 attenuates cell senescence by promoting the ubiquitination and degradation of the core circadian regulator BMAL1.
+|title=Human Obesity Induces Dysfunction and Early Senescence in Adipose Tissue-Derived Mesenchymal Stromal/Stem Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32041778
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32274385
+|abstract=Chronic inflammatory conditions like obesity may adversely impact the biological functions underlying the regenerative potential of mesenchymal stromal/stem cells ([[MSC]]). Obesity can impair [[MSC]] function by inducing cellular senescence, a growth-arrest program that transitions cells to a pro-inflammatory state. However, the effect of obesity on adipose tissue-derived [[MSC]] in human subjects remains unclear. We tested the hypothesis that obesity induces senescence and dysfunction in human [[MSC]]. [[MSC]] were harvested from abdominal subcutaneous fat collected from obese and age-matched non-obese subjects ([i]n[/i] = 40) during bariatric or kidney donation surgeries, respectively. [[MSC]] were characterized, their migration and proliferation assessed, and cellular senescence evaluated by gene expression of cell-cycle arrest and senescence-associated secretory phenotype markers. [i]In vitro[/i] studies tested [[MSC]] effect on injured human umbilical vein endothelial cells (HUVEC) function. Mean age was 59 ± 8 years, 66% were females. Obese subjects had higher body-mass index (BMI) than non-obese. [[MSC]] from obese subjects exhibited lower proliferative capacities than non-obese-[[MSC]], suggesting decreased function, whereas their migration remained unchanged. Senescent cell burden and phenotype, manifested as [i]p16[/i], [i]p53[/i], [i]IL-6[/i], and [i]MCP-1[/i] gene expression, were significantly upregulated in obese subjects' [[MSC]]. BMI correlated directly with expression of [i]p16[/i], [i]p21[/i], and [i]IL-6[/i]. Furthermore, co-incubation with non-obese, but not with obese-[[MSC]], restored VEGF expression and tube formation that were blunted in injured HUVEC. Human obesity triggers an early senescence program in adipose tissue-derived [[MSC]]. Thus, obesity-induced cellular injury may alter efficacy of this endogenous repair system and hamper the feasibility of autologous transplantation in obese individuals.
+|keywords=* adipose tissue
-|keywords=* E3 ubiquitin ligase
+* cellular dysfunction
-* STIP1 homology and U-box-containing protein 1 (STUB1)
+* cellular senescence
-* brain and muscle ARNT-like 1 (BMAL1, ARNTL, MOP3)
+* mesenchymal stem cells
-* cell cycle regulation
+* obesity
-* circadian clock
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7113401
-* hydrogen peroxide
-* proteasome
-* protein degradation
-* senescence
-* ubiquitylation (ubiquitination)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7135990
 }}
-==ASB7==
 {{medline-entry
-|title=[[ASB7]] Is a Novel Regulator of Cytoskeletal Organization During Oocyte Maturation.
+|title=miR-155-5p inhibition rejuvenates aged mesenchymal stem cells and enhances cardioprotection following infarction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33251222
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32196916
+|abstract=Aging impairs the functions of human mesenchymal stem cells ([[MSC]]s), thereby severely reducing their beneficial effects on myocardial infarction (MI). MicroRNAs (miRNAs) play crucial roles in regulating the senescence of [[MSC]]s; however, the underlying mechanisms remain unclear. Here, we investigated the significance of miR-155-5p in regulating [[MSC]] senescence and whether inhibition of miR-155-5p could rejuvenate aged [[MSC]]s (A[[MSC]]s) to enhance their therapeutic efficacy for MI. Young [[MSC]]s (Y[[MSC]]s) and A[[MSC]]s were isolated from young and aged donors, respectively. The cellular senescence of [[MSC]]s was evaluated by senescence-associated β-galactosidase (SA-β-gal) staining. Compared with Y[[MSC]]s, A[[MSC]]s exhibited increased cellular senescence as evidenced by increased SA-β-gal activity and decreased proliferative capacity and paracrine effects. The expression of miR-155-5p was much higher in both serum and [[MSC]]s from aged donors than young donors. Upregulation of miR-155-5p in Y[[MSC]]s led to increased cellular senescence, whereas downregulation of miR-155-5p decreased A[[MSC]] senescence. Mechanistically, miR-155-5p inhibited mitochondrial fission and increased mitochondrial fusion in [[MSC]]s via the AMPK signaling pathway, thereby resulting in cellular senescence by repressing the expression of Cab39. These effects were partially reversed by treatment with AMPK activator or mitofusin2-specific siRNA (Mfn2-siRNA). By enhancing angiogenesis and promoting cell survival, transplantation of anti-miR-155-5p-A[[MSC]]s led to improved cardiac function in an aged mouse model of MI compared with transplantation of A[[MSC]]s. In summary, our study shows that miR-155-5p mediates [[MSC]] senescence by regulating the Cab39/AMPK signaling pathway and miR-155-5p is a novel target to rejuvenate A[[MSC]]s and enhance their cardioprotective effects.
+|keywords=* mesenchymal stem cells
-|keywords=* ASBs
+* miR-155-5p
-* maternal aging
+* myocardial infarction
-* meiosis
+* rejuvenation
-* oocyte
+* senescence
-* reproduction
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189985
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7674779
 }}
-==ASL==
 {{medline-entry
-|title=Increased blood-brain barrier permeability to water in the aging brain detected using noninvasive multi-TE [[ASL]] MRI.
+|title=Mesenchymal Stem Cell Derived Extracellular Vesicles in Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32910547
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32154253
+|abstract=Aging is associated with high prevalence of chronic degenerative diseases that take a large part of the increasing burden of morbidities in a growing demographic of elderly people. Aging is a complex process that involves cell autonomous and cell non-autonomous mechanisms where senescence plays an important role. Senescence is characterized by the loss of proliferative potential, resistance to cell death by apoptosis and expression of a senescence-associated secretory phenotype (SASP). SASP includes pro-inflammatory cytokines and chemokines, tissue-damaging proteases, growth factors; all contributing to tissue microenvironment alteration and loss of tissue homeostasis. Emerging evidence suggests that the changes in the number and composition of extracellular vesicles (EVs) released by senescent cells contribute to the adverse effects of senescence in aging. In addition, age-related alterations in mesenchymal stem/stromal cells ([[MSC]]s) have been associated to dysregulated functions. The loss of functional stem cells necessary to maintain tissue homeostasis likely directly contributes to aging. In this review, we will focus on the characteristics and role of EVs isolated from senescent [[MSC]]s, the potential effect of [[MSC]]-derived EVs in aging and discuss their therapeutic potential to improve age-related diseases.
 |keywords=* aging
-* aquaporin-4
+* clinical translation
-* arterial spin labeling
+* extracellular vesicles
-* blood-brain barrier
+* mesenchymal stem cells
-* blood-brain interface
+* regenerative medicine
-* water permeability
+* senescence
-|full-text-url=https://sci-hub.do/10.1002/mrm.28496
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7047768
 }}
 {{medline-entry
-|title=Quantitative Cerebrovascular Reactivity in Normal Aging: Comparison Between Phase-Contrast and Arterial Spin Labeling MRI.
+|title=Molecular Mechanisms Contributing to Mesenchymal Stromal Cell Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32849217
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32098040
+|abstract=Mesenchymal stem/stromal cells ([[MSC]]s) are a reservoir for tissue homeostasis and repair that age during organismal aging. Beside the fundamental in vivo role of [[MSC]]s, they have also emerged in the last years as extremely promising therapeutic agents for a wide variety of clinical conditions. [[MSC]] use frequently requires in vitro expansion, thus exposing cells to replicative senescence. Aging of [[MSC]]s (both in vivo and in vitro) can affect not only their replicative potential, but also their properties, like immunomodulation and secretory profile, thus possibly compromising their therapeutic effect. It is therefore of critical importance to unveil the underlying mechanisms of [[MSC]] senescence and to define shared methods to assess [[MSC]] aging status. The present review will focus on current scientific knowledge about [[MSC]] aging mechanisms, control and effects, including possible anti-aging treatments.
+|keywords=* MSC senescence
-|keywords=* MRI
+* in vitro aging
-* aging
+* in vivo aging
-* arterial spin labeling
+* mesenchymal stem/stromal cells (MSC)
-* cerebrovascular reactivity
+* rejuvenating strategies
-* phase-contrast
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072652
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7411174
 }}
 {{medline-entry
-|title=Correcting Task fMRI Signals for Variability in Baseline CBF Improves BOLD-Behavior Relationships: A Feasibility Study in an Aging Model.
+|title=Inhibition of DNA Methyltransferase by RG108 Promotes Pluripotency-Related Character of Porcine Bone Marrow Mesenchymal Stem Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32425745
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32125888
+|abstract=Mesenchymal stem/stromal cells ([[MSC]]s) have been identified in almost all adult human tissues and been used in numerous clinical trials for a variety of diseases. Studies have shown that [[MSC]]s would undergo cellular senescence when cultured over a long term, which is brought on by increased epigenetic modifications, including DNA methylation. However, the mechanism of [[MSC]]s senescence is not well studied. In this study, the effects of RG108, a DNA methyltransferase inhibitor (DNMTi), on senescence, apoptosis, and pluripotency gene expressions in porcine bone marrow (pBM)-[[MSC]]s were investigated. First, we determined the optimized dose and time of RG108 treatment in pBM-[[MSC]]s to be 10 μM for 48 hours, respectively. Under these conditions, the pluripotency genes ([i]NANOG[/i], [i]POU5F1[/i]), the anti-senescence genes ([i]TERT[/i], [i]bFGF[/i]), and the anti-apoptosis gene ([i]BCL2[/i]) were increased, whereas the apoptotic gene ([i]BAX[/i]) was decreased. RG108 protected against apoptosis when pBM-[[MSC]] induces apoptosis with H O  for 1.5 hours. We also found that RG108 significantly induced the expression of [i]NANOG[/i] and [i]POU5F1[/i] by decreasing DNA methylation in gene promoter regions. These results indicate that an optimized dose of RG108 may promote the pluripotency-related character of pBM-[[MSC]]s through improving cellular anti-senescence, anti-apoptosis, and pluripotency, which provide a better cell origin for stem cell therapy.
+|keywords=* RG108
-|keywords=* BOLD deactivation
+* apoptosis
-* aging
+* pluripotency
-* cerebral blood flow
+* porcine bone marrow mesenchymal stem cells
-* domain-general
+* senescence
-* language fMRI
+|full-text-url=https://sci-hub.do/10.1089/cell.2019.0060
-* semantic fluency
-* sensitization
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7205008
 }}
-==ASXL1==
 {{medline-entry
-|title=[[ASXL1]] mutation in clonal hematopoiesis.
+|title=Extracellular Vesicles of Stem Cells to Prevent BRONJ.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31945396
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32119600
+|abstract=Extracellular vesicles (EVs), several tens to hundreds of nanometers in size, are vesicles secreted by cells for intercellular communication. EVs released from mesenchymal stem cells ([[MSC]]-EVs) have the potential to treat multiple diseases. This study aimed to determine the effects of [[MSC]]-EVs on bisphosphonate-related osteonecrosis of the jaw (BRONJ), whose pathogenesis and treatment are not yet established. To this end, zoledronic acid (ZOL) was administered to bone marrow cells and fibroblasts in vitro. In vivo, a BRONJ model was produced by administering ZOL to rats and extracting teeth. Each [[MSC]]-EV-treated and nontreated group was compared histologically and molecularly. In vitro, the nontreated group showed an increased number of β-galactosidase-positive cells and expression of senescence-associated genes [i]p21, pRB[/i] and senescence-related inflammatory cytokines. Conversely, [[MSC]]-EV administration decreased the number of senescent cells and expression levels of [i]p21, pRB[/i] and inflammatory cytokines. In vivo, in the nontreated group, the socket was partially uncovered by the oral epithelium, leaving an exposed bone. Conversely, in the [[MSC]]-EV-treated group, the socket was healed. Besides, in the nontreated group, β-galactosidase-positive cells existed in the socket and colocalized with the CD90 and periostin-positive cells. However, there were few β-galactosidase-positive cells in the [[MSC]]-EV-treated group. Furthermore, gene expression of stem cell markers [i]Bmi1[/i] and [i]Hmga2[/i] and the vascular endothelial marker [i]VEGF[/i] was significantly increased in the [[MSC]]-EV-treated group, compared with that in the nontreated group. These results indicate that [[MSC]]-EVs prevent ZOL-induced senescence in stem cells, osteoblasts, and fibroblasts and reduce inflammatory cytokines. Furthermore, administration of [[MSC]]-EVs prevented senescence of cells involved in wound healing and the spread of chronic inflammation around senescent cells, thereby promoting angiogenesis and bone regeneration and preventing BRONJ.
-|mesh-terms=* Aged
+|keywords=* bisphosphonate-associated osteonecrosis of the jaw
-* Aging
+* cellular senescence
-* Animals
+* exosomes
-* Clonal Evolution
+* mesenchymal stem cells
-* Codon, Nonsense
+* wound healing
-* Hematologic Neoplasms
+* zoledronic acid
-* Hematopoiesis
+|full-text-url=https://sci-hub.do/10.1177/0022034520906793
-* Humans
-* Myeloproliferative Disorders
-* Neoplasm Proteins
-* Repressor Proteins
-|full-text-url=https://sci-hub.do/10.1016/j.exphem.2020.01.002
 }}
-==ATF4==
+==MTOR==
 {{medline-entry
-|title=Endoplasmic Reticulum Stress Mediates Vascular Smooth Muscle Cell Calcification via Increased Release of Grp78-Loaded Extracellular Vesicles.
+|title=The roles of [[MTOR]] and miRNAs in endothelial cell senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33297752
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32246301
+|abstract=Accumulation of senescent cells in vascular endothelium is known to contribute to vascular aging and increases the risk of developing cardiovascular diseases. The involvement of classical pathways such as p53/p21 and p16/pRB in cellular senescence are well described but there are emerging evidence supporting the increasingly important role of mammalian target of rapamycin ([[MTOR]]) as driver of cellular senescence via these pathways or other effector molecules. MicroRNAs (miRNAs) are a highly conserved group of small non-coding RNAs (18-25 nucleotides), instrumental in modulating the expression of target genes associated with various biological and cellular processes including cellular senescence. The inhibition of [[MTOR]] activity is predominantly linked to cellular senescence blunting and prolonged lifespan in model organisms. To date, known miRNAs regulating [[MTOR]] in endothelial cell senescence remain limited. Herein, this review discusses the roles of [[MTOR]] and [[MTOR]]-associated miRNAs in regulating endothelial cell senescence, including the crosstalk between [[MTOR]] Complex 1 ([[MTOR]]C1) and cell cycle pathways and the emerging role of [[MTOR]]C2 in cellular senescence. New insights on how [[MTOR]] and miRNAs coordinate underlying molecular mechanisms of endothelial senescence will provide deeper understanding and clarity to the complexity of the regulation of cellular senescence.
+|keywords=* Endothelium
-|keywords=* aging
+* MTOR
-* arteries
+* MicroRNAs
-* endoplasmic reticulum
+* Senescence
-* vascular calcification
+* Vascular aging
-* warfarin
+|full-text-url=https://sci-hub.do/10.1007/s10522-020-09876-w
-|full-text-url=https://sci-hub.do/10.1161/ATVBAHA.120.315506
 }}
-==ATF6==
+==MTR==
 {{medline-entry
-|title=Cellular proteostasis decline in human senescence.
+|title=Amide proton transfer-weighted magnetic resonance imaging of human brain aging at 3 Tesla.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33257563
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32269932
+|abstract=Amide proton transfer-weighted (APTw) imaging has been revealed to hold great potential in the diagnosis of several brain diseases. The purpose of this proof-of-concept study was to evaluate the feasibility and value of APTw magnetic resonance imaging (MRI) in characterizing normal brain aging. A total of 106 healthy subjects were recruited and scanned at 3.0 Tesla, with APTw and conventional magnetization transfer (MT) sequences. Quantitative image analyses were performed in 12 regions of interest (ROIs) for each subject. The APTw or MT ratio ([[MTR]]) signal differences among five age groups (young, mature, middle-aged, young-old, and middle-old) were assessed using the one-way analysis of variance, with the Benjamini-Hochberg correction for multiple comparisons. The relationship between APTw and [[MTR]] signals and the age dependencies of APTw and [[MTR]] signals were assessed using the Pearson correlation and non-linear regression. There were no significant differences between the APTw or [[MTR]] values for males and females in any of the 12 ROIs analyzed. Among the five age groups, there were significant differences in the three white matter regions in the temporal, occipital, and frontal lobes. Overall, the mean APTw values in the older group were higher than those in the younger group. Positive correlations were observed in relation to age in most brain regions, including four with significant positive correlations (r=0.2065-0.4182) and five with increasing trends. As a comparison, the mean [[MTR]] values did not appear to be significantly different among the five age groups. In addition, the mean APTw and [[MTR]] values revealed significant positive correlations in 10 ROIs (r=0.2214-0.7269) and a significant negative correlation in one ROI (entorhinal cortex, r=-0.2141). Our early results show that the APTw signal can be used as a promising and complementary imaging biomarker with which normal brain aging can be evaluated at the molecular level.
+|keywords=* Aging
+* amide proton transfer imaging
+* biomarkers
+* chemical exchange saturation transfer (CEST)
+* molecular imaging
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7136735
+}}
+==NLRP3==
-|keywords=* UPR
-* chaperones
-* heat shock response
-* protein homeostasis
-* senescence
-|full-text-url=https://sci-hub.do/10.1073/pnas.2018138117
-}}
 {{medline-entry
-|title=Impact of endoplasmic reticulum stress on oocyte aging mechanisms.
+|title=Ginsenoside Rg1 ameliorates glomerular fibrosis during kidney aging by inhibiting NOX4 and [[NLRP3]] inflammasome activation in SAMP8 mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32514562
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32114413
+|abstract=Aging is closely related to the progress of renal fibrosis, which eventually results in renal dysfunction. Ginsenoside Rg1 (Rg1) has been reported to have an extensive anti-aging effect. However, the role and mechanism of Rg1 in aging-related renal fibrosis remain unclear. The present study aimed to evaluate the protective effect and mechanism of Rg1 in renal fibrosis during kidney aging in a model of SAMP8 mice. Taking SAMR1 mice as the control group, SAMP8 mice were administered Apocynin (50 mg/kg), Tempol (50 mg/kg), or Rg1 (5, 10 mg/kg) intragastrically for 9 weeks as treatment groups. The results showed that the elevated levels of blood urea nitrogen, serum creatinine and senescence-associated β-galactosidase (β-Gal) were markedly decreased, the glomerular mesangial proliferation was significantly alleviated and the increased levels of collagen IV and TGF-β1 were significantly downregulated by Rg1 in SAMP8 mice. In addition, the generation of ROS and the expression of NADHP oxidase 4 (NOX4) in the renal cortex were significantly reduced by Rg1 treatment. The expression levels of [[NLRP3]] inflammasome-related proteins and the inflammation-related cytokine IL-1β were also inhibited by Rg1 treatment in the SAMP8 mice. These results suggested that Rg1 could delay kidney aging and inhibit aging-related glomerular fibrosis by reducing NOX4-derived ROS generation and downregulating [[NLRP3]] inflammasome expression.
+|keywords=* Ginsenoside Rg1
+* Kidney aging
+* NADPH oxidase 4 (NOX4)
+* NLRP3 inflammasome
+* Renal fibrosis
+|full-text-url=https://sci-hub.do/10.1016/j.intimp.2020.106339
+}}
+==PC==
-|keywords=* ER stress
+{{medline-entry
-* GRP78
+|title=Pacing During 200-m Competitive Masters Swimming.
-* PERK
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32271289
-* eIF2α
+|abstract=Breen, D, Powell, C, and Anderson, R. Pacing during 200-m competitive masters swimming. J Strength Cond Res 34(7): 1903-1910, 2020-Pacing strategies are key to overall performance outcome, particularly in swimming given the large resistive properties of water. However, no studies examining how swimming stroke, gender, age, or performance level affect pacing strategies during 200-m races. This study aimed to examine masters athletes pacing strategies categorized by stroke, gender, age, and performance level. Data were retrieved from World and European masters swimming championships and contained data for 4,272 performances. Performances were coded for stroke, gender, age, and performance classification ([[PC]]). Performance classification was based on comparison to the appropriate masters world record. Performances were then normalized, with split times being expressed as a percentage faster or slower than average 50-m split time to determine relative pace. Coefficient of variation (CV) of 50-m time was examined across splits. The main effect for stroke was examined at each split, whereas gender, age, and [[PC]] were examined for split-1 pace and CV. An alpha level of 0.05 was set to denote statistical significance. A main effect for stroke was identified at each split (all p < 0.001; (Equation is included in full-text article.)-split-1 = 0.292; (Equation is included in full-text article.)-split-2 = 0.040; (Equation is included in full-text article.)-split-3 = 0.058; (Equation is included in full-text article.)-split-4 = 0.162). A main effect for [[PC]] was identified for split-1 pace and CV within all strokes (all p < 0.001), except for breaststroke (both p > 0.775). Masters athletes exhibit different pacing patterns across strokes, whereas lower ranked athletes also display less even pacing and a faster relative start compared with higher-ranked athletes. Individual analyses of pacing strategies may be necessary.
-* endoplasmic reticulum
+|mesh-terms=* Adult
-* mouse oocyte
+* Age Factors
-* oocyte aging
+* Aged
-* salubrinal
+* Aged, 80 and over
-|full-text-url=https://sci-hub.do/10.1093/molehr/gaaa040
+* Aging
+* Athletes
+* Athletic Performance
+* Competitive Behavior
+* Female
+* Humans
+* Male
+* Middle Aged
+* Sex Factors
+* Swimming
+|keywords=#f
+|full-text-url=https://sci-hub.do/10.1519/JSC.0000000000003621
 }}
 {{medline-entry
-|title=ER stress activates immunosuppressive network: implications for aging and Alzheimer's disease.
+|title=Prostate cancer in Pennsylvania: The role of older age at diagnosis, aggressiveness, and environmental risk factors on treatment and mortality using data from the Pennsylvania Cancer Registry.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32279085
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32212232
+|abstract=To assess: (a) cancer treatment in prostate cancer survivors ([[PC]]S) by age at diagnosis (ADx) and prostate cancer ([[PC]]) aggressiveness; (b) potential impact on [[PC]] mortality; and (c) these results in the context of environmental/behavioral risk factors on [[PC]]S in Pennsylvania. Prostate cancer survivors ages ≥40 years were identified from the 2004-2014 Pennsylvania Cancer Registry ([[PC]]R). Demographic/clinical descriptors and [[PC]] treatment were extracted from [[PC]]R. Prostate cancer aggressiveness was defined by clinical/pathologic Gleason score and tumor stage. Logistic and Cox regression analyses tested associations between treatment received and [[PC]]-specific mortality. County-level data from the Pennsylvania BRFSS were used to estimate cancer-related behavioral risk factors (eg, smoking, physical inactivity, fruit/vegetable consumption [FV], alcohol use) and used as covariates. There were 90 694 [[PC]]S ages 40-105 years (mean age = 66.19 years, SD = 9.25) included. Most were non-Hispanic white men (83%). Prostate cancer survivors ≥75 years were least likely to receive any treatment but men ages 65-74 were more likely to receive combined therapies (OR = 1.47; 95% CI 1.28, 1.69) vs [[PC]]S ages 40-54 years, controlling for covariates. Prostate cancer survivors 55-75+ with aggressive [[PC]] who received any treatment vs no definitive treatment had significantly reduced mortality. Men from counties with high obesity and smoking rates were significantly less likely to receive any treatment than men living in counties with lower rates of these risk factors. Prostate cancer survivors who lived in counties with high rates of physical inactivity and had high rates of sufficient FV consumption were slightly more likely to receive cancer treatment vs no definitive treatment compared to men who lived in counties with high rates of physical activity and lower FV consumption. We observed a general age-related decline in receipt of treatment. Prostate cancer survivors ages ≥75 years were significantly less likely to get any cancer treatment compared to younger [[PC]]S. However, most men with more aggressive disease who received any treatment had greatly reduced [[PC]] mortality, regardless of age. Considering environmental/behavioral risk factors may attenuate [[PC]] risk and inform treatment options.
+|keywords=* aging
+* behavioral risk factors
+* geriatric oncology
+* healthy aging
+* prostate cancer survivorship
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7221418
+}}
+==PCNA==
-|keywords=* Ageing
-* Immunometabolism
-* Immunosenescence
-* Immunosuppression
-* Inflammaging
-* Neurodegeneration
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7220864
-}}
 {{medline-entry
-|title=Towards Age-Related Anti-Inflammatory Therapy: Klotho Suppresses Activation of ER and Golgi Stress Response in Senescent Monocytes.
+|title=[Mechanosensitive protein of Hippo regulatory pathway - transcription coactivator with PZD-binding motif (TAZ) in human skin during aging.]
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31972978
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32145162
+|abstract=The aim of this work was to examine the content of transcription coactivator with PZD-binding motif (TAZ) in fibroblasts and blood vessels of human dermis from the development until deep aging (from 20 weeks of pregnancy until 85 years old), and defining of a role of TAZ in age-dependent changes in the number of fibroblasts and blood vessels in the dermis. TAZ, proliferating cells nuclear antigen ([[PCNA]]), endothelial cells marker CD31 were detected with indirect immunohistochemical technique. Results showed that portion of fibroblasts with positive staining for TAZ in the dermis is decreased from 20 weeks of pregnancy to 40 years old. Percent of TAZ positive fibroblasts in dermis is increased since 41 years old until 60-85 years old group. The content of TAZ in blood vessels in the human dermis is decreased sufficiently from 20 weeks of pregnancy until 40 years old followed by an increase from 41 years old. From 61 to 85 years of life, content of TAZ in dermal vessels was not differ from those in 41-60 age group. Age-related changes in the content of TAZ in fibroblasts and blood vessels is not associated with an age-related decrease in total number and percent of [[PCNA]] positive fibroblasts, the number of blood vessels in the dermis.
+|mesh-terms=* Adolescent
+* Adult
+* Aged
+* Aged, 80 and over
+* Aging
+* Child
+* Child, Preschool
+* Dermis
+* Female
+* Fibroblasts
+* Humans
+* Infant
+* Infant, Newborn
+* Middle Aged
+* Pregnancy
+* Protein-Serine-Threonine Kinases
+* Skin Aging
+* Trans-Activators
+* Young Adult
+|keywords=* CD31
+* PCNA
+* TAZ
+* aging
+* blood vessels
+* fibroblasts
+* skin
-|keywords=* ER stress response
-* Golgi apparatus/complex stress response
-* SASP
-* immunosenescence
-* klotho
-* monocytes
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072557
 }}
-==ATG3==
+==PGC==
 {{medline-entry
-|title=Estrogen Signaling Induces Mitochondrial Dysfunction-Associated Autophagy and Senescence in Breast Cancer Cells.
+|title=[Metabolic Alteration in Aging Process: Metabolic Remodeling in White Adipose Tissue by Caloric Restriction].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32244623
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115557
+|abstract=Caloric restriction (CR) improves whole-body metabolism, suppresses various age-related pathophysiological changes, and extends lifespan. The beneficial actions of CR are regulated in growth hormone (GH)/insulin-like growth factor-1 (IGF-1) signal-dependent and -independent manners. To clarify the GH/IGF-1-independent mechanism, we compared gene expression profiles in white adipose tissue (WAT) between CR and GH/IGF-1 suppression, and found that CR upregulated sterol regulatory element-binding protein 1c (SREBP-1c) regulatory gene expression. To validate the impact of SREBP-1c as a beneficial mediator of CR, we compared the responses to CR between wild-type and SREBP-1c knockout (KO) mice. CR extended lifespan, upregulated gene expression involved in FA biosynthesis, activated mitochondrial biogenesis, and suppressed oxidative stress predominantly in WAT. In contrast, most of these findings were not observed in KO mice. Furthermore, SREBP-1c was implicated in CR-associated mitochondrial activation through upregulation of peroxisome proliferator-activated receptor γ coactivator-1α ([[PGC]]-1α), a master regulator of mitochondrial biogenesis. Sirtuin-3 (SIRT3) regulates mitochondrial quality and is also involved in the beneficial actions of CR. We observed that CR upregulated the mature form of SIRT3 protein and mitochondrial intermediate peptidase (MIPEP), a mitochondrial signal peptidase (MtSPase), in WAT. MIPEP cleaved precursor form of SIRT3 to mature form, and activated certain mitochondrial matrix proteins, suggesting that MIPEP might contribute to maintenance of mitochondrial quality during CR via SIRT3 activation. Taken together, CR induces SREBP-1c-dependent metabolic remodeling, including enhancement of FA biosynthesis and mitochondrial activation, via [[PGC]]-1α, and improvement of mitochondria quality via Mipep in WAT, resulting in beneficial actions.
+|mesh-terms=* Adipose Tissue, White
-|keywords=* Estrogen
+* Aging
-* MCF-7
+* Animals
-* MDA-MB-231
+* Caloric Restriction
-* autophagy
+* Gene Expression
+* Humans
+* Longevity
+* Mice
+* Organelle Biogenesis
+* Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
+* Sirtuin 3
+* Sterol Regulatory Element Binding Protein 1
+* Up-Regulation
+|keywords=* caloric restriction (CR)
+* fatty acid biosynthesis
 * mitochondria
-* senescence
+* white adipose tissue (WAT)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7235898
+|full-text-url=https://sci-hub.do/10.1248/yakushi.19-00193-2
 }}
-==ATG5==
 {{medline-entry
-|title=Autophagy and heat-shock response impair stress granule assembly during cellular senescence.
+|title=Kynurenine aminotransferase isoforms display fiber-type specific expression in young and old human skeletal muscle.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33049246
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32068089
+|abstract=Conversion of kynurenine (KYN) to kynurenic acid (KYNA) is the main pathway for free tryptophan degradation in skeletal muscle and has emerged as an important mechanism of how exercise is linked to promotion of mental health. Metabolism of KYN to KYNA mainly depends on the expression of kynurenine aminotransferases (KATs) that is under control of the mitochondria biogenesis regulator [[PGC]]-1α. We therefore hypothesized that expression of KATs would vary between muscle fibers that differ in mitochondrial content, i.e. oxidative type I vs more glycolytic type II muscle fibers. Moreover, we tested the hypothesis that KAT expression differs with age. Single muscle fibers were isolated from biopsies taken from the vastus lateralis muscle in young and old healthy subjects. In young and old subjects the abundance of KAT I, KAT III and KAT IV was greater in Type I than Type II fibers without age-dependent difference in the KAT isoform expressions. The link to mitochondrial content was further seen as the expression of KAT IV correlated to mitochondrial cytochrome c oxidase IV (COX IV) abundance in both fiber types. In conclusion, we describe for the first time the expression pattern of KAT isoforms with respect to specific fiber types and age in human skeletal muscle.
+|keywords=* Aging
-|keywords=* Ageing
+* Kynurenine aminotransferases
-* Cellular senescence
+* Mitochondria
-* Molecular biology
+* Muscle fiber-type
-* Oxidative stress
+* Skeletal muscle
-* Stress granules
+|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110880
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2020.111382
 }}
-==ATG7==
+==PINK1==
 {{medline-entry
-|title=Age-related impairment of autophagy in cervical motor neurons.
+|title=Compression-induced senescence of nucleus pulposus cells by promoting mitophagy activation via the [[PINK1]]/PARKIN pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33290859
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32281308
+|abstract=The current research aimed to explore the possible relationship between [[PINK1]]/PARKIN-mediated mitophagy and the compression-induced senescence of nucleus pulposus cells (NPCs). Therefore, the stages of senescence in NPCs were measured under compression lasting 0, 24 and 48 hours. The mitophagy-related markers, autophagosomes and mitochondrial membrane potential were tested to determine the levels of [[PINK1]]/PARKIN-mediated mitophagy under compression. The [[PINK1]] and PARKIN levels were also measured by immunohistochemistry of human and rat intervertebral disc (IVD) tissues taken at different degenerative stages. A specific mitophagy inhibitor, cyclosporine A (CSA) and a constructed [[PINK1]]-shRNA were used to explore the relationship between mitophagy and senescence by down-regulating the [[PINK1]]/PARKIN-mediated mitophagy levels. Our results indicated that compression significantly enhanced the senescence of NPCs in a time-dependent manner. Also, [[PINK1]]/PARKIN-mediated mitophagy was found to be activated by the extended duration of compression on NPCs as well as the increased degenerative stages of IVD tissues. After inhibition of [[PINK1]]/PARKIN-mediated mitophagy by CSA and [[PINK1]]-shRNA, the senescence of NPCs induced by compression was strongly rescued. Hence, the excessive degradation of mitochondria in NPCs by mitophagy under continuous compression may accelerate the senescence of NPCs. Regulating [[PINK1]]/PARKIN-mediated mitophagy might be a potential therapeutic treatment for IVD degeneration.
+|keywords=* PARKIN pathway
-|keywords=* Aging
+* PINK1
-* Autophagy
+* compression
-* Motor neuron
+* intervertebral disc
-* Neuromuscular dysfunction
+* mitophagy
-* Spinal cord
+* senescence
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.111193
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7214186
 }}
 {{medline-entry
-|title=Comprehensive Bioinformatics Identifies Key microRNA Players in [[ATG7]]-Deficient Lung Fibroblasts.
+|title=Doxorubicin-induced normal breast epithelial cellular aging and its related breast cancer growth through mitochondrial autophagy and oxidative stress mitigated by ginsenoside Rh2.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32527064
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32100342
+|abstract=Clinical dose of doxorubicin (100 nM) induced cellular senescence and various secretory phenotypes in breast cancer and normal epithelial cells. Herein, we reported the detailed mechanism underlying ginsenoside Rh2-mediated NF-κB inhibition, and mitophagy promotion were evaluated by antibody array assay, western blotting analysis, and immunocytostaining. Ginsenoside Rh2 suppressed the protein levels of TRAF6, p62, phosphorylated IKK, and IκB, which consequently inactivated NF-κB activity. Rh2-mediated secretory phenotype was delineated by the suppressed IL-8 secretion. Senescent epithelial cells showed increased level of reactive oxygen species (ROS), which was significantly abrogated by Rh2, with upregulation on SIRT 3 and SIRT 5 and subsequent increase in SOD1 and SOD2. Rh2 remarkably favored mitophagy by the increased expressions of [[PINK1]] and Parkin and decreased level of PGC-1α. A decreased secretion of IL-8 challenged by mitophagy inhibitor Mdivi-1 with an NF-κB luciferase system was confirmed. Importantly, secretory senescent epithelial cells promoted the breast cancer (MCF-7) proliferation while decreased the survival of normal epithelial cells demonstrated by co-culture system, which was remarkably alleviated by ginsenoside Rh2 treatment. These data included ginsenoside Rh2 regulated ROS and mitochondrial autophagy, which were in large part attributed to secretory phenotype of senescent breast epithelial cells induced by doxorubicin. These findings also suggested that ginsenoside Rh2 is a potential treatment candidate for the attenuation of aging related disease.
+|mesh-terms=* Autophagy
+* Breast Neoplasms
+* Cell Culture Techniques
+* Cell Line, Tumor
+* Doxorubicin
+* Drugs, Chinese Herbal
+* Female
+* Ginsenosides
+* Humans
+* Mitochondria
+* Oxidative Stress
+|keywords=* ROS
+* cancer growth
+* cellular senescence
+* chemotherapy
+* ginsenoside Rh2
+* mitophagy
+|full-text-url=https://sci-hub.do/10.1002/ptr.6636
+}}
+==PLK4==
+{{medline-entry
+|title=A novel lncRNA [[PLK4]] up-regulated by talazoparib represses hepatocellular carcinoma progression by promoting YAP-mediated cell senescence.
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32243714
+|abstract=A growing number of studies recognize that long non-coding RNAs (lncRNAs) are essential to mediate multiple tumorigenic processes, including hepatic tumorigenesis. However, the pathological mechanism of lncRNA-regulated liver cancer cell growth remains poorly understood. In this study, we identified a novel function lncRNA, named polo-like kinase 4 associated lncRNA (lncRNA [[PLK4]], GenBank Accession No. RP11-50D9.3), whose expression was dramatically down-regulated in hepatocellular carcinoma (HCC) tissues and cells. Interestingly, talazoparib, a novel and highly potent poly-ADP-ribose polymerase 1/2 (PARP1/2) inhibitor, could increase lncRNA [[PLK4]] expression in HepG2 cells. Importantly, we showed that talazoparib-induced lncRNA [[PLK4]] could function as a tumour suppressor gene by Yes-associated protein (YAP) inactivation and induction of cellular senescence to inhibit liver cancer cell viability and growth. In summary, our findings reveal the molecular mechanism of talazoparib-induced anti-tumor effect, and suggest a potential clinical use of talazoparib-targeted lncRNA [[PLK4]]/YAP-dependent cellular senescence for the treatment of HCC.
-|keywords=* autophagy
+|keywords=* Yes-associated protein
-* bioinformatics
+* cellular senescence
-* functional network analysis
+* hepatocellular carcinoma
-* lung fibrosis
+* polo-like kinase 4 associated lncRNA
-* miR
+* talazoparib
-* proteomics
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7205816
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7312768
 }}
 {{medline-entry
-|title=Regulation of autophagy by DNA G-quadruplexes.
+|title=Differential expression of AURKA/[[PLK4]] in quiescence and senescence of osteosarcoma U2OS cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32420812
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32200684
+|abstract=This study aimed to identify co-expressed differentially expressed genes (DEGs) in quiescence and senescence of osteosarcoma (OS) U2OS cells and investigate their biological functions. GSE94805 from Gene Expression Omnibus database was extracted, involving 12 samples of OS U2OS cells (4 quiescence, 4 senescence, and 4 control samples). After analysis of DEGs by limma package, VENN analysis was performed to identify co-expressed DEGs in quiescence and senescent. The Cytoscape software was used to construct an interactive network of co-expressed DEGs. Finally, box-plot was drawn for the co-expressed DEGs in sub-network. Besides, the relation literatures were selected in GenCLiP database for the co-expressed DEGs. Seven hundred and forty-three DEGs (255 up-regulated genes, 488 down-regulated genes) were obtained in quiescence and 2135 DEGs (1189 up-regulated genes, 946 down-regulated genes) in senescence. Through VENN analysis, 448 DEGs (131 up-regulated genes, 317 down-regulated genes) were co-expressed in quiescent and senescence. In the co-expressed DEGs network, 896 nodes (448 nodes in quiescent, 448 nodes in senescent) were obtained. Finally, 16 co-expressed DEGs were obtained in the sub-network analysis, in which Aurora kinase A (AURKA) and polo-like kinase ([[PLK4]]) had been reported in OS. AURKA and [[PLK4]] might be the key genes in quiescence and senescence of OS U2OS cells.
+|keywords=* AURKA
+* Osteosarcoma
+* PLK4
+* quiescence
+* senescence
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217361
+}}
+==PRDX3==
-|keywords=* G-quadruplex
-* aging
-* astrocytes
-* autophagy
-* neurodegeneration
-* neurons
-|full-text-url=https://sci-hub.do/10.1080/15548627.2020.1769991
-}}
 {{medline-entry
-|title=[[ATG7]] is essential for secretion of iron from ameloblasts and normal growth of murine incisors during aging.
+|title=Proteomic analyses reveal that ginsenoside Rg3([i]S[/i]) partially reverses cellular senescence in human dermal fibroblasts by inducing peroxiredoxin.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31880208
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32148389
+|abstract=The cellular senescence of primary cultured cells is an irreversible process characterized by growth arrest. Restoration of senescence by ginsenosides has not been explored so far. Rg3([i]S[/i]) treatment markedly decreased senescence-associated β-galactosidase activity and intracellular reactive oxygen species levels in senescent human dermal fibroblasts (HDFs). However, the underlying mechanism of this effect of Rg3([i]S[/i]) on the senescent HDFs remains unknown. We performed a label-free quantitative proteomics to identify the altered proteins in Rg3([i]S[/i])-treated senescent HDFs. Upregulated proteins induced by Rg3([i]S[/i]) were validated by real-time polymerase chain reaction and immunoblot analyses. Finally, 157 human proteins were identified, and variable peroxiredoxin (PRDX) isotypes were highly implicated by network analyses. Among them, the mitochondrial [[PRDX3]] was transcriptionally and translationally increased in response to Rg3([i]S[/i]) treatment in senescent HDFs in a time-dependent manner. Our proteomic approach provides insights into the partial reversing effect of Rg3 on senescent HDFs through induction of antioxidant enzymes, particularly [[PRDX3]].
+|keywords=* Ginsenoside Rg3(S)
+* Human dermal fibroblast
+* Label-free quantitative proteomics
+* Restoration
+* Senescence
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7033328
+}}
+==PSMD14==
-|keywords=* ATG7
-* Aging
-* ameloblast
-* autophagy
-* epithelium
-* ferritin
-* hyperplasia
-* iron
-* secretion
-* tooth
-|full-text-url=https://sci-hub.do/10.1080/15548627.2019.1709764
-}}
 {{medline-entry
-|title=Enhancing Autophagy Diminishes Aberrant Ca  Homeostasis and Arrhythmogenesis in Aging Rabbit Hearts.
+|title=Upregulation of deubiquitinase [[PSMD14]] in lung adenocarcinoma (LUAD) and its prognostic significance.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31636573
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32226511
+|abstract=[[PSMD14]] is a 19S-proteasome-associated deubiquitinating enzyme that facilitates protein degradation by the 20S proteasome core particle. Although accumulating evidence indicates that [[PSMD14]] has emerged as a critical oncogenic factor by promoting tumor growth, the expression and function of [[PSMD14]] in non-small cell lung cancer (NSCLC) remain largely unknown. In this study, we assessed [[PSMD14]] expression and correlated it with clinical-pathological features and patient survival in NSCLC. We also determined the roles of [[PSMD14]] in the regulation of lung adenocarcinoma (LUAD) cell growth. The results showed that [[PSMD14]] expression was significantly upregulated in human NSCLC tissues compared with adjacent non-cancerous tissues. The [[PSMD14]] level was associated with tumor size, lymph node invasion, and TNM stage in LUAD patients. Importantly, high [[PSMD14]] expression was associated with poor overall survival (OS) and disease-free survival (DFS) in LUAD patients. Further, knockdown of [[PSMD14]] significantly inhibited cell growth and caused G1 arrest and cellular senescence by increasing p21 stability in LUAD cells. [[PSMD14]] knockdown also promoted cell apoptosis by increasing cleaved caspase-3 levels in H1299 cells. [[PSMD14]] may serve as a potential prognostic marker and therapeutic target for LUAD patients.
+|keywords=* PMSD14
+* apoptosis
+* deubiquitinating enzyme
+* lung adenocarcinoma
+* prognosis
+* senescence
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7086243
+}}
+==PTH==
-|keywords=* aging
+{{medline-entry
-* autophagy
+|title=Parathyroid hormone ameliorates temporomandibular joint osteoarthritic-like changes related to age.
-* calcium
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32154622
-* cardiac physiology
+|abstract=Ageing could be a contributing factor to the progression of temporomandibular joint osteoarthritis (TMJ OA), whereas its pathogenesis and potential therapeutic strategy have not been comprehensively investigated. We generated ageing mouse models (45-week and 60-week; 12-week mice as control) and intermittently injected 45-week mice with parathyroid hormone ([[PTH]](1-34)) or vehicle for 4 weeks. Cartilage and subchondral bone of TMJ were analysed by microCT, histological and immunostaining. Western blot, qRT-PCR, ChIP, ELISA and immunohistochemical analysis were utilized to examination the mechanism of [[PTH]](1-34)'s function. We showed apparent OA-like phenotypes in ageing mice. [[PTH]] treatment could ameliorate the degenerative changes and improve bone microarchitecture in the subchondral bone by activating bone remodelling. Moreover, [[PTH]] inhibited phosphorylation level of Smad3, which can combine with p16  gene promoter region, resulting in reduced senescent cells accumulation and increased cellular proliferation of marrow mesenchymal stem cells (MSCs). ELISA also showed relieved levels of specific senescent-associated secretory phenotype (SASP) in ageing mice after [[PTH]] treatment. In summary, [[PTH]] may reduce the accumulation of senescent cells in subchondral bone by inhibiting p16  and improve bone marrow microenvironment to active bone remodelling process, indicating [[PTH]] administration could be a potential preventative and therapeutic treatment for age-related TMJ OA.
-* ryanodine receptor
+|mesh-terms=* Aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6787934
+* Animals
+* Calcium-Regulating Hormones and Agents
+* Cells, Cultured
+* Disease Models, Animal
+* Male
+* Mice
+* Mice, Inbred C57BL
+* Osteoarthritis
+* Osteogenesis
+* Parathyroid Hormone
+* Temporomandibular Joint
+|keywords=* cellular senescence
+* cyclin-dependent kinase inhibitor P16INK4A
+* marrow mesenchymal stem cells
+* osteoarthritis
+* temporomandibular joint disorders
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7162802
 }}
-==ATM==
+==PTTG1==
 {{medline-entry
-|title=S[[ATM]]F Suppresses the Premature Senescence Phenotype of the [[ATM]] Loss-of-Function Mutant and Improves Its Fertility in [i]Arabidopsis[/i].
+|title=[Down-regulated [[PTTG1]] expression promotes the senescence of human prostate cancer LNCaP-AI].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33143308
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32216239
+|abstract=To investigate the effect of the down-regulated expression of pituitary tumor-transforming gene 1 ([[PTTG1]]) on the senescence of human castration-resistant prostate cancer LNCaP-AI cells. Human castration-resistant prostate cancer LNCaP-AI cells were induced in vitro and transfected with siRNA targeting [[PTTG1]] (the siRNA-[[PTTG1]] group), the reagent lip3000 only (the mock group) or siRNA negative control vector (the NC group). All the cells were cultured in fetal bovine serum (FBS) or charcoal-stripped bovine serum (CSS) and counted with the cell counting chamber. The senescence characteristics of the transfected LNCaP-AI cells were examined by senescence-associated β-galactosidase (SA-β-Gal) staining, and the expressions of the senescence-related β-galactosidase-1-like proteins (Glb1), the cyclin-dependent kinase inhibitors p-21CIP1 and p-27Kip1, and the chromatin-regulating heterochromatin protein 1γ (HP1γ) were detected by Western blot. The expression of [[PTTG1]] in the human prostate cancer LNCaP-AI cells was significantly reduced in the siRNA-[[PTTG1]] group compared with those in the mock and NC groups (0.21 ± 0.01 vs 0.56 ± 0.02 and 0.61 ± 0.02, P < 0.05). Culture with FBS markedly increased while that with CSS decreased the number of LNCaP-AI cells transfected with siRNA, but both FBS and CSS enhanced the proliferation of the LNCaP-AI cells in the mock and NC groups. SA-β-Gal staining revealed that reducing the expression of [[PTTG1]] induced a remarkably higher positive rate of the LNCaP-AI cells in the siRNA-[[PTTG1]] than in the mock and NC groups (［63.5 ± 2.35］% vs ［11.3 ± 1.24］% and ［12.4 ± 1.15］%, P < 0.05). The siRNA-[[PTTG1]] group, in comparison with the mock and NC groups, showed a significantly down-regulated expression of [[PTTG1]] (0.21 ± 0.01 vs 0.56 ± 0.02 and 0.61 ± 0.02, P < 0.05), but up-regulated expressions of p-21CIP1 (0.32 ± 0.03 vs 0.20 ± 0.02 and 0.21 ± 0.03, P < 0.05), p-27Kip1 (0.38 ± 0.02 vs 0.20 ± 0.03 and 0.22 ± 0.01, P < 0.05), Glb1 (0.24 ± 0.01 vs 0.13 ± 0.01 and 0.15 ± 0.01, P < 0.05), and HP1γ (0.41 ± 0.01 vs 0.26 ± 0.01 and 0.27 ± 0.02, P < 0.05) in the LNCaP-AI cells. Down-regulated expression of [[PTTG1]] induces senescence of human castration-resistant prostate cancer LNCaP-AI cells.
+|mesh-terms=* Cell Line, Tumor
+* Cell Proliferation
+* Humans
+* Male
+* Prostatic Neoplasms, Castration-Resistant
+* RNA, Small Interfering
+* Securin
+* beta-Galactosidase
+|keywords=*  LNCaP-AI cell
+*  castration-resistant prostate cancer
+*  cellular senescence
+*  pituitary tumor-transforming gene-1
+* prostate cancer
-|keywords=* ATM
-* DNA damage
-* SATMF
-* fertility
-* leaf senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7662627
 }}
+==RELB==
 {{medline-entry
-|title=[[ATM]] mediated-p53 signaling pathway forms a novel axis for senescence control.
+|title=New control of the senescence barrier in breast cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32949791
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32158912
+|abstract=Normal cells exposed to cancer-causing events respond by triggering cellular senescence, a stress response which halts cell proliferation and constitutes a protective anti-cancer barrier. We have uncovered a previously unknown signaling pathway implicating p21-activated kinase 4 (PAK4) in the control of senescence in breast cancer, via the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) subunit [[RELB]] and the CCAAT-enhancer-binding protein beta (C/EBPβ).
-|keywords=* ATM inhibition
+|keywords=* CEBPB
-* Metabolic reprogrammer
+* Cellular senescence
-* Mitochondria
+* PAK4
-* P53
+* RELB
-* Senescence alleviation
+* p21-activated kinase
-|full-text-url=https://sci-hub.do/10.1016/j.mito.2020.09.002
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7051141
 }}
+==REST==
 {{medline-entry
-|title=Non-canonical [[ATM]]/MRN activities temporally define the senescence secretory program.
+|title=[Brain and Neuronal Aging: Aged Brain Controls via Gene Expression Fidelity and Master Regulatory Factors].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32785991
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115559
+|abstract=Providing plausible strategies for brain aging protection should be a critical concern for countries with large elderly populations including Japan. Age-related cognitive impairments and movement disorders, such as Alzheimer's and Parkinson's diseases, are caused by neurodegeneration that primarily initiates in the hippocampus and the midbrain substantia nigra, respectively. Neurons are postmitotic, and therefore, the accuracy of cellular metabolism should be crucial for maintaining neural functions throughout their life. Thus accuracy of protein synthesis is a critical concern in discussing mechanisms of aging. The essence of the so-called "error catastrophe theory" of aging was on the fidelity of ribosomal translation and/or aminoacylation of tRNA. There is evidence that reduced protein synthesis accuracy results in neurodegeneration. Similarly, reduced proteostasis via autophagy and proteasomes in aging is crucial for protein quality control and well documented as a risk for aging. In both neurodegeneration and protein quality controls, various proteins are involved in their regulation, but recent evidence suggests that repressor element-1 silencing transcription factor ([[REST]]) could be a master regulatory protein that is crucial for orchestrating the neural protecting events in human brain aging. [[REST]] is induced in the aged brain, and protects neurons against oxidative stress and protein toxicity. Interestingly, [[REST]] is identical with neuron-restrictive silencer factor (NRSF), the master regulator of neural development. Thus NRSF/[[REST]] play important roles in both neurogenesis and neurodegeneration. In this review, I summarize the interesting scientific crossover, and discuss the potential use of NRSF/[[REST]] as a pharmaceutical target for controlling aging, particularly in relation to brain aging.
+|mesh-terms=* Aged
+* Aged, 80 and over
+* Aging
+* Animals
+* Brain
+* Gene Expression
+* Gene Expression Regulation, Developmental
+* Humans
+* Neurodegenerative Diseases
+* Protein Biosynthesis
+* Repressor Proteins
+* Ribosomes
+|keywords=* aging
+* brain
+* gene expression
+* neurodegeneration
+* ribosome
+* translational fidelity
+|full-text-url=https://sci-hub.do/10.1248/yakushi.19-00193-4
+}}
+==RET==
-|keywords=* DNA damage response
-* MRN complex
-* NF-κB
-* chromatin
-* senescence secretome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7534619
-}}
 {{medline-entry
-|title=[[ATM]] is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging.
+|title=Resistance exercise training promotes fiber type-specific myonuclear adaptations in older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32201398
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32134710
+|abstract=Aging induces physiological decline in human skeletal muscle function and morphology, including type II fiber atrophy and an increase in type I fiber frequency. Resistance exercise training ([[RET]]) is an effective strategy to overcome muscle mass loss and improve strength, with a stronger effect on type II fibers. In the present study, we sought to determine the effect of a 12-wk progressive [[RET]] program on the fiber type-specific skeletal muscle hypertrophic response in older adults. Nineteen subjects [10 men and 9 women (71.1 ± 4.3 yr)] were studied before and after the 12-wk program. Immunohistochemical analysis was used to quantify myosin heavy chain (MyHC) isoform expression, cross-sectional area (CSA), satellite cell abundance, myonuclear content, and lipid droplet density. [[RET]] induced an increase in MyHC type II fiber frequency and a concomitant decrease in MyHC type I fiber frequency. Mean CSA increased significantly only in MyHC type II fibers (+23.3%, [i]P[/i] < 0.05), but myonuclear content increased only in MyHC type I fibers ([i]P[/i] < 0.05), with no change in MyHC type II fibers. Satellite cell content increased ~40% in both fiber types ([i]P[/i] > 0.05). [[RET]] induced adaptations to the capillary supply to satellite cells, with the distance between satellite cells and the nearest capillary increasing in type I fibers and decreasing in type II fibers. Both fiber types showed similar decrements in intramuscular lipid density with training ([i]P[/i] < 0.05). Our data provide intriguing evidence for a fiber type-specific response to [[RET]] in older adults and suggest flexibility in the myonuclear domain of type II fibers during a hypertrophic stimulus.  In older adults, progressive resistance exercise training ([[RET]]) increased skeletal muscle fiber volume and cross-sectional area independently of myonuclear accretion, leading to an expansion of the myonuclear domain. Fiber type-specific analyses illuminated differential adaptation; type II fibers underwent hypertrophy and exhibited myonuclear domain plasticity, whereas myonuclear accretion occurred in type I fibers in the absence of a robust hypertrophic response. [[RET]] also augmented satellite cell-capillary interaction and reduced intramyocellular lipid density to improve muscle quality.
+|keywords=* aging
-|keywords=* ATM
+* hypertrophy
-* DNA damage response
+* myonuclear domain
-* NF-κB
+* skeletal muscle
-* aging
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191507
-* cellular senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7138542
 }}
-{{medline-entry
+==RHO==
-|title=[[ATM]] suppresses leaf senescence triggered by DNA double-strand break through epigenetic control of senescence-associated genes in Arabidopsis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32163596
-|keywords=*
-Arabidopsis thaliana
-* ATM
-* DNA repair
-* double-strand breaks
-* histone methylation
-* leaf senescence
-|full-text-url=https://sci-hub.do/10.1111/nph.16535
-}}
 {{medline-entry
-|title=Glioblastoma Cells Do Not Affect Axitinib-Dependent Senescence of HUVECs in a Transwell Coculture Model.
+|title=SARS-CoV-2 receptor ACE2 and TMPRSS2 are primarily expressed in bronchial transient secretory cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32098270
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32246845
+|abstract=The SARS-CoV-2 pandemic affecting the human respiratory system severely challenges public health and urgently demands for increasing our understanding of COVID-19 pathogenesis, especially host factors facilitating virus infection and replication. SARS-CoV-2 was reported to enter cells via binding to ACE2, followed by its priming by TMPRSS2. Here, we investigate ACE2 and TMPRSS2 expression levels and their distribution across cell types in lung tissue (twelve donors, 39,778 cells) and in cells derived from subsegmental bronchial branches (four donors, 17,521 cells) by single nuclei and single cell RNA sequencing, respectively. While TMPRSS2 is strongly expressed in both tissues, in the subsegmental bronchial branches ACE2 is predominantly expressed in a transient secretory cell type. Interestingly, these transiently differentiating cells show an enrichment for pathways related to [[RHO]] GTPase function and viral processes suggesting increased vulnerability for SARS-CoV-2 infection. Our data provide a rich resource for future investigations of COVID-19 infection and pathogenesis.
-|mesh-terms=* Ataxia Telangiectasia Mutated Proteins
+|mesh-terms=* Adult
-* Axitinib
+* Aging
-* Cell Line, Tumor
+* Angiotensin-Converting Enzyme 2
-* Cellular Senescence
+* Bronchi
-* Coculture Techniques
+* COVID-19
+* Cells, Cultured
+* Chronic Disease
+* Coronavirus Infections
+* Epithelial Cells
+* Female
+* Gene Expression
 * Gene Expression Profiling
-* Glioblastoma
+* Germany
-* Human Umbilical Vein Endothelial Cells
+* Goblet Cells
 * Humans
-* Phosphorylation
+* Lung
-|keywords=* Axitinib
+* Male
-* endothelial cells
+* Middle Aged
-* glioblastoma
+* Pandemics
-* senescence
+* Peptidyl-Dipeptidase A
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7073100
+* Pneumonia, Viral
+* Reference Standards
+* Sequence Analysis, RNA
+* Serine Endopeptidases
+* Sex Characteristics
+* Single-Cell Analysis
+* Smoking
+* Tissue Banks
+|keywords=*
+FURIN
+* COVID-19
+* Human Cell Atlas
+* epithelial differentiation
+* respiratory tract
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7232010
 }}
+==RPE==
 {{medline-entry
-|title=Declining BRCA-Mediated DNA Repair in Sperm Aging and its Prevention by Sphingosine-1-Phosphate.
+|title=CSF1R blockade induces macrophage ablation and results in mouse choroidal vascular atrophy and [[RPE]] disorganization.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31916095
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32234210
+|abstract=The choroid, which provides vascular supply to the outer retina, demonstrates progressive degeneration in aging and age-related macular degeneration (AMD). However mechanisms that maintain or compromise choroidal homeostasis are obscure. We discovered that the ablation of choroidal macrophages via CSF1R blockade was associated with choroidal vascular atrophy and retinal pigment epithelial ([[RPE]]) changes including structural disruption, downregulation of visual cycle genes, and altered angiogenic factor expression. Suspending CSF1R blockade following ablation enabled spontaneous macrophage regeneration, which fully restored original macrophage distributions and morphologies. Macrophage regeneration was accompanied by arrested vascular degeneration and ameliorated pathological [[RPE]] alterations. These findings suggest that choroidal macrophages play a previously unappreciated trophic role in maintaining choroidal vasculature and [[RPE]] cells, implicating insufficiency in choroidal macrophage function as a factor in aging- and AMD-associated pathology. Modulating macrophage function may constitute a strategy for the therapeutic preservation of the choroid and [[RPE]] in age-related retinal disorders.
+|keywords=* RPE disorganization
-|keywords=* Aging
+* aging
-* DNA fragmentation
+* choroid
-* Gene expression
+* choroidal macrophage
-* Sperm
+* choroidal vasculature
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7065969
+* immunology
+* inflammation
+* mouse
+* neuroscience
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156269
 }}
 {{medline-entry
-|title=BRCA-related [[ATM]]-mediated DNA double-strand break repair and ovarian aging.
+|title=Extracellular microparticles exacerbate oxidative damage to retinal pigment epithelial cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31822904
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32173468
+|abstract=Oxidative stress-induced retinal pigment epithelial cell ([[RPE]]) dysfunction is a primary contributing factor to early dry age-related macular degeneration (AMD). Oxidative injury to the retina may promote extracellular vesicles (EVs) released from [[RPE]]. In this study, we investigated the effects of oxidative-induced [[RPE]] cell-derived microparticles (RMPs) on [[RPE]] cell functions. The oxidative stress induced more RMPs released from [[RPE]] cells in vitro and in vivo, and significant more RMPs were released from aged [[RPE]] cells than that from younger [[RPE]] cells. RMPs were taken up by [[RPE]] cells in a time-dependent manner; however, blockage of CD36 attenuated the uptake process. Furthermore, the decrease of [[RPE]] cell viability by RMPs treatment was associated with an increased expression of cyclin-dependent kinase inhibitors p15 and p21. RMPs enhanced senescence and interrupted phagocytic activity of [[RPE]] cells as well. The present study demonstrated that RMPs produce a strong effect of inducing [[RPE]] cell degeneration. This finding further supports the postulate that RMPs exacerbate oxidative stress damage to [[RPE]] cells, which may uncover a potentially relevant process in the genesis of dry AMD.
-|mesh-terms=* Aging
+|keywords=* Extracellular vesicles
-* Animals
+* Oxidative stress
-* Ataxia Telangiectasia
+* Phagocytosis
-* BRCA1 Protein
+* RPE cell Dysfunction
-* BRCA2 Protein
+* RPE cell-Derived microparticles (RMPs)
-* DNA Breaks, Double-Stranded
+* Retinal pigment epithelial cell (RPE)
-* DNA Repair
+* Senescence
-* Female
+|full-text-url=https://sci-hub.do/10.1016/j.yexcr.2020.111957
-* Fertility
-* Fertility Preservation
-* Humans
-* Mice
-* Oocytes
-* Ovarian Follicle
-* Ovarian Reserve
-* Ovary
-|keywords=*
-          BRCA
-*
-          BRCA1/2
-* DNA repair
-* anti-Mullerian hormone
-* chemotherapy
-* mutations
-* oocyte
-* ovarian aging
-* ovarian reserve
-* ovarian response
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6935693
 }}
 {{medline-entry
-|title=[[ATM]] Deficiency Accelerates DNA Damage, Telomere Erosion, and Premature T Cell Aging in HIV-Infected Individuals on Antiretroviral Therapy.
+|title=Water-based continuous and interval training in older women: Cardiorespiratory and neuromuscular outcomes (WATER study).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31781094
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32145293
+|abstract=The purpose of this study was to investigate the effects of two water-based aerobic programs on cardiorespiratory and neuromuscular outcomes in older women. Forty-one women (60 to 75 years old) volunteered to participate in the study. Participants were randomized into a water-based continuous (CTG; n = 21; 63.9 ± 2.5 years) or an interval (ITG; n = 20; 64.8 ± 3.6 years) aerobic training group. Both training programs were performed for 12 weeks (45-min sessions twice a week), with exercise intensity based on rating of perceived exertion (Borg's [[RPE]] 6-20 Scale). Pre and post training assessments of cardiorespiratory and neuromuscular outcomes were performed. Data analyses were conducted using Generalized Estimating Equations and Bonferroni post-hoc test (α = 0.05). After the intervention, the CTG and the ITG displayed similar improvements in time to exhaustion (8% vs. 11%), peak oxygen uptake (9% vs. 7%), maximal dynamic knee extension strength (5% vs. 6%), dynamic muscular endurance of knee extensors (10% vs. 11%), maximal vastus lateralis electromyographic signal amplitude (13% vs. 35%), as well as an increase in muscle thickness (5% vs. 6%) and decrease in muscle echo intensity (-2% vs. -3%) of the quadriceps femoris. In conclusion, older women benefited from water-based exercise training prescribed based on participants' [[RPE]], with both the interval and the continuous training programs resulting in similar increases in the cardiorespiratory and neuromuscular parameters.
-|mesh-terms=* Anti-Retroviral Agents
+|keywords=* Aerobic capacity
-* Ataxia Telangiectasia Mutated Proteins
+* Aerobic training
-* Cellular Senescence
+* Aging
-* DNA Damage
+* Aquatic exercise
-* HIV Infections
+* Interval exercise
-* Humans
+* Muscle echo intensity
-* T-Lymphocytes
+* Muscle strength
-* Telomere
+* Muscle thickness
-|keywords=* ATM
+|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110914
-* DNA damage repair
-* HIV
-* T cell homeostasis
-* apoptosis
-* immune aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6856652
 }}
+==S100B==
 {{medline-entry
-|title=SMG1 heterozygosity exacerbates haematopoietic cancer development in Atm null mice by increasing persistent DNA damage and oxidative stress.
+|title=Aging protects rat cortical slices against to oxygen-glucose deprivation induced damage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31565865
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32064981
+|abstract= In present study, we aimed to clarify effect of aging on the susceptibility of brain tissue to neurodegeneration induced by ischemia.  Damage induced by oxygen-glucose deprivation (OGD) followed by reoxygenation (REO) were compared in cortical slices prepared from young (3 months of age) and aged (22-24 months of age) male Sprague Dawley rats.  After incubation of the slices in an oxygen and glucose containing control condition, 2,3,5-triphenyl tetrazolium chloride (TTC) staining intensity was found significantly high in aged cortical slices. Although thirty minutes incubation of the slices in OGD medium followed by REO (OGD-REO) caused similar decline in TTC staining in young and aged cortical slices, staining intensity was still significantly higher in the slices prepared from aged animals. Thirty minutes of OGD-REO, on the other hand, also caused more increase in lactate dehydrogenase (LDH) leakage from young slices. While water contents of the slices were almost equal under control condition, it was significantly high in young cortical slices after OGD-REO incubations. In contrary to these findings, OGD and REO caused more increases in [[S100B]] output from aged rat cortical slices. [[S100B]] levels in brain regions including the cerebral cortex were also found higher in aged rats.  All these results indicate that, cortical slices prepared from aged male rats are significantly less responsive to [i]in vitro[/i] OGD-REO induced alterations. Since protein [[S100B]] outputs were almost doubled from aged cortical slices, a possible involvement of this enhanced [[S100B]] output seems to be likely.
-|mesh-terms=* Animals
+|keywords=* Aging
-* Ataxia Telangiectasia Mutated Proteins
+* LDH
-* Carcinogenesis
+* S100B
-* Cells, Cultured
+* edema
-* DNA Damage
+* oxygen-glucose deprivation
-* Embryo, Mammalian
+|full-text-url=https://sci-hub.do/10.1080/00207454.2020.1730830
-* Fibroblasts
-* Gamma Rays
-* Hematologic Neoplasms
-* Heterozygote
-* Kaplan-Meier Estimate
-* Longevity
-* Lymphoma
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Oxidative Stress
-* Protein-Serine-Threonine Kinases
-|keywords=* DNA damage
-* cancer
-* inflammation
-* lymphoma
-* oxidative stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850945
 }}
+==SAG==
 {{medline-entry
-|title=LncRNA RP11-670E13.6, interacted with hnRNPH, delays cellular senescence by sponging microRNA-663a in UVB damaged dermal fibroblasts.
+|title=Neurogenesis in the inner ear: the zebrafish statoacoustic ganglion provides new neurons from a Neurod/Nestin-positive progenitor pool well into adulthood.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31444317
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32165493
+|abstract=The vertebrate inner ear employs sensory hair cells and neurons to mediate hearing and balance. In mammals, damaged hair cells and neurons are not regenerated. In contrast, hair cells in the inner ear of zebrafish are produced throughout life and regenerate after trauma. However, it is unknown whether new sensory neurons are also formed in the adult zebrafish statoacoustic ganglion ([[SAG]]), the sensory ganglion connecting the inner ear to the brain. Using transgenic lines and marker analysis, we identify distinct cell populations and anatomical landmarks in the juvenile and adult [[SAG]]. In particular, we analyze a Neurod/Nestin-positive progenitor pool that produces large amounts of new neurons at juvenile stages, which transitions to a quiescent state in the adult [[SAG]]. Moreover, BrdU pulse chase experiments reveal the existence of a proliferative but otherwise marker-negative cell population that replenishes the Neurod/Nestin-positive progenitor pool at adult stages. Taken together, our study represents the first comprehensive characterization of the adult zebrafish [[SAG]] showing that zebrafish, in sharp contrast to mammals, display continued neurogenesis in the [[SAG]] well beyond embryonic and larval stages.
-|mesh-terms=* Cell Proliferation
+|mesh-terms=* Adult Stem Cells
-* Cellular Senescence
+* Aging
-* Fibroblasts
+* Animals
-* Heterogeneous-Nuclear Ribonucleoprotein Group F-H
+* Animals, Genetically Modified
-* Humans
+* Basic Helix-Loop-Helix Transcription Factors
-* MicroRNAs
+* Cell Differentiation
-* RNA, Long Noncoding
+* Ear, Inner
-* Skin
+* Embryo, Nonmammalian
-* Skin Aging
+* Ganglia, Sensory
-* Ultraviolet Rays
+* Gene Expression Regulation, Developmental
-|keywords=* cellular senescence
+* Hair Cells, Auditory
-* dermal fibroblast
+* Larva
-* lncRNA
+* Nerve Tissue Proteins
-* microRNA
+* Nestin
-* ultraviolet B
+* Neural Stem Cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6738423
+* Neurogenesis
+* Sensory Receptor Cells
+* Stem Cell Niche
+* Zebrafish
+|keywords=* Inner ear
+* Neuronal stem cells
+* PNS
+* Zebrafish
+|full-text-url=https://sci-hub.do/10.1242/dev.176750
 }}
-{{medline-entry
+==SCN2B==
-|title=Tel1/[[ATM]] Signaling to the Checkpoint Contributes to Replicative Senescence in the Absence of Telomerase.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31391264
-|mesh-terms=* Amino Acid Substitution
-* Ataxia Telangiectasia Mutated Proteins
-* Cell Cycle Checkpoints
-* Cell Division
-* Cellular Senescence
-* DNA Damage
-* DNA Replication
-* DNA, Single-Stranded
-* DNA-Binding Proteins
-* Intracellular Signaling Peptides and Proteins
-* Mutant Proteins
-* Protein-Serine-Threonine Kinases
-* Saccharomyces cerevisiae
-* Saccharomyces cerevisiae Proteins
-* Telomerase
-* Telomere
-* Telomere Shortening
-|keywords=* Tel1
-* checkpoint
-* replicative senescence
-* telomere
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6781906
-}}
-==ATP7A==
 {{medline-entry
-|title=Adipocyte-specific disruption of ATPase copper transporting α in mice accelerates lipoatrophy.
+|title=MicroRNA‑449a regulates the progression of brain aging by targeting [[SCN2B]] in SAMP8 mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31396659
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32124967
+|abstract=Our previous study demonstrated that the expression of sodium channel voltage‑gated beta 2 ([[SCN2B]]) increased with aging in senescence‑accelerated mouse prone 8 (SAMP8) mice, and was identified to be associated with a decline in learning and memory, while the underlying mechanism is unclear. In the present study, multiple differentially expressed miRNAs, which may be involved in the process of aging by regulating target genes, were identified in the prefrontal cortex and hippocampus of SAMP8 mice though miRNA microarray analysis. Using bioinformatics prediction, [[SCN2B]] was identified to be one of the potential target genes of miR‑449a, which was downregulated in the hippocampus. Previous studies demonstrated that miR‑449a is involved in the occurrence and progression of aging by regulating a variety of target genes. Therefore, it was hypothesized that miR‑449a may be involved in the process of brain aging by targeting [[SCN2B]]. To verify this hypothesis, the following experiments were conducted: A reverse transcription‑quantitative polymerase chain reaction assay revealed that the expression level of miR‑449a was significantly decreased in the prefrontal cortex and hippocampus of 12‑month old SAMP8 mice; a dual‑luciferase reporter assay verified that miR‑449a regulated [[SCN2B]] expression by binding to the 3'‑UTR 'seed region'; an anti‑Ago co‑immunoprecipitation combined with Affymetrix microarray analyses demonstrated that the target mRNA highly enriched with Ago‑miRNPs was confirmed to be [[SCN2B]]. Finally, overexpression of miR‑449a or inhibition of [[SCN2B]] promoted the extension of hippocampal neurons in vitro. The results of the present study suggested that miR‑449a was downregulated in the prefrontal cortex and hippocampus of SAMP8 mice and may regulate the process of brain aging by targeting [[SCN2B]].
-|mesh-terms=* 3T3-L1 Cells
+|mesh-terms=* Aging
-* Adipocytes
-* Adipose Tissue, White
-* Aging
 * Animals
-* Body Weight
+* Brain
-* Copper
+* Gene Expression Regulation
-* Copper-Transporting ATPases
+* Male
-* Diet, High-Fat
-* Energy Metabolism
-* Insulin Resistance
-* Lipid Metabolism
-* Lipodystrophy
-* Lipolysis
 * Mice
-* Mice, Knockout
+* Mice, Transgenic
-|keywords=* ATP7A
+* MicroRNAs
-* Adipose tissues
+* Voltage-Gated Sodium Channel beta-2 Subunit
-* Copper
+|keywords=#f
-* Insulin resistance
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053848
-* Lipoatrophy
-|full-text-url=https://sci-hub.do/10.1007/s00125-019-4966-2
 }}
-==ATR==
+==SCO1==
 {{medline-entry
-|title=Bloodstain age estimation through infrared spectroscopy and Chemometric models.
+|title=Real-Time PCR Analysis of Metabolism-Related Genes in a Long-Lived Model of C. elegans.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33077037
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32219749
+|abstract=In the nematode Caenorhabditis elegans, the mammalian tumor suppressor p53 ortholog CEP-1 (C. elegans p53-like protein) is associated not only with the stress response, germline apoptosis, and meiotic chromosome segregation but also with longevity through the modification of energy metabolism during aging. The mitochondrial respiration-related gene sco-1 in C. elegans is orthologous to the human [[SCO1]] gene and a target of p53/CEP-1. Using quantitative real-time polymerase chain reaction (PCR) analysis, we recently found that the expression levels of sco-1 gene were increased in wild-type C. elegans in an aging-related manner and decreased in long-lived cep-1 mutants. Here, we describe the relative quantitative strategy using a commercial real-time PCR system to detect more accurately differences in the levels of expressed genes between long-lived and wild-type C. elegans strains. To estimate the expression levels of target genes compared with wild-type using relative quantification, we used the expression levels of an endogenous control gene, such as a housekeeping gene. In addition, it is critical to normalize differences in the expression levels of the common housekeeping gene among the strains analyzed for an accurate comparison of the quantitative expression levels of target genes.
+|keywords=* Caenorhabditis elegans
-|keywords=* Aging
+* Energy metabolism
-* Bloodstains
+* Longevity
-* Chemometric
+* TaqMan real-time PCR
-* Forensic chemistry
+* p53/CEP-1
-* MLR
+|full-text-url=https://sci-hub.do/10.1007/978-1-0716-0471-7_12
-* PLSR
-|full-text-url=https://sci-hub.do/10.1016/j.scijus.2020.07.004
 }}
-{{medline-entry
+==SFPQ==
-|title=Artificial Intelligence and fourier-transform infrared spectroscopy for evaluating water-mediated degradation of lubricant oils.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32887052
-|keywords=* ANN
-* Artificial neural networks
-* FTIR
-* LDA
-* Linear discriminant analysis
-* Lubricant oil aging
-|full-text-url=https://sci-hub.do/10.1016/j.talanta.2020.121312
-}}
 {{medline-entry
-|title=Senescence Induction by Combined Ionizing Radiation and DNA Damage Response Inhibitors in Head and Neck Squamous Cell Carcinoma Cells.
+|title=Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32883016
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32267831
+|abstract=Long noncoding RNAs (lncRNAs) play important roles in the development of vascular diseases. However, the effect of lncRNA NORAD on atherosclerosis remains unknown. This study aimed to investigate the effect NORAD on endothelial cell injury and atherosclerosis. Ox-LDL-treated human umbilical vein endothelial cells (HUVECs) and high-fat-diet (HFD)-fed ApoE  mice were used as [i]in vitro[/i] and [i]in vivo[/i] models. Results showed that NORAD-knockdown induced cell cycle arrest in G0/G1 phase, aggravated ox-LDL-induced cell viability reduction, cell apoptosis, and cell senescence along with the increased expression of Bax, P53, P21 and cleaved caspase-3 and the decreased expression of Bcl-2. The effect of NORAD on cell viability was further verified via NORAD-overexpression. NORAD- knockdown increased ox-LDL-induced reactive oxygen species, malondialdehyde, p-IKBα expression levels and NF-κB nuclear translocation. Proinflammatory molecules ICAM, VCAM, and IL-8 were also increased by NORAD- knockdown. Additionally, we identified the strong interaction of NORAD and IL-8 transcription repressor [[SFPQ]] in HUVECs. In ApoE  mice, NORAD-knockdown increased the lipid disorder and atherosclerotic lesions. The results have suggested that lncRNA NORAD attenuates endothelial cell senescence, endothelial cell apoptosis, and atherosclerosis via NF-κB and p53-p21 signaling pathways and IL-8, in which NORAD-mediated effect on IL-8 might through the direct interaction with [[SFPQ]].
+|keywords=* IL-8
-|keywords=* ATM
+* NORAD
-* ATR
+* cell apoptosis
-* DNA damage response inhibitor
+* cell senescence
-* DNAPK
+* ox-LDL
-* HNSCC
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185106
-* homologous recombination
-* ionizing radiation
-* kinase inhibitor
-* radiosensitivity
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7563880
 }}
-{{medline-entry
+==SGK1==
-|title=Kinetics of thermal degradation and lifetime study of poly(vinylidene fluoride) (PVDF) subjected to bioethanol fuel accelerated aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32775731
-|keywords=* Activation energy
-* Aging
-* Bioethanol fuel
-* Kinetics analysis
-* Lifetime prediction
-* Materials chemistry
-* Materials science
-* Poly(vinylidene fluoride)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7398943
-}}
 {{medline-entry
-|title=Supraphysiological protection from replication stress does not extend mammalian lifespan.
+|title=Epigenetic Regulation of KL (Klotho) via H3K27me3 (Histone 3 Lysine [K] 27 Trimethylation) in Renal Tubule Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32253367
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32223380
+|abstract=KL (klotho) levels decline with age, which is an important mechanistic driver of aging. [i]KL[/i] gene deficiency is associated with hypertension. The purpose of this study is to investigate the potential role of H3K27me3 (histone 3 lysine [K] 27 trimethylation) in the regulation of [i]KL[/i] gene expression and examine the related molecular pathways that may drive kidney cell aging. Kidneys were collected from 6-month-old WT (wild type; young WT), 30-month-old WT (aged WT), and 6- (young) and 20-month-old (aged) [i]KL[/i] mutant mice, respectively. We demonstrated that the H3K27me3 level was increased in kidneys of aged WT and KL mutant mice versus young WT mice. Elevation of H3K27me3 levels was likely due to downregulation of the H3K27 (histone H3 Lys 27)-specific demethylase JMJD3 (the Jumonji domain containing-3) in the aged kidneys. Inhibition of PRC2 (polycomb repressive complex C2; histone trimethyltransferase) decreased the H3K27me3 levels leading to an increase in the expression of KL in cultured primary renal tubule cells assessed by Western blot and [i]KL[/i] promoter activity assays. The chromatin immunoprecipitation qPCR assay revealed that H3K27me3 was physically associated with the [i]KL[/i] promoter region. Furthermore, aging impaired the [[SGK1]] (serum- and glucocorticoid-induced protein kinase 1)/FOXO3a (the forkhead box class O 3a) signaling leading to upregulation of p53 and p16 (aging markers) in the kidney of aged WT mice. KL may regulate the [[SGK1]]/FOXO3 signaling, which was decreased due to KL deficiency. Thus, aging-associated downregulation of [i]KL[/i] gene expression may be partly attributed to upregulation of H3K27me3 levels. Downregulation of KL may impair the [[SGK1]]/FOXO3 signaling contributing to kidney cell aging.
+|keywords=* AKT
-|keywords=* DNA damage
+* EZH2
 * aging
-* cancer
+* mTOR
-* mouse models
+* p53
-* replication stress
+|full-text-url=https://sci-hub.do/10.1161/HYPERTENSIONAHA.120.14642
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185120
 }}
-{{medline-entry
+==SI==
-|title=Assessing the Retest Reliability of Prefrontal EEG Markers of Brain Rhythm Slowing in the Eyes-Closed Resting State.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32253926
-|keywords=* EEG
-* EEG slowing
-* brain aging
-* dominant frequency
-* prefrontal
-|full-text-url=https://sci-hub.do/10.1177/1550059420914832
-}}
 {{medline-entry
-|title=Effects of Hydrogen Peroxide and Sodium Hypochlorite Aging on Properties and Performance of Polyethersulfone Ultrafiltration Membrane.
+|title=Survival time after marked reduction in oral intake in terminally ill noncancer patients: A retrospective study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31635217
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32161695
+|abstract=The prediction of short-term survival is important for noncancer patients and their families. Although a markedly reduced oral intake by cancer patients suggests a poor prognosis, the survival times of noncancer patients after its onset remain unclear. We herein investigated the time from a marked reduction in oral intake to death in noncancer patients as well as factors associated with their subsequent survival. We conducted a retrospective medical record review of noncancer patients who died in our hospital between April 2017 and April 2018. We recorded the day when oral intake markedly decreased and the date of death. We extracted data on age, gender, the Charlson Comorbidities Index, mean daily fluid volume, laboratory test results, and vital signs converted to the Shock Index ([[SI]]). We used Cox's proportional hazards models to assess relationships between these factors and survival times after the onset of a markedly reduced oral intake. We analyzed data from 44 noncancer patients. The median time from the onset of a markedly reduced oral intake to death was 16.5 days. Based on Cox's proportional hazards models, only [[SI]] ≧ 1.0 at the onset of a markedly reduced oral intake correlated with survival times (hazard ratio: 5.89, 95% confidence interval (CI): 1.71-20.1, [i]P[/i] = .005). Noncancer patients died a median of 16.5 days after the onset of a markedly reduced oral intake, and [[SI]] ≧1.0 correlated with subsequent survival times. These results will provide novel insights into the prognosis of noncancer patients at the end of life.
-|mesh-terms=* Humic Substances
+|keywords=* elderly
-* Hydrogen Peroxide
+* geriatrics
-* Hydrophobic and Hydrophilic Interactions
+* palliative medicine
-* Membranes, Artificial
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7060293
-* Polymers
-* Sodium Hypochlorite
-* Sulfones
-* Ultrafiltration
-|keywords=* chemical cleaning
-* hydrogen peroxide (H2O2)
-* membrane aging
-* polyethersulfone (PES) ultrafiltration (UF) membrane
-* sodium hypochlorite (NaClO)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6843545
 }}
 {{medline-entry
-|title=NF-κB signaling in skin aging.
+|title=Adherence to Mediterranean diet moderates the association between multimorbidity and depressive symptoms in older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31634486
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109694
+|abstract=Adherence to Mediterranean Diet (Med-Diet) has been associated with a lower incidence of chronic diseases and may be associated with lower risk for depression. The aim of the present study was to investigate (i) the association of adherence to Med-Diet with depressive symptoms and multimorbidity in a cohort of geriatric medical outpatients, and (ii) the role of Med-Diet in mediating the association between depressive symptoms and multimorbidity. A total of 143 geriatric patients (mean age: 73.1 ± 8.35) were included. Adherence to Med-Diet was evaluated using a validated 14-item questionnaire; depressive and cognitive symptoms were assessed through the 15-item Geriatric Depression Scale (GDS) and Mini Mental State Examination (MMSE) respectively; multimorbidity was evaluated using the Cumulative Illness Rating Scale for Geriatrics (CIRSG-[[SI]]). Significant associations were found between MDQ score, GDS and CIRSG-[[SI]] (MDQ score and GDS: r= -0.206, p = 0.014; MDQ score and CIRSG-[[SI]]: r= -0.247, p = 0.003; GDS and CIRSG-[[SI]]: r = 0.251; p = 0.003). These associations remained significant after adjusting for potential confounding factors. A mediational model analysis showed that the direct effect of CIRSG-[[SI]] on GDS was significant (b = 1.330; se = 0.59; p = 0.028) with this effect being counterbalanced by higher MDQ scores (indirect effect of CIRS-G on GDS through MDQ: b = 0.382; se = 0.19; p = 0.048). These findings (i) add to the accumulating evidence that Med-Diet may have a positive impact on mental health in the elderly, and (ii) suggest that Med-Diet may contribute, at least in part, to protect geriatric patients with multimorbidity from the development of depressive symptoms, ultimately promoting healthy aging.
-|mesh-terms=* Animals
+|mesh-terms=* Aged
-* Cellular Senescence
+* Aged, 80 and over
+* Cohort Studies
+* Depression
+* Diet, Mediterranean
+* Healthy Aging
 * Humans
-* NF-kappa B
+* Multimorbidity
-* Phenotype
+* Surveys and Questionnaires
-* Signal Transduction
+|keywords=* Aging
-* Skin Aging
+* Depressive symptoms
-* Skin Neoplasms
+* Mediterranean diet
-|keywords=* NF-κB
+* Mental health
-* Senescence-associated secretory phenotype
+* Multimorbidity
-* Skin aging
+|full-text-url=https://sci-hub.do/10.1016/j.archger.2020.104022
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2019.111160
 }}
+==SIRT1==
 {{medline-entry
-|title=Development of a w/o emulsion using ionic liquid strategy for transdermal delivery of anti - aging component α - lipoic acid: Mechanism of different ionic liquids on skin retention and efficacy evaluation.
+|title=Lymphocyte senescence in COPD is associated with decreased sirtuin 1 expression in steroid resistant pro-inflammatory lymphocytes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31634554
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32270742
+|abstract=The class III NAD-dependent histone deacetylase (HDAC) sirtuin 1 ([[SIRT1]]) is an important regulator of senescence, aging, and inflammation. [[SIRT1]]de-acetylates chromatin histones, thereby silencing inflammatory gene transcription. We have reported increased steroid-resistant senescent pro-inflammatory CD28nullCD8+ T cells in patients with chronic obstructive pulmonary disease (COPD). We hypothesized that [[SIRT1]] is reduced in these cells in COPD, and that treatment with [[SIRT1]] activators (resveratrol, curcumin) and agents preventing NAD depletion (theophylline) would upregulate [[SIRT1]] and reduce pro-inflammatory cytokine expression in these steroid-resistant cells. Blood was collected from [i]n[/i] = 10 COPD and [i]n[/i] = 10 aged-matched controls. Expression of CD28, [[SIRT1]], and pro-inflammatory cytokines was determined in CD8+ and CD8- T and natural killer T (NKT)-like cells cultured in the presence of ±1 µM prednisolone, ±5 mg/L theophylline, ±1 µM curcumin, ±25 µM resveratrol, using flow cytometry and immunofluorescence. There was an increase in the percentage of CD28nullCD8+ T and NKT-like cells in COPD patients compared with controls. Decreased [[SIRT1]] expression was identified in CD28nullCD8+T and NKT-like cells compared with CD28+ counterparts from both patients and controls (e.g. CD28null 11 ± 3% [i]versus[/i] CD28+ 57 ± 9%). Loss of [[SIRT1]] was associated with increased production of IFNγ and TNFα, steroid resistance, and disease severity. [[SIRT1]] expression was upregulated in the presence of all drugs and was associated with a decrease in steroid resistance and IFNγ and TNFα production by CD28nullCD8+T and NKT-like cells. The presence of the [[SIRT1]] inhibitor, EX-527 negated [by 92 ± 12% (median ± SEM)] the effect of the [[SIRT1]] activator SRT720 on the percentage of CD8+ T cells producing IFNγ and TNFα. Steroid resistance in pro-inflammatory CD28nullCD8+ T and NKT-like cells is associated with decreased [[SIRT1]] expression. Treatment with prednisolone, in combination with theophylline, curcumin or resveratrol increases [[SIRT1]] expression, restores steroid sensitivity, and inhibits pro-inflammatory cytokine production from these cells and may reduce systemic inflammation in COPD. [i]The reviews of this paper are available via the supplemental material section.[/i]
-|mesh-terms=* Administration, Cutaneous
+|keywords=* CD28nullCD8+ T and NKT-like cells
-* Animals
+* COPD
-* Emulsions
+* IFNγ and TNFα
-* Hydroxyproline
+* SIRT1
-* Ionic Liquids
+* lymphocyte senescence
-* Male
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7153179
-* Rats, Wistar
-* Skin
-* Skin Absorption
-* Skin Aging
-* Thioctic Acid
-* Ultraviolet Rays
-|keywords=* Anti – aging efficacy
-* Ionic liquids
-* Skin retention
-* Solubility
-* Α – lipoic acid
-|full-text-url=https://sci-hub.do/10.1016/j.ejps.2019.105042
 }}
 {{medline-entry
-|title=Effect of Nitrogen-Doped Graphene Oxide on the Aging Behavior of Nitrile-Butadiene Rubber.
+|title=Therapeutic effects of hydro-alcoholic leaf extract of Withania somnifera on age-induced changes in daily rhythms of Sirt1, Nrf2 and Rev-erbα in the SCN of male Wistar rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31658636
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32249404
+|abstract=The temporal expression pattern of the circadian clock genes are known to be altered/attenuated with advance in age. Withania somnifera (WS) essentially consists of numerous active constituents including withanolides is known to have antioxidant, anti-inflammatory and adaptogenic properties. We have earlier demonstrated therapeutic effects of hydro-alcoholic leaf extract of WS on the age-induced alterations in the levels and daily rhythms of various clock genes such as rBmal1, rPer1, rPer2 and rCry1. We have now studied effects of hydro-alcoholic leaf extract of WS on the age-induced alterations in the levels and daily rhythms of expression of [[SIRT1]] (an NAD  dependent histone deacetylase and a modulator of clock) and NRF2 (a clock controlled gene and a master transcription factor regulating various endogenous antioxidant enzymes) in addition to rRev-erbα in SCN of adult [3 months (m)], middle-aged (12 m) and old-aged (24 m) male Wistar rats. The daily rhythms of rNrf2 expression showed 6 h phase delay in middle age and 12 h phase advance in old age. WS restored rSirt1 daily rhythms and phase in old age whereas it restored the phase of rNrf2 in the SCN of both middle and old aged animals. At protein level, [[SIRT1]] expression showed phase advances in 12 m and 24 m whereas NRF2 daily rhythms were abolished in both the age groups. WS restored the phase and daily rhythms of [[SIRT1]] as well as NRF2 in 12 m old rats. However, rRev-erbα expression was found insensitive to WS treatment in all the age groups studied. Pairwise correlation analysis demonstrated significant stoichiometric interactions among rSirt1, rNrf2 and rRev-erbα in 3 m which altered with aging significantly. WS treatment resulted in differential restorations of such interactions.
+|keywords=* Aging
-|keywords=* aging resistance
+* Ashwagandha
-* graphene oxide
+* Circadian clock
-* nitrile-butadiene rubber
+* NRF2
-* nitrogen-doped
+* SCN
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6835680
+* SIRT1
+|full-text-url=https://sci-hub.do/10.1007/s10522-020-09875-x
 }}
-==AVP==
 {{medline-entry
-|title=Plasma oxytocin and vasopressin levels in young and older men and women: Functional relationships with attachment and cognition.
+|title=The Serum Concentration of Anti-Aging Proteins, Sirtuin1 and αKlotho in Patients with End-Stage Kidney Disease on Maintenance Hemodialysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31606581
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32214805
+|abstract=Sirtuin1 ([[SIRT1]]) acts as an anti-aging protein due to anti-apoptotic, anti-oxidative and anti-inflammatory effect and is implicated in several diseases including diabetes or cardiovascular problems. [[SIRT1]] renal overexpression indicates oxidative stress. Similarly, αKlotho was primarily exposed as anti-aging factor. It is primary produced in kidney. It's deficiency is associated with progression of chronic kidney disease and heart disorders. The aim of the study was to assess the serum concentration of sirtuin1 and αKlotho in hemodialysis (HD) patients compared to healthy volunteers in regard to age, blood pressure control, residual kidney function (RKF), diabetes, cardiovascular disease, dialysis vintage and type of dialyzer. The serum level of [[SIRT1]] and αKlotho was evaluated using ELISA tests in 103 HD patients, median age 67 years and in 21 volunteers. Blood pressure, RRF, echocardiography and dialysis parameters were assessed. HD group was divided according to the presence/absence of RKF. The serum [[SIRT1]] level was higher (28.4 vs 2.71ng/mL, p<0.0001) and αKlotho was lower (433.9 vs 756.6pg/mL, p<0.0001) in HD then in control group. αKlotho was lower in those without RKF (387.2 vs 486.2pg/mL, p=0.028). [[SIRT1]] positively correlated with hemodialysis vintage. αKlotho negatively correlated with left ventricular posterior wall thickness. There was no significant relationship between [[SIRT1]] and αKlotho level and age, blood pressure control, type of dialyzer, Kt/V and diabetes. Multivariate analysis revealed association of [[SIRT1]] with ejection fraction (B -0.72; p=0.32). Elevated [[SIRT1]] and lower αKlotho concentration are associated with impaired kidney function. The decrease in levels of αKlotho may also indicate heart hypertrophy in hemodialysis patients. The role of anti-aging proteins, particularly [[SIRT1]] as biomarkers/predictors of oxidative stress, inflammation and cardiovascular diseases need further examination.
-|mesh-terms=* Adolescent
+|mesh-terms=* Age Factors
-* Adult
-* Age Factors
 * Aged
-* Aged, 80 and over
 * Aging
-* Anxiety
+* Biomarkers
-* Avoidance Learning
+* Blood Pressure
-* Cognition
+* Cardiovascular Diseases
-* Cohort Studies
+* Case-Control Studies
+* Diabetes Complications
+* Echocardiography
 * Female
+* Glucuronidase
+* Heart Ventricles
 * Humans
+* Kidney
+* Kidney Failure, Chronic
 * Male
 * Middle Aged
-* Object Attachment
+* Renal Dialysis
-* Oxytocin
+* Sirtuin 1
-* Sex Factors
+* Stroke Volume
-* Vasopressins
+|keywords=* chronic kidney disease
-* Young Adult
+* hemodialysis
-|keywords=* Age
+* sirtuin1
-* Attachment anxiety
+* αKlotho
-* Oxytocin
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7084123
-* Processing speed
-* Sex
-* Vasopressin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6943921
 }}
-==B4GALT1==
 {{medline-entry
-|title=Expression of β-1,4-galactosyltransferases during Aging in Caenorhabditis elegans.
+|title=Small extracellular vesicles deliver miR-21 and miR-217 as pro-senescence effectors to endothelial cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33171474
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32158519
+|abstract=The role of epigenetics in endothelial cell senescence is a cutting-edge topic in ageing research. However, little is known of the relative contribution to pro-senescence signal propagation provided by microRNAs shuttled by extracellular vesicles (EVs) released from senescent cells. Analysis of microRNA and DNA methylation profiles in non-senescent (control) and senescent (SEN) human umbilical vein endothelial cells (HUVECs), and microRNA profiling of their cognate small EVs (sEVs) and large EVs demonstrated that SEN cells released a significantly greater sEV number than control cells. sEVs were enriched in miR-21-5p and miR-217, which target DNMT1 and [[SIRT1]]. Treatment of control cells with SEN sEVs induced a miR-21/miR-217-related impairment of DNMT1-[[SIRT1]] expression, the reduction of proliferation markers, the acquisition of a senescent phenotype and a partial demethylation of the locus encoding for miR-21. MicroRNA profiling of sEVs from plasma of healthy subjects aged 40-100 years showed an inverse U-shaped age-related trend for miR-21-5p, consistent with senescence-associated biomarker profiles. Our findings suggest that miR-21-5p/miR-217 carried by SEN sEVs spread pro-senescence signals, affecting DNA methylation and cell replication.
+|keywords=* Cellular senescence
-|keywords=* Biomarker
+* DNMT1
-* Glycosylation
+* SIRT1
-* Lifespan regulation
+* extracellular vesicles
-* bre-4
+* microRNAs
-* sqv-3
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7048230
-|full-text-url=https://sci-hub.do/10.1159/000510722
 }}
-==BACE1==
 {{medline-entry
-|title=Electric Stimulation of Neurogenesis Improves Behavioral Recovery After Focal Ischemia in Aged Rats.
+|title=Spatiotemporal gating of [[SIRT1]] functions by O-GlcNAcylation is essential for liver metabolic switching and prevents hyperglycemia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32742258
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32152092
+|abstract=Inefficient physiological transitions are known to cause metabolic disorders. Therefore, investigating mechanisms that constitute molecular switches in a central metabolic organ like the liver becomes crucial. Specifically, upstream mechanisms that control temporal engagement of transcription factors, which are essential to mediate physiological fed-fast-refed transitions are less understood. [[SIRT1]], a NAD -dependent deacetylase, is pivotal in regulating hepatic gene expression and has emerged as a key therapeutic target. Despite this, if/how nutrient inputs regulate [[SIRT1]] interactions, stability, and therefore downstream functions are still unknown. Here, we establish nutrient-dependent O-GlcNAcylation of [[SIRT1]], within its N-terminal domain, as a crucial determinant of hepatic functions. Our findings demonstrate that during a fasted-to-refed transition, glycosylation of [[SIRT1]] modulates its interactions with various transcription factors and a nodal cytosolic kinase involved in insulin signaling. Moreover, sustained glycosylation in the fed state causes nuclear exclusion and cytosolic ubiquitin-mediated degradation of [[SIRT1]]. This mechanism exerts spatiotemporal control over [[SIRT1]] functions by constituting a previously unknown molecular relay. Of note, loss of [[SIRT1]] glycosylation discomposed these interactions resulting in aberrant gene expression, mitochondrial dysfunctions, and enhanced hepatic gluconeogenesis. Expression of nonglycosylatable [[SIRT1]] in the liver abrogated metabolic flexibility, resulting in systemic insulin resistance, hyperglycemia, and hepatic inflammation, highlighting the physiological costs associated with its overactivation. Conversely, our study also reveals that hyperglycosylation of [[SIRT1]] is associated with aging and high-fat-induced obesity. Thus, we establish that nutrient-dependent glycosylation of [[SIRT1]] is essential to gate its functions and maintain physiological fitness.
+|mesh-terms=* Acetylglucosamine
-|keywords=* aging
+* Aging
-* behavior
+* Animals
-* electrical stimulation
+* Fasting
-* neurogenesis
+* Gluconeogenesis
-* rats
+* Glycosylation
-* stroke
+* HEK293 Cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7365235
+* Homeostasis
+* Humans
+* Hyperglycemia
+* Insulin Resistance
+* Liver
+* Male
+* Mice
+* Mice, Inbred C57BL
+* Obesity
+* Phosphorylation
+* Protein Processing, Post-Translational
+* Sirtuin 1
+* Spatio-Temporal Analysis
+|keywords=* PGC1α
+* fed–fast cycle
+* gluconeogenesis
+* insulin signaling
+* ubiquitinylation
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7104039
 }}
 {{medline-entry
-|title=Disruption of synaptic expression pattern and age-related DNA oxidation in a neuronal model of lead-induced toxicity.
+|title=Hydrogen Sulfide Inhibits Homocysteine-Induced Neuronal Senescence by Up-Regulation of [[SIRT1]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32058320
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32132865
+|abstract=Homocysteine (Hcy) accelerates neuronal senescence and induces age-related neurodegenerative diseases. Silence signal regulating factor 1 ([[SIRT1]]) prolongs lifespan and takes neuroprotective effects. We have previously demonstrated that hydrogen sulfide (H S) prevents Hcy-induced apoptosis of neuronal cells and has neuroprotective effect. In the present work, we aimed to investigate whether H S protects HT22 cells against Hcy-induced neuronal senescence and whether [[SIRT1]] mediates this role of H S. We found that Hcy induced cellular senescence in HT22 cells, as determined by β-galactosidase staining, expressions of P16 , P21 , and trypan blue Staining, which are the markers of cellular senescence. However, sodium hydrosulfide (NaHS, the donor of H S) significantly reversed Hcy-induced cellular senescence. Interestingly, NaHS not only up-regulated the expression of [[SIRT1]] in HT22 cells but also reversed Hcy-downregulated the expression of [[SIRT1]] in HT22 cells. Furthermore, we found that pretreatment with Sirtinol (an inhibitor of [[SIRT1]]) markedly reversed the protection of NaHS against Hcy-induced HT22 cells senescence and apoptosis. Our findings illustrated that H S protects HT22 cells against Hcy-induced senescence by up-regulating [[SIRT1]].
+|keywords=* SIRT1
-|keywords=* Aging mice
+* cell senescence
-* Brain-derived neurotrophic factor precursor
+* homocysteine
-* Latent expression pattern
+* hydrogen sulfide
-* Lead
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053352
-* Pubertal exposure
-* Synaptic deficits
-* Tau phosphorylation
-|full-text-url=https://sci-hub.do/10.1016/j.etap.2020.103350
 }}
-==BAD==
 {{medline-entry
-|title=I  imidazoline receptor modulation protects aged SAMP8 mice against cognitive decline by suppressing the calcineurin pathway.
+|title=[[SIRT1]] and aging related signaling pathways.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33128688
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32084459
+|abstract=Aging is a biological phenomenon in which the structure and function of organisms declining with the increasing of age. It has become a major risk factor of human diseases, including diabetes, cancers, cardiovascular diseases and neurodegenerative diseases. Silencing information regulator 2 related enzyme 1(sirtuin1, [[SIRT1]]) is an NAD -dependent deacetylase, which has been reported to be involved in the regulation of cellular senescence and aging. The expression of [[SIRT1]] is diminished with aging in mice. By contrast, increased expression of [[SIRT1]] is sufficient to extend lifespan in yeast, caenorhabditis elegans and mice. In this review, the relationship between [[SIRT1]] and aging and various signaling networks associated with aging, including NF-κB, AMPK, mTOR, P53, PGC1α, and FoxOs will be discussed. Meanwhile, the potential therapeutic strategies of targeting [[SIRT1]] to anti-aging are also addressed.
 |keywords=* Aging
-* Alzheimer’s disease
+* Deacetylate
-* Behavior
+* NAD(+)
-* I2 imidazoline receptors
+* SIRT1
-* NFAT
+* Signaling pathways
-* Neuroinflammation
+|full-text-url=https://sci-hub.do/10.1016/j.mad.2020.111215
-* Neuroprotection
-|full-text-url=https://sci-hub.do/10.1007/s11357-020-00281-2
 }}
-==BAK1==
 {{medline-entry
-|title=Developmental Attenuation of Neuronal Apoptosis by Neural-Specific Splicing of Bak1 Microexon.
+|title=Tropisetron protects against brain aging via attenuating oxidative stress, apoptosis and inflammation: The role of [[SIRT1]] signaling.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32710818
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32088214
+|abstract=The aim of this study was to elucidate the signaling pathway involved in the anti-aging effect of tropisetron and to clarify whether it affects mitochondrial oxidative stress, apoptosis and inflammation in the aging mouse brain by upregulating Sirtuin 1 or silent information regulator 1 ([[SIRT1]]). Aging was induced by d-galactose (DG) at the dose of 200 mg/kg body weight/day subcutaneously injected to male mice for six weeks. Tropisetron was simultaneously administered intraperitoneally once a day at three various doses (1, 3 and 5 mg/kg body weight). Oxidative stress and mitochondrial dysfunction markers were evaluated. Nitric oxide (NO) and pro-inflammatory cytokines levels including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were studied. Besides, the expressions of apoptosis-associated genes (Bax and Bcl-2) and the aging-related gene ([[SIRT1]]) were determined by the real time polymerase chain reaction (RT-PCR). In addition, histopathological alterations were assessed. Tropisetron reversed the induction of oxidative damage, mitochondrial dysfunction and overproduction of inflammatory mediators induced by DG in the brain tissue. In addition, tropisetron suppressed DG-induced apoptosis and found to significantly elevate [[SIRT1]] gene expression. Besides, tropisetron could markedly alleviate DG-induced abnormal changes in the brain morphology. Tropisetron exhibited anti-aging effects in the context of DG-induced senescence in mouse brain through various pathways. Our results suggest that tropisetron may attenuate DG-induced brain aging via [[SIRT1]] signaling activation.
-|mesh-terms=* Animals
+|mesh-terms=* Aging
+* Animals
+* Antioxidants
 * Apoptosis
 * Brain
-* Cell Line, Tumor
+* Drug Administration Schedule
-* Cells, Cultured
+* Galactose
-* Female
+* Gene Expression Regulation
-* Heterogeneous-Nuclear Ribonucleoproteins
+* Inflammation
+* Injections, Intraperitoneal
+* Injections, Subcutaneous
+* Interleukin-6
 * Male
 * Mice
-* Mice, Inbred C57BL
+* Mitochondria
-* Mutation
+* Neurons
-* Neural Stem Cells
+* Nitric Oxide
-* Neurogenesis
+* Oxidative Stress
-* Nonsense Mediated mRNA Decay
+* Proto-Oncogene Proteins c-bcl-2
-* Polypyrimidine Tract-Binding Protein
+* Reactive Oxygen Species
-* RNA Splicing
+* Serotonin 5-HT3 Receptor Antagonists
-* bcl-2 Homologous Antagonist-Killer Protein
+* Sirtuin 1
-|keywords=* AS-NMD
+* Tropisetron
-* BAK
+* Tumor Necrosis Factor-alpha
-* BCL2 family proteins
+* bcl-2-Associated X Protein
-* NMD
+|keywords=* Aging
-* PTB
+* Brain
-* PTBP
+* Neurotoxicity
-* PTBP2
+* Sirtuin 1
-* UPF2
+* Tropisetron
-* alternative splicing
+* d-galactose
-* cell death
+|full-text-url=https://sci-hub.do/10.1016/j.lfs.2020.117452
-* neural development
-* neurogenesis
-* neuronal lifespan
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7529960
 }}
-==BANF1==
+==SIRT3==
 {{medline-entry
-|title=An additional case of Néstor-Guillermo progeria syndrome diagnosed in early childhood.
+|title=[i][[SIRT3]][/i] Transfection of Aged Human Bone Marrow-Derived Mesenchymal Stem Cells Improves Cell Therapy-Mediated Myocardial Repair.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32783369
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32228121
+|abstract=Sirtuin 3 ([[SIRT3]]) is a deacetylase important for antioxidant protection, cell longevity, and aging. We hypothesized that [[SIRT3]] improve oxidative resistance of aged cells and improve cell therapy in aged patients. [i]In vitro[/i], the proliferation and oxidative resistance of human mesenchymal stem cells (hMSCs) significantly declined with age. The expression and activity of antioxidant enzymes, including catalase (CAT) and manganese superoxide dismutase (MnSOD), increased after transfection of [i][[SIRT3]][/i] in hMSCs from older donors (O-hMSCs). The protein level of Forkhead box O3a (FOXO3a) in nucleus increased after [[SIRT3]] overexpression. The antioxidant capacity of O-hMSCs increased after [[SIRT3]] overexpression. 3-Amino-1,2,4-triazole (3-AT, CAT inhibitor) or diethyldithiocarbamate (DETC, SOD inhibitor) that was used to inhibit CAT or SOD activity significantly blocked the antioxidant function of [[SIRT3]]. When two inhibitors were used together, the antioxidant function of [[SIRT3]] almost disappeared. Following myocardial infarction and intramyocardial injections of O-hMSCs in rats [i]in vivo[/i], the survival rate of O-hMSCs increased by [i][[SIRT3]][/i] transfection. The cardiac function of rats was improved after [[SIRT3]]-overexpressed O-hMSC transplantation. The infarct size, collagen content, and expression levels of matrix metalloproteinase 2 (MMP2) and MMP9 decreased. Besides, the protein level of vascular endothelial growth factor A and vascular density increased after cell transplantation with [[SIRT3]]-modified O-hMSCs. These results indicate that damage resistance of hMSCs decline with age and [[SIRT3]] might protect O-hMSCs against oxidative damage by activating CAT and MnSOD through transferring FOXO3a into nucleus. Meanwhile, the therapeutic effect of aged hMSC transplantation can be improved by [[SIRT3]] overexpression.
+|keywords=* O-hMSC transplantation
-|keywords=* BANF1
+* SIRT3
-* Néstor-Guillermo progeria syndrome
+* aging
-* premature aging
+* gene modification
-* progeria
+* myocardial infarction
-* whole exome sequencing
+* myocardial repair
-|full-text-url=https://sci-hub.do/10.1002/ajmg.a.61777
+|full-text-url=https://sci-hub.do/10.1089/rej.2019.2260
 }}
-==BATF==
 {{medline-entry
-|title=LncRNA-ES3 inhibition by Bhlhe40 is involved in high glucose-induced calcification/senescence of vascular smooth muscle cells.
+|title=17β-estradiol inhibits H O -induced senescence in HUVEC cells through upregulating [[SIRT3]] expression and promoting autophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32483833
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32172411
+|abstract=17β-estradiol (17β-E ) has been implicated in inhibiting the senescence of vascular endothelial cells (VEC) and slowing down the process of atherosclerosis. However, the underlying molecular mechanisms are still unknown. In this study, we examined the roles of [[SIRT3]] in 17β-E -induced autophagy and 17β-E -mediated inhibition of hydrogen peroxide (H O )-induced senescence in Human umbilical vein endothelial cells (HUVEC). Cellular senescence was measured by immunoblot analysis with antibodies against phosphorylated Rb and senescence-associated β-galactosidase staining. Immunoblot analysis with antibodies against LC3 and p62 was performed to determine autophagy flux. Our findings show that 17β-E  activates [[SIRT3]] promoter and upregulates [[SIRT3]] gene expression in HUVEC cells. siRNA-mediated silencing of [[SIRT3]] gene expression inhibits 17β-E -induced processing of LC3-I to LC3-II and degradation of p62, two widely-used makers of autophagy. [[SIRT3]] knockdown also blocks 17β-E -induced inhibition of cellular senescence triggered by H O . Our data further reveal that [[SIRT3]] knockdown impairs 17β-E -induced co-localization of LC3 and VDAC1, a marker protein on mitochondria, when HUVEC cells were co-treated with H O . Together, our findings suggest that 17β-E  upregulates [[SIRT3]] gene expression by activating [[SIRT3]] promoter and then promotes autophagy, which in turn serves to remove dysfunctional mitochondria caused by H O  and consequently inhibit H O -induced senescence in HUVEC cells.
+|keywords=* 17β-estradiol
-|keywords=* Bhlhe40
+* Autophagy
-* VSMC calcification/senescence
+* SIRT3
-* diabetes
+* Senescence
-* lncRNA-ES3
+|full-text-url=https://sci-hub.do/10.1007/s10522-020-09868-w
-* microRNA
-* vascular aging
-|full-text-url=https://sci-hub.do/10.1111/nyas.14381
 }}
-==BAX==
 {{medline-entry
-|title=Clearance of therapy-induced senescent tumor cells by the senolytic ABT-263 via interference with BCL-X  -[[BAX]] interaction.
+|title=CR6 interacting factor 1 deficiency induces premature senescence via [[SIRT3]] inhibition in endothelial cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32652830
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109515
+|abstract=Vascular endothelial cell senescence is an important cause of cardiac-related diseases. Mitochondrial reactive oxygen species (mtROS) have been implicated in cellular senescence and multiple cardiovascular disorders. CR6 interacting factor 1 (CRIF1) deficiency has been shown to increase mtROS via the inhibition of mitochondrial oxidative phosphorylation; however, the mechanisms by which mtROS regulates vascular endothelial senescence have not been thoroughly explored. The goal of this study was to investigate the effects of CRIF1 deficiency on endothelial senescence and to elucidate the underlying mechanisms. CRIF1 deficiency was shown to increase the activity of senescence-associated β-galactosidase along with increased expression of phosphorylated p53, p21, and p16 proteins. Cell cycle arrested in the G0/G1 phase were identified in CRIF1-deficient cells using the flow cytometry. Furthermore, CRIF1 deficiency was also shown to increase cellular senescence by reducing the expression of Sirtuin 3 ([[SIRT3]]) via ubiquitin-mediated degradation of transcription factors PGC1α and NRF2. Downregulation of CRIF1 also attenuated the function of mitochondrial antioxidant enzymes including manganese superoxide dismutase (MnSOD), Foxo3a, nicotinamide-adenine dinucleotide phosphate, and glutathione via the suppression of [[SIRT3]]. Interestingly, overexpression of [[SIRT3]] in CRIF1-deficient endothelial cells not only reduced mtROS levels by elevating expression of the antioxidant enzyme MnSOD but also decreased the expression of cell senescence markers. Taken together, these results suggest that CRIF1 deficiency induces vascular endothelial cell senescence via ubiquitin-mediated degradation of the transcription coactivators PGC1α and NRF2, resulting in decreased expression of [[SIRT3]].
+|keywords=* Antioxidant system
+* Mitochondria
+* Oxidative stress
+* Senescence
+* Vascular endothelial cell
+|full-text-url=https://sci-hub.do/10.1016/j.freeradbiomed.2020.02.017
+}}
+==SOX9==
-|keywords=* ABT-263
-* BCL-XL
-* chemotherapy
-* radiation
-* senescence
-* senolytic
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7530780
-}}
 {{medline-entry
-|title=CREB Signaling Mediates Dose-Dependent Radiation Response in the Murine Hippocampus Two Years after Total Body Exposure.
+|title=Positive Effects of a Young Systemic Environment and High Growth Differentiation Factor 11 Levels on Chondrocyte Proliferation and Cartilage Matrix Synthesis in Old Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31657930
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32067417
+|abstract=To investigate the effects of a young systemic environment and growth differentiation factor 11 (GDF-11) on aging cartilage. A heterochronic parabiosis model (2-month-old mouse and 12-month-old mouse [Y/O]), an isochronic parabiosis model (12-month-old mouse and 12-month-old mouse [O/O]), and 12-month-old mice alone (O) were evaluated. Knee joints and chondrocytes from old mice were examined by radiography, histology, cell proliferation assays, immunohistochemistry, Western blotting, and quantitative reverse transcriptase-polymerase chain reaction 16 weeks after parabiosis surgery. GDF-11 was injected into 12-month-old mouse joints daily for 16 weeks. Cartilage degeneration, cell proliferation, and osteoarthritis-related gene expression were evaluated. Osteoarthritis Research Society International scores in old mice were significantly lower in the Y/O group than in the O/O and O groups (both P < 0.05). The percentage of 5-ethynyl-2'-deoxyuridine-positive chondrocytes in old mice was significantly higher in the Y/O group than in the other groups (P < 0.05). Type II collagen (CII) and [[SOX9]] messenger RNA levels differed in cartilage from old mice in the Y/O group compared to the O/O and O groups (both P < 0.05). RUNX-2, CX, and matrix metalloproteinase 13 levels were significantly lower in cartilage from old mice in the Y/O group compared to the O/O and O groups (both P < 0.05). Similar results were obtained for protein expression levels and after GDF-11 treatment in vitro and in vivo. Phosphorylated Smad2/3 (pSmad2/3) levels were higher in the recombinant GDF-11-treated group than in the control group. A young systemic environment promotes chondrocyte proliferation and cartilage matrix synthesis in old mice. GDF-11, a "young factor," contributes to these effects through the up-regulation of pSmad2/3.
+|mesh-terms=* Adolescent
-|keywords=* CREB signaling
+* Aged
-* aging
+* Aging
-* brain
-* hippocampus
-* ionizing radiation
-* label-free proteomics
-|full-text-url=https://sci-hub.do/10.1021/acs.jproteome.9b00552
-}}
-==BAZ2B==
-{{medline-entry
-|title=Two conserved epigenetic regulators prevent healthy ageing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32103178
-|mesh-terms=* Aging
 * Animals
-* Caenorhabditis elegans
+* Arthroplasty, Replacement, Knee
-* Caenorhabditis elegans Proteins
+* Bone Morphogenetic Proteins
-* Cognition
+* Cartilage, Articular
-* Cognitive Dysfunction
+* Cell Proliferation
-* Epigenesis, Genetic
+* Chondrocytes
-* Healthy Aging
+* Collagen Type II
-* Histone-Lysine N-Methyltransferase
+* Collagen Type X
-* Histones
+* Core Binding Factor Alpha 1 Subunit
+* Extracellular Matrix
+* Female
+* Growth Differentiation Factors
 * Humans
-* Longevity
+* In Vitro Techniques
-* Lysine
+* Knee Joint
 * Male
-* Memory
+* Matrix Metalloproteinase 13
-* Methylation
 * Mice
-* Mitochondria
+* Osteoarthritis, Knee
-* Neurons
+* Parabiosis
-* Proteins
+* Phosphorylation
-* RNA Interference
+* RNA, Messenger
-* Spatial Learning
+* Reverse Transcriptase Polymerase Chain Reaction
-* Transcription Factors, General
+* SOX9 Transcription Factor
+* Smad2 Protein
-|full-text-url=https://sci-hub.do/10.1038/s41586-020-2037-y
+* Smad3 Protein
+* Stifle
+* Young Adult
+|keywords=#f
+|full-text-url=https://sci-hub.do/10.1002/art.41230
 }}
-==BCL6==
+==SRD5A2==
 {{medline-entry
-|title=Ecto-NTPDase CD39 is a negative checkpoint that inhibits follicular helper cell generation.
+|title=Extract of Plumbago zeylanica enhances the growth of hair follicle dermal papilla cells with down-regulation of 5α-reductase type II.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32452837
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32125089
+|abstract=Cellular senescence, a phenomenon of irreversible growth arrest of mammalian cells, is involved in various age-related phenomena in organisms. Hair follicle dermal papilla (DP) cells play important roles in the regulation of hair growth and loss. We examined the implication of cellular senescence of DP cells in androgenetic alopecia (AGA), the most common form of male hair loss, and searched for the compounds that have a beneficial effect on the prevention of AGA. Expression of the 5α-reductase type II ([[SRD5A2]]) gene, which plays a key role in the development of AGA, was examined by quantitative RT-PCR and Western blotting analysis in DP cells. Besides, DP cells were cultured with the extracts of herbs used in traditional Ayurvedic medicine to search for the compounds that have a beneficial effect on the growth of DP cells. We found that expression of the [[SRD5A2]] was up-regulated in senescent DP cells. We also found that the herbal extract of Plumbago zeylanica (root) enhanced the growth of DP cells and down-regulated the expression of [[SRD5A2]] in DP cells. Further, plumbagin, an ingredient of P zeylanica, would be responsible for the above effects of P zeylanica. These results suggested the possibility that senescent DP cells may have a role in the development of AGA through up-regulating [[SRD5A2]] expression, and the P zeylanica extract and plumbagin may suppress its development through enhancing the growth of DP cells and down-regulating [[SRD5A2]] expression in DP cells.
+|keywords=*
+P zeylanica
-|keywords=* Adaptive immunity
+* 5α-reductase
-* Aging
+* dermal papilla
-* Cellular senescence
+* hair
-* T cells
+* plumbagin
-* Vaccines
+* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7324201
+|full-text-url=https://sci-hub.do/10.1111/jocd.13355
 }}
-==BCR==
+==SST==
 {{medline-entry
-|title=The presence of CLL-associated stereotypic B cell receptors in the normal [[BCR]] repertoire from healthy individuals increases with age.
+|title=Examination on how emotion regulation mediates the relationship between future time perspective and well-being: a counter-evidence to the socioemotional selectivity theory.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31485252
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32158369
+|abstract=Previous studies have shown that older people maintain higher well-being than younger people despite their physical and cognitive functioning declining with age. This paradoxical phenomenon has been explained by the socioemotional selectivity theory ([[SST]]), in which a limited future time perspective (FTP) is an antecedent that leads to higher well-being through the use of adaptive emotion regulation. However, few empirical studies have examined the mediation process assumed in the [[SST]]. Moreover, it is unclear whether time left in life (TLL), which was originally referred to in the [[SST]] and is thought to be a different concept from FTP, relates to emotion regulation and well-being. Therefore, the current study investigated how emotion regulation mediates the relationship between FTP, TLL, and well-being by using a cross-sectional questionnaire that was responded to by 1393 Japanese adults (age range 20-89 years, [i]M[/i] = 54.23, SD = 19.01). The results of correlation and mediation analyses indicated that, in contrast to the assumption of the [[SST]], limited (expanded) FTP and TLL generally lead to lower (higher) well-being through the mediation of maladaptive (adaptive) emotion regulation. Although there are some methodological limitations, the findings imply that the relationship between FTP, TLL, and emotion regulation that is assumed in the [[SST]] should be reconsidered and that TLL should be thought of as a distinct variable from FTP.
 |keywords=* Aging
-* B-lymphocyte
+* Emotion regulation
-* BCR repertoire
+* Future time perspective
-* CLL
+* Socioemotional selectivity theory
-* Stereotypic BCR
+* Time left in life
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6714092
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7040126
 }}
-==BDNF==
+==STAT3==
 {{medline-entry
-|title=Influence of [i][[BDNF]][/i] Genetic Polymorphisms in the Pathophysiology of Aging-related Diseases.
+|title=Atorvastatin-induced senescence of hepatocellular carcinoma is mediated by downregulation of hTERT through the suppression of the IL-6/[[STAT3]] pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33269104
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32257389
+|abstract=Hepatocellular carcinoma (HCC), a hepatic malignancy, has a poor prognosis and contributes to cancer-related death worldwide. Cellular senescence is an anticancer therapeutic strategy that causes irreversible cell cycle arrest and enables immune-mediated clearance of cancer cells. Atorvastatin, an HMG-CoA reductase inhibitor, has been shown to inhibit tumor growth and induce apoptosis or autophagy in malignant tumors. However, whether atorvastatin can induce HCC cell senescence and the mechanisms involved are poorly understood. The effects of atorvastatin-induced senescence were examined in both HCC cells and mouse xenograft models. The phenomenon and mechanism of senescence were examined by cell cycle analysis, senescence-associated β-galactosidase (SA-β-gal) staining and western blotting in HCC cells, and HCC tissues from mice were analyzed by immunohistochemical (IHC) staining. We demonstrated that atorvastatin induced cell growth inhibition and G0/G1 phase cell cycle arrest, leading to senescence in HCC cells. Atorvastatin-induced senescence was independent of p53, p14, and p16, and atorvastatin not only decreased the secretion of IL-6, a major senescence-associated secretory phenotype (SASP) factor, and the phosphorylation of [[STAT3]] but also inhibited the expression of hTERT, a catalytic subunit of telomerase. Supplementation with exogenous IL-6 reversed both atorvastatin-induced suppression of [[STAT3]] phosphorylation and hTERT expression and atorvastatin-induced senescence. Overexpression of constitutively activated [[STAT3]] rescued HCC cells from atorvastatin-induced hTERT suppression and senescence. Moreover, atorvastatin decreased tumor growth in mouse xenograft models. Consistent with these results, atorvastatin decreased the IL-6, p-[[STAT3]], and hTERT levels and increased β-gal expression in tumor sections. Taken together, these data indicate that atorvastatin can induce atypical cellular senescence in HCC cells to inhibit tumor growth, an effect mediated by downregulation of hTERT through suppression of the IL-6/[[STAT3]] pathway.
+|keywords=* Cancer therapy
+* Senescence
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7105491
+}}
+==STS==
-|keywords=* Aging
-* BDNF gene
-* aging-related diseases
-* polymorphism
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673859
-}}
 {{medline-entry
-|title=Moderators of the Impact of (Poly)Phenols Interventions on Psychomotor Functions and [[BDNF]]: Insights from Subgroup Analysis and Meta-Regression.
+|title=The WRKY53 transcription factor enhances stilbene synthesis and disease resistance by interacting with MYB14 and MYB15 in Chinese wild grape.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32961777
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32080737
+|abstract=Resveratrol is notable not only for its functions in disease resistance in plants but also for its health benefits when it forms part of the human diet. Identification of new transcription factors helps to reveal the regulatory mechanisms of stilbene synthesis. Here, the WRKY53 transcription factor was isolated from the Chinese wild grape, Vitis quinquangularis. Vqwrky53 was expressed in a variety of tissues and responded to powdery mildew infection and to exogenous hormone application. VqWRKY53 was located in the nucleus and had transcriptional activation activity in yeast. A yeast two-hybrid assay and a bimolecular fluorescence complementation assay confirmed that VqWRKY53 interacted physically with VqMYB14 and VqMYB15, which have previously been reported to regulate stilbene synthesis. When Vqwrky53 was overexpressed in grape leaves, the expression of Vq[[STS]]32 and Vq[[STS]]41 and the content of stilbenes were increased. A yeast one-hybrid assay demonstrated that VqWRKY53 could bind directly to the promoters of [[STS]] genes. Overexpression of Vqwrky53 activated β-glucuronidase expression, driven by [[STS]] promoters, and co-expressing Vqwrky53 with VqMYB14 and VqMYB15 showed stronger regulatory functions. Heterologous overexpression of Vqwrky53 in Arabidopsis accelerated leaf senescence and disease resistance to PstDC3000.
+|keywords=* Chinese wild grape (Vitis quinquangularis)
+* WRKY transcription factor
+* disease resistance
+* leaf senescence
+* stilbene
+* transcriptional regulation
+|full-text-url=https://sci-hub.do/10.1093/jxb/eraa097
+}}
+==SUCNR1==
-|keywords=* aging
-* antioxidant
-* brain functions
-* brain plasticity
-* cognition
-* psychomotor functions
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7551086
-}}
 {{medline-entry
-|title=Astroglia-Derived [[BDNF]] and MSK-1 Mediate Experience- and Diet-Dependent Synaptic Plasticity.
+|title=[The effect of Mexidol on cerebral mitochondriogenesis at a young age and during aging].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32708382
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32105271
+|abstract=To study the ability of mexidol to induce cerebral mitochondriogenesis in the brain of young and aging rats. Expression level of marker proteins of cerebral mitochondriogenesis was evaluated during treatment with mexidol (20, 40, 100 mg/kg; 20 days; intraperitoneally) in the cerebral cortex of young (3 month) and aging (6, 9, 12, and 15 month) outbred male rats, using the Western blot analysis. It has been shown for the first time that the course injections of mexidol in doses of 40 and 100 mg/kg is accompanied by dose-dependent induction of the succinate receptor [[SUCNR1]] and protein markers of mitochondrial biogenesis: transcription coactivator PGC-1α, transcription factors (NRF1, TFAM), catalytic subunits of respiratory enzymes (NDUV2, NDUV2,cytb, COX2) and ATP synthase (ATP5A) in the cerebral cortex of young and aging outbred male rats. Mexidol-dependent overexpression of subunits of mitochondrial enzymes and PGC-1α is observed only with the course of the drug. The results indicate the ability of mexidol to induce cerebral mitochondriogenesis and eliminate mitochondrial dysfunction in young and aging animals and, thus, exert an effect on one of the key pathogenetic links of the development of disorders in aging and neurodegenerative diseases.
+|mesh-terms=* Age Factors
-|keywords=* AMPA receptors
+* Aging
-* Arc/Arg3.1
+* Animals
-* GABA receptors
+* Male
-* TrkB receptors
+* Mitochondria
+* Neurodegenerative Diseases
+* Picolines
+* Rats
+* Receptors, G-Protein-Coupled
+* Transcription Factors
+|keywords=* Western blot analysis
 * aging
-* calcium signalling
+* cerebral mitochondriogenesis
-* dendritic spines
+* mexidol
-* diet
+* mitochondrial dysfunction
-* enriched environment
+* rats
-* glia-neuron interactions
+* respiratory enzyme subunits
-* ion conductance microscopy
+* succinate receptor
-* synaptic scaling
+* transcriptional coactivator PGC-1α
-* synaptic strength
+|full-text-url=https://sci-hub.do/10.17116/jnevro202012001162
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7407492
 }}
+==TEC==
 {{medline-entry
-|title=[[BDNF]] reverses aging-related microglial activation.
+|title=Gender Disparity Impacts on Thymus Aging and LHRH Receptor Antagonist-Induced Thymic Reconstitution Following Chemotherapeutic Damage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32664974
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32194555
+|abstract=One of the main consequences of thymus aging is the decrease in naïve T cell output. This condition accelerates at the onset of puberty, and presents as a major clinical complication for cancer patients who require cytoablative therapy. Specifically, the extensive use of chemotherapeutics, such as cyclophosphamide, in such treatments damage thymic structure and eliminate the existing naïve T cell repertoire. The resulting immunodeficiency can lead to increased incidence of opportunistic infections, tumor growth relapse and/or autoimmune diseases, particularly in older patients. Thus, strategies aimed at rejuvenating the aged thymus following chemotherapeutic damage are required. Previous studies have revealed that sex hormone deprivation in male mice is capable of regenerating the thymic microenvironment following chemotherapy treatment, however, further investigation is crucial to identify gender-based differences, and the molecular mechanisms involved during thymus regeneration. Through phenotypic analyzes, we identified gender-specific alterations in thymocytes and thymic epithelial cell ([[TEC]]) subsets from the onset of puberty. By middle-age, females presented with a higher number of thymocytes in comparison to males, yet a decrease in their Aire  medullary [[TEC]]/thymocyte ratio was observed. This reduction could be associated with an increased risk of autoimmune disease in middle-aged women. Given the concurrent increase in female Aire  c[[TEC]]/thymocyte ratio, we proposed that there may be an impediment in Aire  m[[TEC]]  differentiation, and Aire  c[[TEC]]  as its upstream precursor. The regenerative effects of LHRH receptor antagonist, degarelix, on [[TEC]] subsets was also less pronounced in middle-aged females compared to males, possibly due to slower progression of thymic involution in the former, which presented with greater [[TEC]]  proportions. Furthermore, following cyclophosphamide treatment, degarelix enhanced thymocyte and mature [[TEC]] subset recovery, with faster recovery kinetics observed in females. These events were found to involve both reactivation and proliferation of thymic epithelial progenitor cells. Taken together, the findings from this study portray a relationship between gender disparity and thymus aging, and highlight the potential benefits of LHRH receptor antagonist treatment for thymic regeneration. Further research is required, however, to determine how gender may impact on the mechanisms underpinning these events.
+|keywords=* aging
-|keywords=* Aging
+* chemotherapy
-* BDNF
+* gender
-* CREB
+* luteinizing hormone-releasing hormone
-* Microglial activation
+* regeneration
-* NF-кB
+* sex hormone deprivation
-* TrkB
+* thymic epithelial cell
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7362451
+* thymus
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7062683
 }}
+==TEF==
 {{medline-entry
-|title=High Supervised Resistance Training in Elderly Women: The Role of Supervision Ratio.
+|title=Expression of human HSP27 in yeast extends replicative lifespan and uncovers a hormetic response.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32509119
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32189112
+|abstract=Human HSP27 is a small heat shock protein that modulates the ability of cells to respond to heat shock and oxidative stress, and also functions as a chaperone independent of ATP, participating in the proteasomal degradation of proteins. The expression of HSP27 is associated with survival in mammalian cells. In cancer cells, it confers resistance to chemotherapy; in neurons, HSP27 has a positive effect on neuronal viability in models of Alzheimer's and Parkinson's diseases. To better understand the mechanism by which HSP27 expression contributes to cell survival, we expressed human HSP27 in the budding yeast Saccharomyces cerevisiae under control of different mutant [[TEF]] promoters, that conferred nine levels of graded basal expression, and showed that replicative lifespan and proteasomal activity increase as well as the resistance to oxidative and thermal stresses. The profile of these phenotypes display a dose-response effect characteristic of hormesis, an adaptive phenomenon that is observed when cells are exposed to increasing amounts of stress or toxic substances. The hormetic response correlates with changes in expression levels of HSP27 and also with its oligomeric states when correlated to survival assays. Our results indicate that fine tuning of HSP27 concentration could be used as a strategy for cancer therapy, and also for improving neuronal survival in neurodegenerative diseases.
 |keywords=* Aging
-* exercise
+* Cancer
-* functional capacity
+* HSP27
-* muscle strength
+* Hormesis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7241618
+* Neurodegeneratve diseases
+* Proteasome
+|full-text-url=https://sci-hub.do/10.1007/s10522-020-09869-9
 }}
+==TERT==
 {{medline-entry
-|title=Metformin regulates astrocyte reactivity in Parkinson's disease and normal aging.
+|title=Unravelling Cellular Mechanisms of Stem Cell Senescence: An Aid from Natural Bioactive Molecules.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32497590
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32244882
+|abstract=Cellular senescence plays a role in the onset of age-related pathologies and in the loss of tissue homeostasis. Natural compounds of food or plants exert an important antioxidant activity, counteracting the formation of harmful free radicals. In the presence of an intense stressing event, cells activate specific responses to counteract senescence or cell death. In the present paper, we aimed at evaluating the levels of expression of specific markers of senescence, in order to demonstrate that extracts from [i]Myrtus Communis L[/i]. can prevent premature senescence in ADSCs exposed to oxidative stress. Cells were cultured in the presence of [i]Myrtus[/i] extracts for 12-24 and 48 h and then incubated with H O  to induce senescence. We then evaluated the expression of senescence-related markers p16, p19, p21, p53, [[TERT]], c-Myc, and the senescence-associated β-Galactoidase activity. Our results showed that pre-treatment with [i]Myrtus[/i] extracts protects cells from premature senescence, by regulating the cell cycle, and inducing the expression of [[TERT]] and c-Myc. These findings suggest a potential application of these natural compounds in the prevention and treatment of various diseases, counteracting premature senescence and preserving tissue functions.
+|keywords=* cellular mechanisms
-|keywords=* Aging
+* gene expression
-* Dorsal striatum
+* nutraceuticals
-* Metformin
+* oxidative stress
-* Parkinson's disease
+* senescence
-* Reactive astrocyte
+* stem cells
-|full-text-url=https://sci-hub.do/10.1016/j.neuropharm.2020.108173
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7150900
 }}
 {{medline-entry
-|title=Aging-Induced Brain-Derived Neurotrophic Factor in Adipocyte Progenitors Contributes to Adipose Tissue Dysfunction.
+|title=Expression of telomerase reverse transcriptase positively correlates with duration of lithium treatment in bipolar disorder.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32489703
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32114208
+|abstract=Bipolar disorder (BD) may be associated with accelerated cellular aging. However, previous studies on telomere length (TL), an important biomarker of cellular aging, have yielded mixed results in BD. We aimed to evaluate the hypothesis that BD is associated with telomere shortening and whether this is counteracted by long-term lithium treatment. We also sought to determine whether long-term lithium treatment is associated with increased expression of telomerase reverse transcriptase ([[TERT]]), the catalytic subunit of telomerase. We determined TL and [[TERT]] expression in 100 BD I patients and 100 healthy controls. We also genotyped three single nucleotide polymorphisms associated with TL. [[TERT]] expression was significantly increased in BD I patients currently on lithium treatment. [[TERT]] expression was also significantly positively correlated with duration of lithium treatment in patients treated for 24 months or more. However, we did not find any significant effect of lithium treatment on TL. Neither did we find significant differences in TL between BD patients and controls. We suggest that long-term lithium treatment is associated with an increase in the expression of [[TERT]]. We hypothesize that an increase in [[TERT]] expression may contribute to lithium's mood stabilizing and neuroprotective properties by improving mitochondrial function and decreasing oxidative stress.
+|mesh-terms=* Adult
+* Aging
+* Antimanic Agents
+* Bipolar Disorder
+* Cellular Senescence
+* Female
+* Humans
+* Lithium
+* Lithium Compounds
+* Male
+* Middle Aged
+* Mitochondria
+* Oxidative Stress
+* Polymorphism, Single Nucleotide
+* Real-Time Polymerase Chain Reaction
+* Telomerase
+* Telomere
+* Telomere Homeostasis
+* Telomere Shortening
+|keywords=* Affective disorder
+* Aging
+* Mitochondria
+* Oxidative stress
+* TERT
+* Telomere
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7334059
+}}
+==TF==
-|keywords=* BDNF
-* adipocyte progenitors
-* adipose tissue
-* aging
-* sympathetic innervation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7220283
-}}
 {{medline-entry
-|title=The Role of [[BDNF]] on Aging-Modulation Markers.
+|title=Expression of Transferrin and Albumin in the Sperm-Storage Tubules of Japanese Quail and their Possible Involvement in Long-Term Sperm Storage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32397504
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32174770
+|abstract=Because of the presence of sperm storage tubules (SSTs) in the utero-vaginal junction (UVJ) in the oviduct, once ejaculated sperm enter the female reproductive tract, they can survive for a prolonged period in domestic birds; however, the specific mechanisms involved in sperm maintenance within the SST remain to be elucidated. In this study, we showed that transferrin ([[TF]]) and albumin (ALB) are expressed in SSTs. When UVJ extracts were subjected to size-exclusion column chromatography, we obtained fractions that extend sperm longevity [i]in vitro[/i]. LC-MS/MS analysis of the two major proteins in the fractions identified these proteins as [[TF]] and ALB. Immunohistochemical analysis using specific antisera against [[TF]] and ALB indicated that both proteins were localized not only in the SSTs, but also in the surface epithelium of the UVJ. When the ejaculated sperm were incubated with either purified [[TF]] or ALB, sperm viability increased after 24 h. These results indicated that oviductal [[TF]] and ALB are involved in the process of sperm storage in SSTs and may open a new approach for technological improvement to prolong sperm longevity [i]in vitro[/i].
+|keywords=* Japanese quail
-|keywords=* BBB
+* albumin
-* astrocytes
+* sperm longevity
-* brain aging
+* sperm storage tubules
-* in vivo model
+* transferrin
-* low dose BDNF
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7063080
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7287884
 }}
-{{medline-entry
+==TG==
-|title=Spermidine and spermine delay brain aging by inducing autophagy in SAMP8 mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32268299
-|keywords=* aging
-* autophagy
-* mitochondrial dysfunction
-* polyamine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185103
-}}
 {{medline-entry
-|title=Microglia senescence occurs in both substantia nigra and ventral tegmental area.
+|title=Awareness of major cardiovascular risk factors and its relationship with markers of vascular aging: Data from the Brisighella Heart Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32275335
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32249143
+|abstract=General population awareness about cardiovascular risk factors is usually low. The aim of the present study was to evaluate the vascular aging of subjects aware and not aware to be hypertensive, hypercholesterolemic, hypertriglyceridemic or diabetics in a general population sample. We interviewed 1652 subjects without atherosclerotic cardiovascular diseases (M: 46.6%, F: 53.4%) about their awareness of hypertension, hypercholesterolemia, hypertriglyceridemia or type 2 diabetes. Then we compared the augmentation index and pulse wave velocity of subjects aware and not aware of the investigated cardiovascular risk factors. 1049 participants declared not to be hypertensive, while 32 were not sure. Among them, respectively, 23.5% and 50% were hypertensive. Subjects not aware of their hypertension had significantly higher aortic blood pressure than aware ones (p < 0.001). 841 participants declared not to be hypercholesterolemic, while 60 were not sure. Among them, respectively, 18.1% and 40% were hypercholesterolemic. Subjects not aware of their hypercholesterolemia had significantly higher augmentation index than the aware ones (p < 0.05). 1226 participants declared not to be hypertriglyceridemic, while 200 were not sure. Among them, respectively, 19.2% and 44% were hypertriglyceridemic. Subjects not aware of their hypertriglyceridemia had significantly higher [[TG]] levels aware ones (p < 0.05), although this seemed to not related to increased arterial stiffness. 1472 participants declared not to be diabetic, while 20 were not sure. Among them, respectively, 2.0% and 25.0% were diabetics. Subjects not aware of their diabetes had significantly higher augmentation index than the aware ones (p < 0.05). In conclusion, the lack of awareness of hypertension and hypercholesterolemia is relatively frequent in the general population and is associated to significantly higher arterial stiffness.
+|mesh-terms=* Adolescent
-|keywords=* Parkinson's disease
+* Adult
-* aging-dependent neurodegeneration
+* Age Factors
-* dopamine neurons
+* Aged
-* microglia complexity
+* Aged, 80 and over
-* stereological analyses
+* Aging
-* tyrosine hydroxylase; microglia senescence
+* Biomarkers
-|full-text-url=https://sci-hub.do/10.1002/glia.23834
+* Blood Glucose
+* Blood Pressure
+* Cardiovascular Diseases
+* Cholesterol
+* Cross-Sectional Studies
+* Diabetes Mellitus
+* Female
+* Humans
+* Hypercholesterolemia
+* Hypertension
+* Hypertriglyceridemia
+* Italy
+* Male
+* Middle Aged
+* Risk Assessment
+* Risk Factors
+* Triglycerides
+* Vascular Stiffness
+* Young Adult
+|keywords=* Arterial aging
+* Awareness
+* Epidemiology
+* Pulse wave velocity
+* Risk factors
+|full-text-url=https://sci-hub.do/10.1016/j.numecd.2020.03.005
 }}
 {{medline-entry
-|title=Towards an understanding of the physical activity-[[BDNF]]-cognition triumvirate: A review of associations and dosage.
+|title=Characterisation of the dynamic nature of lipids throughout the lifespan of genetically identical female and male Daphnia magna.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32171785
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32221338
+|abstract=Lipids play a significant role in regulation of health and disease. To enhance our understanding of the role of lipids in regulation of lifespan and healthspan additional studies are required. Here, UHPLC-MS/MS lipidomics was used to measure dynamic changes in lipid composition as a function of age and gender in genetically identical male and female Daphnia magna with different average lifespans. We demonstrate statistically significant age-related changes in triglycerides ([[TG]]), diglycerides (DG), phosphatidylcholine, phosphatidylethanolamine, ceramide and sphingomyelin lipid groups, for example, in males, 17.04% of [[TG]] lipid species decline with age whilst 37.86% increase in relative intensity with age. In females, 23.16% decrease and 25.31% increase in relative intensity with age. Most interestingly, the rate and direction of change can differ between genetically identical female and male Daphnia magna, which could be the cause and/or the consequence of the different average lifespans between the two genetically identical genders. This study provides a benchmark dataset to understand how lipids alter as a function of age in genetically identical female and male species with different average lifespan and ageing rate.
 |mesh-terms=* Aging
-* Brain-Derived Neurotrophic Factor
+* Animals
-* Cognition
+* Daphnia
-* Exercise
+* Diglycerides
-* Healthy Aging
-* Humans
-|keywords=* Ageing
-* BDNF
-* Brain
-* Physical activity
-|full-text-url=https://sci-hub.do/10.1016/j.arr.2020.101044
-}}
-{{medline-entry
-|title=Impact of [[BDNF]] and sex on maintaining intact memory function in early midlife.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31948671
-|mesh-terms=* Brain
-* Brain-Derived Neurotrophic Factor
-* Cognition
 * Female
-* Humans
+* Lipid Metabolism
-* Magnetic Resonance Imaging
+* Longevity
 * Male
-* Memory
+* Phosphatidylcholines
-* Memory, Short-Term
+* Sphingomyelins
-* Menopause
+* Triglycerides
-* Middle Aged
+|keywords=#f
-* Neuroprotective Agents
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7101400
-* Neuropsychological Tests
-* Reproduction
-* Sex Characteristics
-|keywords=* Aging
-* BDNF
-* Hormones
-* Memory
-* Menopause
-* Sex differences
-|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2019.12.014
 }}
-{{medline-entry
+==TH==
-|title=Testosterone replacement causes dose-dependent improvements in spatial memory among aged male rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31901624
-|keywords=* Aging
-* BDNF
-* Object location memory
-* Radial arm maze
-* Spatial memory
-* Testosterone
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7080566
-}}
 {{medline-entry
-|title=The effects of aerobic exercise intensity on memory in older adults.
+|title=Quantitative proteomic profiling of the rat substantia nigra places glial fibrillary acidic protein at the hub of proteins dysregulated during aging: Implications for idiopathic Parkinson's disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31665610
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32270889
+|abstract=There is a strong correlation between aging and onset of idiopathic Parkinson's disease, but little is known about whether cellular changes occur during normal aging that may explain this association. Here, proteomic and bioinformatic analysis was conducted on the substantia nigra (SN) of rats at four stages of life to identify and quantify protein changes throughout aging. This analysis revealed that proteins associated with cell adhesion, protein aggregation and oxidation-reduction are dysregulated as early as middle age in rats. Glial fibrillary acidic protein (GFAP) was identified as a network hub connecting the greatest number of proteins altered during aging. Furthermore, the isoform of GFAP expressed in the SN varied throughout life. However, the expression levels of the rate-limiting enzyme for dopamine production, tyrosine hydroxylase ([[TH]]), were maintained even in the oldest animals, despite a reduction in the number of dopamine neurons in the SN pars compact(SNc) as aging progressed. This age-related increase in [[TH]] expression per neuron would likely to increase the vulnerability of neurons, since increased dopamine production would be an additional source of oxidative stress. This, in turn, would place a high demand on support systems from local astrocytes, which themselves show protein changes that could affect their functionality. Taken together, this study highlights key processes that are altered with age in the rat SN, each of which converges upon GFAP. These findings offer insight into the relationship between aging and increased challenges to neuronal viability, and indicate an important role for glial cells in the aging process.
+|keywords=* RRID:AB_11145309
-|keywords=* BDNF
+* RRID:AB_2109791
-* activité physique
+* RRID:AB_228307
+* RRID:AB_228341
+* RRID:AB_2336820
+* RRID:AB_2631098
+* RRID:AB_390204
+* RRID:MGI:5651135
+* RRID:SCR_001881
+* RRID:SCR_002798
+* RRID:SCR_003070
+* RRID:SCR_004946
+* RRID:SCR_005223
 * aging
-* cognition
+* dopaminergic neuron
-* entraînement par intervalles de haute intensité
+* glial fibrillary acidic protein
-* executive functions
+* proteome
-* exercice
+* proteomics
-* exercise
+* substantia nigra
-* fonctions exécutives
+|full-text-url=https://sci-hub.do/10.1002/jnr.24622
-* high-intensity interval training
-* memory
-* mémoire
-* physical activity
-* vieillissement
-|full-text-url=https://sci-hub.do/10.1139/apnm-2019-0495
 }}
-{{medline-entry
+==TNC==
-|title=Protective effects of vitamin D on neurophysiologic alterations in brain aging: role of brain-derived neurotrophic factor ([[BDNF]]).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31524100
-|keywords=* BDNF
-* Brain aging
-* neurophysiologic alterations
-* neuroprotection
-* vitamin D supplementation
-|full-text-url=https://sci-hub.do/10.1080/1028415X.2019.1665854
-}}
 {{medline-entry
-|title=Differential Effects of Physical Exercise, Cognitive Training, and Mindfulness Practice on Serum [[BDNF]] Levels in Healthy Older Adults: A Randomized Controlled Intervention Study.
+|title=Tenascin-C expression controls the maturation of articular cartilage in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31498125
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32066496
+|abstract=Expression of the de-adhesive extracellular matrix protein tenascin-C ([[TNC]]) is associated with the early postnatal development of articular cartilage which is both load-dependent and associated with chondrocyte differentiation. We assessed morphological changes in the articular cartilage of [[TNC]] deficient mice at postnatal ages of 1, 4 and 8 weeks compared to age-matched wildtype mice. Cartilage integrity was assessed based on hematoxylin and eosin stained-sections from the tibial bone using a modified Mankin score. Chondrocyte density and cartilage thickness were assessed morphometrically. [[TNC]] expression was localized based on immunostaining. At 8 weeks of age, the formed tangential/transitional zone of the articular cartilage was 27% thicker and the density of chondrocytes in the articular cartilage was 55% lower in wildtype than the [[TNC]]-deficient mice. [[TNC]] protein expression was associated with chondrocytes. No relevant changes were found in mice at 1 and 4 weeks of age. The findings indicate a role of tenascin-C in the post-natal maturation of the extracellular matrix in articular cartilage. This might be a compensatory mechanism to strengthen resilience against mechanical stress.
-|mesh-terms=* Aged
-* Brain-Derived Neurotrophic Factor
-* Cognition
-* Correlation of Data
-* Exercise
-* Female
-* Healthy Aging
-* Healthy Lifestyle
-* Humans
-* Learning
-* Male
-* Mindfulness
-* Neuropsychological Tests
-* Outcome Assessment, Health Care
-|keywords=* Aging
-* brain-derived neurotrophic factor
-* cognitive training
-* mindfulness
-* physical exercise
-|full-text-url=https://sci-hub.do/10.3233/JAD-190756
-}}
-{{medline-entry
-|title=Dietary Supplementation with Fish Oil or Conjugated Linoleic Acid Relieves Depression Markers in Mice by Modulation of the Nrf2 Pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31398773
 |mesh-terms=* Aging
 * Animals
-* Antidepressive Agents
+* Cartilage, Articular
-* Autoimmunity
+* Cell Count
-* Biomarkers
+* Genotype
-* Brain
+* Mice
-* Brain-Derived Neurotrophic Factor
+* Tenascin
-* Depression
+|keywords=* Adhesion
-* Dietary Supplements
+* Articular cartilage
-* Docosahexaenoic Acids
+* Cartilage defect
-* Fatty Acid Elongases
+* Cell density
-* Fatty Acids
+* Knock-out mouse
-* Fish Oils
+* Load
-* Inflammation
+* Tenascin C
-* Linoleic Acids, Conjugated
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7027060
-* Liver
-* Male
-* Mice, Inbred MRL lpr
-* NF-E2-Related Factor 2
-* Oxidative Stress
-* Stearoyl-CoA Desaturase
-* Tumor Necrosis Factor-alpha
-|keywords=* brain derived neurotrophic factor
-* brain fatty acid profile
-* conjugated linoleic acid
-* depression
-* fish oil
-* nuclear erythroid related factor-2
-|full-text-url=https://sci-hub.do/10.1002/mnfr.201900243
 }}
-==BGN==
+==TNF==
 {{medline-entry
-|title=Alterations of local functional connectivity in lifespan: A resting-state fMRI study.
+|title=Synergistic Antitumor Efficacy of Magnetohyperthermia and Poly(lactic-co-glycolic acid)-Encapsulated Selol in Ehrlich Breast Adenocarcinoma Treatment in Elderly Swiss Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32462815
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32252879
+|abstract=Nanobiotechnology strategies for cancer treatments are currently being tested with increasing interest, except in elderly groups. It is well established that breast cancer incidence increases with age and that traditional therapies usually generate severe adverse effects, especially for elderly groups. To investigate if the benefits of nanotechnology could be extended to treating cancer in this group, citrate-coated maghemite nanoparticles (NpCit) were used for magnetohyperthermia (MHT) in combination with the administration of PLGA-Selol nanocapsule (NcSel), a formulation with antioxidant and antitumor activity. The combined therapies significantly inhibited breast Ehrlich tumor growth and prevented metastases to the lymph nodes, liver and lungs until 45 days after tumor induction, a better result than the group undergoing conventional drug treatment. The levels of [[TNF]]-α, associated with poor prognosis in Ehrlich tumor, were also normalized. Therefore, the results evidenced the potential use of these therapies for future clinical trials in elderly breast cancer patients.
+|mesh-terms=* Adenocarcinoma
-|keywords=* four-dimensional spatial-temporal consistency of local neural activity
+* Aging
-* lifespan
+* Animals
-* local functional connectivity
-* local functional connectivity density
-* resting-state fMRI
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7375100
-}}
-==BHLHE40==
-{{medline-entry
-|title=Thyroid hormone induces cellular senescence in prostate cancer cells through induction of DEC1.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32360904
-|mesh-terms=* Basic Helix-Loop-Helix Transcription Factors
 * Cell Line, Tumor
-* Cell Proliferation
+* Glycols
-* Cellular Senescence
-* Cyclin-Dependent Kinase Inhibitor p15
-* Homeodomain Proteins
 * Humans
-* Male
+* Mice
-* Prostatic Neoplasms
+* Nanoparticles
-* Thyroid Hormones
+* Polylactic Acid-Polyglycolic Acid Copolymer
-|keywords=* BHLHE40
+* Selenium Compounds
-* Cellular senescence
+|keywords=#f
-* DEC1
+|full-text-url=https://sci-hub.do/10.1166/jbn.2020.2890
-* Prostate cancer
-* Thyroid hormone
-|full-text-url=https://sci-hub.do/10.1016/j.jsbmb.2020.105689
 }}
-==BLM==
 {{medline-entry
-|title=[Olmesartan inhibits age-associated migration and invasion of human aortic vascular smooth muscle cells by upregulating miR-3133 axis].
+|title=Pinitol suppresses [[TNF]]-α-induced chondrocyte senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32895132
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32200264
+|abstract=Osteoarthritis (OA) is a highly prevalent joint disorder that is tightly correlated with age. As the body ages, cell replication and function decline until homeostasis can no longer be maintained. This process involves cellular senescence as well as replicative senescence. Telomere length, cell cycle arrest, expression of p16 and p53, and the release of senescence-associated β-galactosidase (SA-β-Gal) are all markers of cell senescence. In OA joints, chondrocytes undergo cellular senescence prematurely, thereby ceasing to synthesize and maintain cartilage tissue. Upregulation of proinflammatory cytokines, such as tumor necrosis factor-α ([[TNF]]-α), and oxidative stress induced by overproduction of reactive oxygen species (ROS) are key events in the pathogenesis of OA. In the present study, we investigated the effects of pinitol, a naturally occurring compound, on the effects of [[TNF]]-α on chondrocyte senescence and cell cycle arrest. We found that pinitol has a favorable safety profile in terms of cell viability. Pinitol significantly inhibited cellular senescence and cell cycle arrest in the G0/G1 phase induced by [[TNF]]-α. We also found that pinitol could inhibit [[TNF]]-α-induced increased telomerase activity and expression of p16 and p53. Importantly, we found that the effects of pinitol may be mediated through rescue of Nrf2 signaling, which is recognized as a key protective factor in OA. This finding was verified through a Nrf2 silencing experiment using Nrf2 siRNA. Together, our findings reveal the potential of pinitol as a safe therapeutic option for the prevention of OA-associated chondrocyte senescence and oxidative stress.
-|mesh-terms=* Cell Movement
+|keywords=* Cellular senescence
-* Cell Proliferation
+* Nrf2
-* Cells, Cultured
+* Osteoarthritis
+* Pinitol
+* TNF-α
+|full-text-url=https://sci-hub.do/10.1016/j.cyto.2020.155047
+}}
+{{medline-entry
+|title=[Aging of skin fibroblasts: genetic and epigenetic factors.]
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32160428
+|abstract=Gerontocosmetology is the rapid developing knowledge area that has a very large applied meaning. Herewith a lot of information about skin aging and geroprotectors for skin rejuvenation hasn't a scientific background. Thus, understanding the fundamental mechanisms of skin aging becomes the actual task of molecular gerontology. Skin fibroblasts are the polyfunctional cell population that synthesize a number of biologically active substances and participate in maintaining of extracellular matrix homeostasis, skin hydratation and endocrine and immune function. In the review genetic (accumulation of nuclear and mitochondrial DNA mistakes) and epigenetic factors of skin fibroblasts aging are described. Role of AP-1, NF-κB, c-jun, CCN1, TGF-β, [[TNF]]-α, MMP-1, MMP-3, MMP-8, MMP-9 and glycation in skin fibroblasts aging are discussed. There are some data about decreasing of skin fibroblasts ability to migration and synthesis of paxillins and aquaporin-3 (AQP3) during aging. Role of hormonal regulation in skin fibroblasts aging are described. Geroprotective action of melatonin to skin fibroblasts are showed. Reviewed molecular-cellular aspects of skin fibroblasts aging can be take into consideration for scientific background of using of cosmetic products for retarding of skin aging rate.
+|mesh-terms=* Cells, Cultured
+* Epigenesis, Genetic
+* Fibroblasts
 * Humans
-* Imidazoles
+* Skin Aging
-* Matrix Metalloproteinase 2
-* MicroRNAs
-* Muscle, Smooth, Vascular
-* Myocytes, Smooth Muscle
-* Tetrazoles
 |keywords=* aging
-* invasion
+* melatonin
-* microRNA
+* signal molecules
-* migration
+* skin fibroblasts
-* olmesartan
-* vascular smooth muscle cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7225100
 }}
-==BMI1==
 {{medline-entry
-|title=Senescence Induced by [[BMI1]] Inhibition Is a Therapeutic Vulnerability in H3K27M-Mutant DIPG.
+|title=Functional and traditional training improve muscle power and reduce proinflammatory cytokines in older women: A randomized controlled trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33086074
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32151735
+|abstract=Aging is a natural process that, even in the nonattendance of complex diseases, is associated with a numerous behavioral change that attributes reduced muscle mass, power, strength and function. In addition, aging linked to low-grade inflammatory status, characterized by increased plasma concentrations of inflammatory cytokines such as [[TNF]]-α and IL-6. Physical exercise is the main non-pharmacological strategy for improving the physical fitness of the aged individuals. However, it is still controversial whether exercise can reduce aging-mediated inflammation. To analyze the effects of functional (FT) and traditional (TT) training practice on muscle power and inflammatory profile in physically active older women. The study has been performed for twenty-six weeks in which twenty-four weeks utilized for training sessions and two weeks for physical and biochemical assessments. Forty-three older women (age FT: 64.25 ± 4.70, range: 60-75; TT: 64.90 ± 3.03, range: 60-71; Control: 65.91 ± 5.79, range: 60-75) were randomly divided into three groups: Functional (FT; n = 16); Traditional (TT; n = 16) training groups; and Control Group (CG; n = 11) respectively. Muscle power tests were performed by push (Bench press) and squatting (Squat) actions. The jumping ability was performed through Counter Movement Jump (CMJ). In addition, isometric strength were assessed by Hand Grip Test. Plasma cytokine concentration was measured using flow cytometry. Functional and traditional training sessions subjected to aged women demonstrated a significant enhancement in their physical activity and muscle power. The trained individuals from above two groups showed significant improvements in all analyzed parameters excluding hand-grip. Functional and traditional training exercise reduced the plasma concentrations of [[TNF]]-α (FT: p = 0.0001; TT: p = 0.0410) and whereas FT group has reduced IL-6 (p = 0.0072), but did not affect the alterations of pre and post measurements of IL-2 (FT: p = 0.0651; TT: p = 0.2146) and IL-10 values (FT: p = 0.2658; TT: p = 0.3116). There was no significant difference in any of the test parameters between FT and TT groups. The functional and traditional training practices showed equivalent beneficial outcomes by increasing muscle power and reducing systemic markers associated with inflammation.
+|keywords=* Aging
-|keywords=* BH3 mimetics
+* Cytokines.
-* BMI1
+* Dynapenia
-* DIPG
+* Inflamm-aging
-* H3K27M mutant
+|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110920
-* H3WT
-* PTC 028
-* RNAi screen
-* SASP
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7574900
 }}
-==BMP2==
 {{medline-entry
-|title=Interleukin-1β-Induced Senescence Promotes Osteoblastic Transition of Vascular Smooth Muscle Cells.
+|title=Associations of [[TNF]]-α -308 G>A and [[TNF]]-β 252 A>G with Physical Function and BNP-Rugao Longevity and Ageing Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32126555
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115620
+|abstract=To explore the associations of [[TNF]]-α -308 G>A (rs1800629) and [[TNF]]-β 252 A>G (rs909253) with physical function and plasma B-type natriuretic peptide (BNP). Data of 1747 community-dwelling elders from the ageing arm of the Rugao Longevity and Ageing Study was used. Physical function was measured by handgrip strength, Timed Up and Go (TUG) test and 5-meter walking test (5MWT). AA genotype of the [[TNF]]-α -308 G>A was associated with higher mean time of TUG test and 5MWT (multivariable adjusted β=5.75 and 5.70, respectively, p<0.05), compared with GG genotype. For the [[TNF]]-β 252 A>G polymorphism, GG genotype was associated with higher mean time of TUG test and 5MWT (multivariable adjusted β=1.55 and 0.83, respectively, p<0.05) and lower handgrip strength (multivariable adjusted β=-0.69, p<0.05), compared with AA genotype. Further, GG was associated with greater odds of low handgrip strength (OR=1.47, 95% CI=1.06-2.04), low speed of TUG test (OR=1.87, 95% CI=1.20-2.01) and elevated BNP (OR=1.30, 95% CI=1.08-1.84). GG also interacted with elevated BNP to be associated with greater odds of low handgrip strength and 5MWT. [[TNF]]-β 252 A>G was associated with physical function measurements, plasma BNP level, and odds of elevated BNP in an elderly population. [[TNF]]-β 252 A>G also interacted with elevated BNP to be associated with greater odds of physical function measurements.
-|mesh-terms=* Adult
+|mesh-terms=* Aged
-* Aged
 * Aged, 80 and over
+* Aging
 * Female
 * Humans
-* Interleukin-1beta
+* Longevity
 * Male
-* Middle Aged
+* Natriuretic Peptide, Brain
-* Muscle, Smooth, Vascular
+* Tumor Necrosis Factor-alpha
-* Osteoblasts
+|keywords=* Physical function
-|keywords=* Interleukin-1β
+* TNF-α -308 G>A polymorphism
-* Osteoblastic transition
+* TNF-β 252 A>G polymorphism
-* Senescence
+* plasma BNP
-* Vascular calcification
+* population study.
-|full-text-url=https://sci-hub.do/10.1159/000504298
+|full-text-url=https://sci-hub.do/10.1007/s12603-020-1336-1
 }}
-==BMP4==
 {{medline-entry
-|title=Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome.
+|title=3D TECA hydrogel reduces cellular senescence and enhances fibroblasts migration in wound healing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32896271
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32104405
+|abstract=This study was designed to investigate the effect of 3D TECA hydrogel on the inflammatory-induced senescence marker, and to assess the influence of the gel on the periodontal ligament fibroblasts (PDLFs) migration in wound healing [i]in vitro[/i]. PDLFs were cultured with 20 ng/ml [[TNF]]-α to induce inflammation in the presence and absence of 50 µM 3D TECA gel for 14 d. The gel effect on the senescence maker secretory associated-β-galactosidase (SA-β-gal) activity was measured by a histochemical staining. Chromatin condensation and DNA synthesis of the cells were assessed by 4',6-diamidino-2-phenylindole and 5-ethynyl-2'-deoxyuridine fluorescent staining respectively. For evaluating fibroblasts migration, scratch wound healing assay and Pro-Plus Imaging software were used. The activity of senescence marker, SA-β-gal, was positive in the samples with [[TNF]]-α-induced inflammation. SA-β-gal percentage is suppressed (>65%, [i]P[/i] < 0.05) in the treated cells with TECA gel as compared to the non-treated cells. Chromatin foci were obvious in the non-treated samples. DNA synthesis was markedly recognized by the fluorescent staining in the treated compared to non-treated cultures. Scratch wound test indicated that the cells migration rate was significantly higher (14.9 µm /h, [i]P[/i] < 0.05) in the treated versus (11 µm /h) for control PDLFs. The new formula of 3D TECA suppresses the inflammatory-mediated cellular senescence and enhanced fibroblasts proliferation and migration. Therefore, 3D TECA may be used as an adjunct to accelerate repair and healing of periodontal tissues.
+|keywords=* 3D TECA
-|keywords=* aging
+* Cellular senescence
-* direct reprogramming
+* Fibroblast migration
-* endothelial cell
+* SA-β-gal
-* human
+* TNF-α
-* hutchinson-gilford progeria syndrome
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7032142
-* medicine
+}}
-* mouse
+{{medline-entry
-* smooth muscle cell
+|title=Regulatory Effect of Anwulignan on the Immune Function Through Its Antioxidation and Anti-Apoptosis in D-Galactose-Induced Aging Mice.
-* vascular barrier
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32099340
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7478891
+|abstract=Aging is a spontaneous and inevitable phenomenon of biology, which can lead to the gradual deterioration of tissues and organs. One of the age-related deterioration processes is immunosenescence, which leads to changes in the function of immune systems, including immune cells and associated cytokines. A proper modulation of immune responses can improve the age-related immunosenescence process and then reach healthy aging. [i]Schisandra sphenanthera[/i], a traditional Chinese medicine, has been used as both a medicine and a nutritional supplement for thousands of years. Anwulignan, a monomer compound of [i]Schisandra sphenanthera[/i] lignans, has been reported to possess an immunomodulatory effect. Therefore, this study was designed to further explore whether Anwulignan could also modulate the immune functions in aging model mice and the underlying mechanism. D-galactose (D-gal) is often used as an inducer of immunosenescence in animals. In this study, a mice model was created by subcutaneous D-gal (220 mg kg ) for successive 42 days. Then, the blood and spleen tissue samples were taken for the analysis and observation of cytokine levels, immunoglobulin levels, leukocyte numbers, and the phagocytic activity of macrophages, as well as the histological changes, the proliferation ability of lymphocytes, and the biochemical parameters in the spleen tissue. Anwulignan significantly increased the serum levels of IL-2, IL-4, IFN-γ, lgG, lgM, and lgA, decreased the content of [[TNF]]-α and IL-6 in the aging mice, and increased the blood leukocyte number, the phagocytic activity, the lymphocyte proliferation, and the spleen index in vitro. Anwulignan also significantly increased the activities of SOD and GSH-Px, decreased the contents of MDA and 8-OHdG in the spleen tissue, up-regulated the expressions of Nrf2, HO-1, and Bcl2, down-regulated the expressions of Keap1, Caspase-3, and Bax in the spleen cells, and reduced the apoptosis of spleen lymphocytes. Anwulignan can restore the immune function that is declined in D-gal-induced aging mice partly related to its antioxidant capacity by activating the Nrf2/ARE pathway and downstream enzymes, as well as its anti-apoptotic effect by regulating Caspase-3 and the ratio of Bcl2 to Bax in the spleen.
+|mesh-terms=* Animals
+* Antioxidants
+* Apoptosis
+* Cytokines
+* Immunologic Factors
+* Immunosenescence
+* Male
+* Medicine, Chinese Traditional
+* Mice
+* Models, Animal
+* NF-E2-Related Factor 2
+* Oxidative Stress
+* Phytochemicals
+* Schisandra
+* Spleen
+|keywords=* Anwulignan
+* anti-apoptosis
+* antioxidation
+* immunosenescence
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996228
 }}
-==BMP7==
 {{medline-entry
-|title=Downregulation of miR-542-3p promotes osteogenic transition of vascular smooth muscle cells in the aging rat by targeting [[BMP7]].
+|title=Pretreatment Frailty Is Independently Associated With Increased Risk of Infections After Immunosuppression in Patients With Inflammatory Bowel Diseases.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31829291
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32105728
+|abstract=Infections are an important adverse effect of immunosuppression for treatment of inflammatory bowel diseases (IBDs). However, risk of infection cannot be sufficiently determined based on patients' ages or comorbidities. Frailty has been associated with outcomes of patients with other inflammatory diseases. We aimed to determine the association between frailty and risk of infections after immunosuppression for IBD. We performed a cohort study of 11,001 patients with IBD, using a validated frailty definition based on International Classification of Disease codes to identify patients who were frail vs fit in the 2 years before initiation of an anti-tumor necrosis factor ([[TNF]]) or immunomodulator therapy, from 1996 through 2010. Our primary outcome was an infection in the first year after treatment. We constructed multivariable logistic regression models, adjusting for clinically pertinent confounders (age, comorbidities, steroid use, and combination therapy) to determine the association between frailty and posttreatment infections. There were 1299 patients treated with an anti-[[TNF]] agent and 2676 patients treated with an immunomodulator. In this cohort, 5% of patients who received anti-[[TNF]] therapy and 7% of patients who received an immunomodulator were frail in the 2 years before immunosuppression. Frail patients were older and had more comorbidities. Higher proportions of frail patients developed infections after treatment (19% after [[TNF]] and 17% after immunomodulators) compared with fit patients (9% after [[TNF]] and 7% after immunomodulators; P < .01 for frail vs fit in both groups). Frail patients had an increased risk of infection after we adjusted for age, comorbidities, and concomitant medications (anti-[[TNF]] adjusted odds ratio, 2.05 [95% confidence interval, 1.07-3.93] and immunomodulator adjusted odds ratio, 1.81 [95% confidence interval, 1.22-2.70]). Frailty was associated with infections after immunosuppression in patients with IBD after we adjust for age and comorbidities. Systematic assessment and strategies to improve frailty might reduce infection risk in patients with IBD.
-|mesh-terms=* Aging
-* Animals
-* Base Sequence
-* Bone Morphogenetic Protein 7
-* Down-Regulation
-* Glycerophosphates
-* MicroRNAs
-* Models, Biological
-* Muscle, Smooth, Vascular
-* Myocytes, Smooth Muscle
-* Osteogenesis
-* Rats
 |keywords=* Aging
-* Mir-542-3p
+* Immunosuppression
-* Osteogenic differentiation
+* Side Effect
-* Vascular smooth muscle cells
+* Thiopurine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6907335
+|full-text-url=https://sci-hub.do/10.1053/j.gastro.2020.02.032
 }}
-==BOC==
+==TP53==
 {{medline-entry
-|title=Protein Requirements of Elderly Chinese Adults Are Higher than Current Recommendations.
+|title=Mutational spectrum and dynamics of clonal hematopoiesis in anemia of older individuals.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32140711
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32243522
+|abstract=Anemia is a major and currently poorly understood clinical manifestation of hematopoietic aging. Upon aging, hematopoietic clones harboring acquired leukemia-associated mutations expand and become detectable, now referred to as clonal hematopoiesis (CH). To investigate the relationship between CH and anemia of the elderly, we explored the landscape and dynamics of CH in older individuals with anemia. From the prospective, population-based Lifelines cohort (n = 167 729), we selected all individuals at least 60 years old who have anemia according to World Health Organization criteria (n = 676) and 1:1 matched control participants. Peripheral blood of 1298 individuals was analyzed for acquired mutations at a variant allele frequency (VAF) of 1% or higher in 27 driver genes. To track clonal evolution over time, we included all available follow-up samples (n = 943). CH was more frequently detected in individuals with anemia (46.6%) compared with control individuals (39.1%; P = .007). Although no differences were observed regarding commonly detected DTA mutations (DNMT3A, TET2, ASXL1) in individuals with anemia compared with control individuals, other mutations were enriched in the anemia cohort, including [[TP53]] and SF3B1. Unlike individuals with nutrient deficiency (P = .84), individuals with anemia of chronic inflammation and unexplained anemia revealed a higher prevalence of CH (P = .035 and P = .017, respectively) compared with their matched control individuals. Follow-up analyses revealed that clones may expand and decline, generally showing only a subtle increase in VAF (mean, 0.56%) over the course of 44 months, irrespective of the presence of anemia. Specific mutations were associated with different growth rates and propensities to acquire an additional hit. In contrast to smaller clones (<5% VAF), which did not affect overall survival, larger clones were associated with increased risk for death.
-|mesh-terms=* Aged
+|mesh-terms=* Age Factors
+* Aged
 * Aging
-* Amino Acids
+* Anemia
-* Body Weight
-* China
-* Dietary Proteins
-* Energy Intake
-* Energy Metabolism
 * Female
+* Hematopoiesis
 * Humans
+* Kaplan-Meier Estimate
 * Male
-* Nutritional Requirements
+* Middle Aged
-* Oxidation-Reduction
+* Mutation
-* Phenylalanine
+* Prospective Studies
-* Recommended Dietary Allowances
+|keywords=#f
-* Tyrosine
+|full-text-url=https://sci-hub.do/10.1182/blood.2019004362
-|keywords=* indicator amino acid oxidation
+}}
-* older adults
+==TRAF3==
-* phenylalanine oxidation
-* protein requirement
-* stable isotope
-|full-text-url=https://sci-hub.do/10.1093/jn/nxaa031
-}}
-==BPI==
 {{medline-entry
-|title=High TARC plasma levels confer protection to long living individuals by inducing M2 profile.
+|title=[[TRAF3]], a Target of MicroRNA-363-3p, Suppresses Senescence and Regulates the Balance Between Osteoblastic and Adipocytic Differentiation of Rat Bone Marrow-Derived Mesenchymal Stem Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33002742
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32111144
+|abstract=Bone marrow-derived mesenchymal stem cells (BMSCs) have the potential to differentiate into osteoblasts or adipocytes, and an imbalance between adipogenesis and osteogenesis causes age-related bone loss. In this study, we determined the influence of tumor necrosis factor receptor-associated factor 3 ([[TRAF3]]) on senescence and osteoblastic and adipocytic differentiation of rat BMSCs. [[TRAF3]] expression increased during osteogenic differentiation but decreased during adipocytic differentiation of rat BMSCs, and compared with day 0 cultures, on day 14, the differences were significant. Overexpression of [[TRAF3]] significantly promoted BMSC osteogenic differentiation and suppressed adipogenic differentiation and senescence. Furthermore, [i]Traf3[/i] was determined to be a target gene of miR-363-3p in BMSCs, and [[TRAF3]] expression in BMSCs was reduced by miR-363-3p overexpression. This overexpression attenuated the effects of [[TRAF3]] on BMSC adipogenic differentiation, osteogenic differentiation, and senescence. Taken together, these results uncovered the mechanism by which [[TRAF3]] promotes BMSC osteogenic differentiation and suppresses adipogenic differentiation and senescence, indicating that the miR-363-3p-[[TRAF3]] axis might be a novel therapeutic target for BMSC-based bone tissue engineering in osteoporosis.
+|keywords=* TRAF3
+* adipogenic differentiation
+* bone marrow-derived mesenchymal stem cells
+* miR-363-3p
+* osteogenic differentiation
+* senescence
+|full-text-url=https://sci-hub.do/10.1089/scd.2019.0276
+}}
+==TRIM21==
-|keywords=* FACS
-* Longevity
-* M2 macrophages
-* Plasma profile
-* TARC
-|full-text-url=https://sci-hub.do/10.1016/j.cyto.2020.155305
-}}
 {{medline-entry
-|title=Circulating [[BPI]]FB4 Levels Associate With and Influence the Abundance of Reparative Monocytes and Macrophages in Long Living Individuals.
+|title=[[TRIM21]] overexpression promotes tumor progression by regulating cell proliferation, cell migration and cell senescence in human glioma.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32547549
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32064156
+|abstract=Molecular biomarkers combined with histopathological examination are of critical importance in the diagnosis and treatment of gliomas. Although recent studies have shown that many tripartite motif-containing (TRIM) family proteins could regulate the cell cycle, cell proliferation, and differentiation in cancers, the precise role of [[TRIM21]] has been unknown in glioma. In this study, we analyzed [[TRIM21]], which was upregulated in gliomas and identified its role in tumor proliferation, migration and drug resistance. By using immunohistochemical analysis, we found that the expression level of [[TRIM21]] was upregulated in glioma specimens and the higher expression level of [[TRIM21]] was associated with poorer clinical outcomes in glioma patients. Moreover, we demonstrated that [[TRIM21]] could act as a regulator of the proliferation, cell cycle, and migration of glioma cells by gain- and loss-of function assays in vitro. In vivo, [[TRIM21]] could also modulate glioma progression in murine intracranial xenografts. Furthermore, we found that [[TRIM21]] suppressed cellular senescence via the p53-p21 pathway, and increased drug resistance in glioma cells by RNA-seq analysis, SA-[i]β[/i]-Gal activity assay, and Cell Counting Kit-8 (CCK-8) assay. These results indicated that [[TRIM21]] is a novel regulator in the diagnosis, prognosis, and therapy of gliomas.
+|keywords=* Glioma
-|keywords=* FACS
+* TRIM21
-* M2 macrophages
+* cell senescence
-* immunity
+* drug resistance
-* longevity
+* p53-p21 pathway
-* patrolling-monocytes
+* prognosis
-* plasma
+|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7017742
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7272600
 }}
-==BPIFB4==
+==TST==
 {{medline-entry
-|title=New Insights for [[BPIFB4]] in Cardiovascular Therapy.
+|title=Adaptations in mechanical muscle function, muscle morphology, and aerobic power to high-intensity endurance training combined with either traditional or power strength training in older adults: a randomized clinical trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32998388
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32239311
+|abstract=There is a lack of information on the effects of power training (PT) as an alternative to traditional strength training ([[TST]]) during concurrent training (CT) in older individuals. This study aimed to verify the neuromuscular adaptations that occurred following 16-week interventions with two CT models in older men: high-intensity interval training (HIIT) combined with either [[TST]] or PT. Thirty-five older men (65.8 ± 3.9 years) were randomly assigned into one of two training groups CTS: [[TST]] + HIIT (n = 18) or CTP: PT + HIIT (n = 17). CTS performed resistance training at intensities ranging from 65 to 80% of 1 RM at slow controlled speed, whereas CTP trained at intensities ranging from 40 to 60% of 1 RM at maximal intentional speed. Lower body one-repetition maximum (1 RM), isometric rate of force development (RFD), countermovement jump (CMJ) muscle power output, quadriceps femoris muscles thickness (QF MT), and peak oxygen uptake (VO ) were assessed before training and after 8 and 16 weeks of CT. Groups improved similarly in all primary outcomes (P < 0.05), with mean increases ranging: 1 RM (from 39.4 to 75.8%); RFD (from 9.9 to 64.8%); and CMJ muscle power (from 1.8 to 5.2%). Significant increases (P < 0.05) were observed in all secondary outcomes (QF MT, specific tension and VO ) with no differences between groups. CT models were effective for improving maximal and explosive force (1 RM, RFD, and CMJ power), QF MT, and VO . Moreover, despite that using lower loading intensities, PT induced similar adaptations to those of [[TST]].
+|keywords=* Aging
+* Concurrent training
+* Explosive force
+* Functional capacity
+* HIIT
+|full-text-url=https://sci-hub.do/10.1007/s00421-020-04355-z
+}}
+==U2AF1==
-|keywords=* BPIFB4
-* aging
-* cardiovascular disease
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7583974
-}}
 {{medline-entry
-|title=LAV-[[BPIFB4]] associates with reduced frailty in humans and its transfer prevents frailty progression in old mice.
+|title=Isobaric tags for relative and absolute quantitation (iTRAQ)-based proteomic analysis of mRNA splicing relevant proteins in aging HSPCs.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31461407
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32141009
+|abstract=HSPC (hematopoietic stem/progenitor cell) aging was closely associated with the organism aging, senile diseases and hematopoietic related diseases. Therefore, study on HSPC aging is of great significance to further elucidate the mechanisms of aging and to treat hematopoietic disease resulting from HSPC aging. Little attention had been paid to mRNA splicing as a mechanism underlying HSPC senescence. We used our lab's patented in vitro aging model of HSPCs to analyze mRNA splicing relevant protein alterations with iTRAQ-based proteomic analysis. We found that not only the notable mRNA splicing genes such as SR, hnRNP, WBP11, Sf3b1, Ptbp1 and [[U2AF1]] but also the scarcely reported mRNA splicing relevant genes such as Rbmxl1, Dhx16, Pcbp2, Pabpc1 were significantly down-regulated. We further verified their gene expressions by qRT-PCR. In addition, we reported the effect of Spliceostatin A (SSA), which inhibits mRNA splicing in vivo and in vitro, on HSPC aging. It was concluded that mRNA splicing emerged as an important factor for the vulnerability of HSPC aging. This study improved our understanding of the role of mRNA splicing in the HSPC aging process.
-|mesh-terms=* Aged
+|keywords=* Aging
-* Aged, 80 and over
+* DEPs
-* Aging
+* HSPC
-* Animals
+* iTRAQ
-* Female
+* mRNA splicing
-* Frailty
+|full-text-url=https://sci-hub.do/10.1007/s40520-020-01509-z
-* Gene Expression Regulation
-* Genotype
-* Humans
-* Longevity
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Mice, Transgenic
-* Phosphoproteins
-* Specific Pathogen-Free Organisms
-|keywords=* BPIFB4
-* aging
-* frailty
-* longevity-associated variant-lav
-* survival
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6738439
 }}
-==BRAF==
+==UCP1==
 {{medline-entry
-|title=Conditional reprograming culture conditions facilitate growth of lower grade glioma models.
+|title=Lack of [[UCP1]] stimulates fatty liver but mediates [[UCP1]]-independent action of beige fat to improve hyperlipidemia in Apoe knockout mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33258947
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32179129
+|abstract=Brown adipose tissue (BAT) plays a critical role in lipid metabolism and may protect from hyperlipidemia; however, its beneficial effect appears to depend on the ambient temperature of the environment. In this study, we investigated the effects of uncoupling protein 1 ([[UCP1]]) deficiency on lipid metabolism, including the pathophysiology of hyperlipidemia, in apolipoprotein E knockout (APOE-KO) mice at a normal (23 °C) and thermoneutral (30 °C) temperature. Unexpectedly, [[UCP1]] deficiency caused improvements in hyperlipidemia, atherosclerosis, and glucose metabolism, regardless of an increase in hepatic lipid deposition, in Ucp1/Apoe double-knockout (DKO) mice fed a high-fat diet at 23 °C, with BAT hyperplasia and robust browning of inguinal white adipose tissue (IWAT) observed. Proteomics and gene expression analyses revealed significant increases in many proteins involved in energy metabolism and strong upregulation of brown/beige adipocyte-related genes and fatty acid metabolism-related genes in browned IWAT, suggesting an induction of beige fat formation and stimulation of lipid metabolism in DKO mice at 23 °C. Conversely, mRNA levels of fatty acid oxidation-related genes decreased in the liver of DKO mice. The favorable phenotypic changes were lost at 30 °C, with BAT whitening and disappearance of IWAT browning, while fatty liver further deteriorated in DKO mice compared with that in APOE-KO mice. Finally, longevity analysis revealed a significant lifespan extension of DKO mice compared with that of APOE-KO mice at 23 °C. Irrespective of the fundamental role of [[UCP1]] thermogenesis, our results highlight the importance of beige fat for the improvement of hyperlipidemia and longevity under the atherogenic status at normal room temperature.
+|keywords=* Apoe knockout mice
-|keywords=* BRAFV600E
+* Beige fat
-* Conditional reprogramming
+* Gene expression
-* NF1
+* Hyperlipidemia
-* Senescence
-* low grade glioma
-|full-text-url=https://sci-hub.do/10.1093/neuonc/noaa263
-}}
-{{medline-entry
-|title=Active notch protects MAPK activated melanoma cell lines from MEK inhibitor cobimetinib.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33202284
-|keywords=* Cobimetinib (PubChem CID: 16222096)
-* MEK
-* Nirogacestat (PubChem CID:46224413)
-* Notch
-* Senescence
-* Uveal melanoma
-|full-text-url=https://sci-hub.do/10.1016/j.biopha.2020.111006
-}}
-{{medline-entry
-|title=Mitochondrial metabolic reprograming via [[BRAF]] inhibition ameliorates senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31421186
-|mesh-terms=* Cell Proliferation
-* Cells, Cultured
-* Cellular Reprogramming
-* Cellular Senescence
-* Drug Evaluation, Preclinical
-* Humans
-* Mitochondria
-* Proto-Oncogene Proteins B-raf
-|keywords=* BRAF
-* Metabolic reprogramming
-* Mitochondrial function
-* SB590885
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2019.110691
-}}
-==BRD2==
-{{medline-entry
-|title=Brd2 haploinsufficiency extends lifespan and healthspan in C57B6/J mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32559200
-|mesh-terms=* Animals
-* Female
-* Fertility
-* Grooming
-* Haploinsufficiency
-* Kidney
 * Longevity
-* Male
+* Uncoupling protein 1
-* Mice
+|full-text-url=https://sci-hub.do/10.1016/j.bbadis.2020.165762
-* Mice, Inbred C57BL
-* Transcription Factors
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7304595
 }}
-==BRD4==
+==VDAC1==
 {{medline-entry
-|title=Inhibition of [[BRD4]] triggers cellular senescence through suppressing aurora kinases in oesophageal cancer cells.
+|title=Changes in the expression of oxidative phosphorylation complexes in the aging intestinal mucosa.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32954665
+|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32173460
+|abstract=Mitochondria produce cellular energy via oxidative phosphorylation (OXPHOS), mediated by respiratory chain complexes I to IV and ATP synthase (complex V). Mitochondrial respiratory complexes have been shown to decline with age in several tissues. As the intestinal epithelium is a tissue with a high energy demand, the aim of the present study was to establish whether the expression profile of OXPHOS subunits in the intestinal mucosa changes during the aging process. Biopsies of intestinal mucosa with no evidence of endoscopic or histomorphologic abnormalities, taken from 55 patients (mean age 42 years, age range 4-82 years; 62% female), were divided into four age groups (4-19, 20-39, 40-59, ≥60 years). Sections from different intestinal segments (terminal ileum, ascending colon, and sigmoid colon/rectum) were stained immunohistochemically (IHC) for subunits of OXPHOS complexes I-V and the voltage-dependent anion-selective channel 1 protein ([[VDAC1]], porin), a marker of mitochondrial mass. Scores for IHC staining were determined by multiplication of the staining intensity and the percentage of positive cells. In addition, the numbers of intestinal crypts staining positive, partly positive, and negative were assessed. The average protein expression levels of OXPHOS subunits increased continuously from childhood onward, peaked in persons aged 20 to 59 years, and declined thereafter. This was seen for complexes II to V in the terminal ileum, complexes I to V in the ascending colon, and complexes I to IV in the sigmoid colon/rectum. Across all age groups, no effect of age on expression of the porin subunit [[VDAC1]] was detected. The number of complex I- and IV-negative crypts in different intestinal segments increased with age. The protein expression levels of OXPHOS complexes increases from childhood onward and declines in elderly individuals, while the numbers of crypts with partial or complete loss of expression of complexes I and IV increase continuously with age. These data suggest that the continued reductions in the levels of mitochondrial OXPHOS complexes in crypts might be compensated in adulthood, but that, ultimately, reduced expression levels occur in persons aged 60 years and older. These findings raise two important questions: first, can the process of aging could be delayed through (pharmacological) intervention of mitochondrial pathways, and second, pathophysiologically, are these findings associated with disorders of the intestinal mucosa, e.g. inflammation?
+|keywords=* Aging
-|keywords=* BRD4
+* Colonic crypt
-* aurora kinase
+* Expression
-* cellular senescence
+* Intestine
-* oesophageal cancer
+* Mitochondria
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7701500
+* OXPHOS
-}}
+|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110924
-{{medline-entry
-|title=[[BRD4]] contributes to LPS-induced macrophage senescence and promotes progression of atherosclerosis-associated lipid uptake.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32392533
-|keywords=* BRD4
-* gene expression
-* inflammation
-* macrophage
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7288959
-}}
-{{medline-entry
-|title=BET Proteins Are Required for Transcriptional Activation of the Senescent Islet Cell Secretome in Type 1 Diabetes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31561444
-|mesh-terms=* Animals
-* Cell Cycle Proteins
-* Cellular Senescence
-* Diabetes Mellitus, Type 1
-* Female
-* Humans
-* Insulin-Secreting Cells
-* Islets of Langerhans
-* Mice
-* Mice, Inbred NOD
-* Paracrine Communication
-* Protein Binding
-* Transcription Factors
-* Transcriptional Activation
-|keywords=* BET proteins
-* beta cells
-* senescence and SASP
-* type 1 diabetes
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6801956
-}}
-==BTK==
-{{medline-entry
-|title=Amelioration of age-related brain function decline by Bruton's tyrosine kinase inhibition.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31736210
-|keywords=* BTK
-* cellular senescence
-* healthspan
-* p53
-* progeria
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6974713
-}}
-==C2==
-{{medline-entry
-|title=[Effects of resistance training on mitochondrial function in skeletal muscle of aging rats].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32744013
-|mesh-terms=* Aging
-* Animals
-* Male
-* Membrane Potential, Mitochondrial
-* Mitochondria, Muscle
-* Muscle, Skeletal
-* Physical Conditioning, Animal
-* Rats
-* Rats, Sprague-Dawley
-* Resistance Training
-|keywords=* fusion protein 2
-* mitochondria
-* quadriceps
-* rats
-* resistance training
-|full-text-url=https://sci-hub.do/10.12047/j.cjap.5861.2020.037
-}}
-{{medline-entry
-|title=Structural and functional characterization of Solanum lycopersicum phosphatidylinositol 3-kinase [[C2]] domain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31972387
-|mesh-terms=* Animals
-* C2 Domains
-* Lycopersicon esculentum
-* Phosphatidylinositol 3-Kinase
-* Plants, Genetically Modified
-* Protein Binding
-* Tobacco
-|keywords=* C2 domain
-* Membrane binding
-* Phosphatidylinositol 3-kinase
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.plaphy.2020.01.014
-}}
-==C3==
-{{medline-entry
-|title=Inverse association between periumbilical fat and longevity mediated by complement [[C3]] and cardiac structure.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33221761
-|keywords=* abdominal obesity
-* cardiac structure
-* complement C3
-* longevity
-* periumbilical fat
-|full-text-url=https://sci-hub.do/10.18632/aging.104113
-}}
-{{medline-entry
-|title=Complement [[C3]] deficiency ameliorates aging related changes in the kidney.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32882264
-|mesh-terms=* Aging
-* Animals
-* Complement C3
-* Inflammation
-* Kidney
-* Kidney Diseases
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-|keywords=* Complement component 3
-* Kidney disorder
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2020.118370
-}}
-{{medline-entry
-|title=Reduced sialylation triggers homeostatic synapse and neuronal loss in middle-aged mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32087947
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Homeostasis
-* Immunity, Innate
-* Mice, Transgenic
-* Neurons
-* Racemases and Epimerases
-* Sialic Acid Binding Immunoglobulin-like Lectins
-* Sialic Acids
-* Synapses
-|keywords=* Aging
-* GNE
-* Glycocalyx
-* Microglia
-* Neurodegeneration
-* Neuroinflammation
-* Sialic acid
-|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.01.008
-}}
-{{medline-entry
-|title=[Comparative analysis of experimental data about the effects of various polyphenols on lifespan and aging.]
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31512417
-|mesh-terms=* Animals
-* Antioxidants
-* Female
-* Longevity
-* Male
-* Mice
-* Mice, Inbred BALB C
-* Polyphenols
-* Survival Analysis
-|keywords=* BP-C3
-* Gompertz model
-* SkQ1
-* aging
-* herbal extracts
-* lifespan
-* metformin
-* polyphenols
-* resveratrol
-* tocopherol
-}}
-==C5==
-{{medline-entry
-|title=The [[C5]]-75 Program: Meeting the Need for Efficient, Pragmatic Frailty Screening and Management in Primary Care.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32638663
-|keywords=* aging
-* case-finding
-* co-morbid conditions
-* comorbidité
-* dépistage
-* fragilité
-* frailty
-* primary care
-* recherche de cas
-* screening
-* soins de première ligne
-* vieillissement
-|full-text-url=https://sci-hub.do/10.1017/S0714980820000161
-}}
-{{medline-entry
-|title=Can a relatively large spinal cord for the dural sac influence severity of paralysis in elderly patients with cervical spinal cord injury caused by minor trauma?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32590805
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Cervical Vertebrae
-* Female
-* Geriatrics
-* Humans
-* Japan
-* Magnetic Resonance Imaging
-* Male
-* Paralysis
-* Severity of Illness Index
-* Spinal Canal
-* Spinal Cord
-* Spinal Cord Injuries
-* Tomography, X-Ray Computed
-* Wounds and Injuries
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7328921
-}}
-==C6==
-{{medline-entry
-|title=Evolution of the Aroma of Treixadura Wines during Bottle Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33049919
-|keywords=* bottle aging
-* flavor profile
-* sensory evaluation
-* volatile composition
-* white wine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7600726
-}}
-{{medline-entry
-|title=D-galactose induces senescence of glioblastoma cells through YAP-CDK6 pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32991321
-|keywords=* CDK6
-* D-galatose
-* YAP
-* cellular senescence
-* glioblastoma
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7585072
-}}
-==C7==
-{{medline-entry
-|title=The Vertebral Artery Convergence to the Cervical Spine in Elders.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32337923
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Cervical Vertebrae
-* Computed Tomography Angiography
-* Cross-Sectional Studies
-* Female
-* Humans
-* Male
-* Middle Aged
-* Retrospective Studies
-* Vertebral Artery
-|keywords=*  angiography
-*  computed tomography
-*  osteoarthritis
-*  spine
-*  vertebral artery
-* aging
-|full-text-url=https://sci-hub.do/10.3897/folmed.61.e39418
-}}
-==C9==
-{{medline-entry
-|title=[[C9]]orf72 in myeloid cells suppresses STING-induced inflammation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32814898
-|mesh-terms=* Aging
-* Amyotrophic Lateral Sclerosis
-* Animals
-* C9orf72 Protein
-* Dendritic Cells
-* Encephalomyelitis, Autoimmune, Experimental
-* Female
-* Humans
-* Inflammation
-* Interferon Type I
-* Membrane Proteins
-* Mice
-* Myeloid Cells
-* Neoplasms
-* T-Lymphocytes
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7484469
-}}
-{{medline-entry
-|title=Glycine-alanine dipeptide repeats spread rapidly in a repeat length- and age-dependent manner in the fly brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31843021
-|mesh-terms=* Aging
-* Alanine
-* Animals
-* Animals, Genetically Modified
-* Brain
-* C9orf72 Protein
-* DNA Repeat Expansion
-* Dipeptides
-* Drosophila
-* Female
-* Glycine
-|keywords=* Ageing
-* C9orf72
-* Dipeptide repeat proteins
-* Drosophila
-* PolyGA
-* Repeat size
-* Spread
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6916080
-}}
-{{medline-entry
-|title=Human iPSC-derived astrocytes from ALS patients with mutated [[C9]]ORF72 show increased oxidative stress and neurotoxicity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31787569
-|mesh-terms=* Amyotrophic Lateral Sclerosis
-* Animals
-* Astrocytes
-* Biomarkers
-* C9orf72 Protein
-* Cells, Cultured
-* Cellular Reprogramming
-* Cellular Senescence
-* Cerebral Cortex
-* Disease Models, Animal
-* Gene Expression Profiling
-* Glutamic Acid
-* Humans
-* Induced Pluripotent Stem Cells
-* Mice
-* Motor Neurons
-* Mutation
-* Oxidative Stress
-* Proteomics
-* Reactive Oxygen Species
-|keywords=* Amyotrophic lateral sclerosis
-* Astrocytes
-* Neurotoxicity
-* Oxidative stress
-* Senescence
-* iPSC
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6921360
-}}
-==C9orf72==
-{{medline-entry
-|title=Carriership of two copies of [[C9orf72]] hexanucleotide repeat intermediate-length alleles is a risk factor for ALS in the Finnish population.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33168078
-|keywords=* ALS
-* Aging
-* C9orf72
-* Case-control analysis
-* Intermediate repeats
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7654028
-}}
-==CA1==
-{{medline-entry
-|title=The relation between tau pathology and granulovacuolar degeneration of neurons.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33069844
-|keywords=* AT8
-* Aging
-* CA1
-* Casein kinase 1δ
-* Congo red
-* Dorsal raphe nucleus
-* Locus coeruleus
-* Neurodegeneration
-* Tau pathology
-|full-text-url=https://sci-hub.do/10.1016/j.nbd.2020.105138
-}}
-{{medline-entry
-|title=Memory and dendritic spines loss, and dynamic dendritic spines changes are age-dependent in the rat.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32950615
-|keywords=* Aging
-* Hippocampus
-* Locomotor activity
-* Memory and learning
-* Prefrontal cortex
-* Pyramidal neurons
-* dendritic spines
-|full-text-url=https://sci-hub.do/10.1016/j.jchemneu.2020.101858
-}}
-{{medline-entry
-|title=Deregulated expression of a longevity gene, Klotho, in the C9orf72 deletion mice with impaired synaptic plasticity and adult hippocampal neurogenesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32887666
-|keywords=* Amyotrophic lateral sclerosis (ALS)
-* C9ORF72
-* Dentate gyrus, adult neurogenesis
-* Frontotemporal dementia (FTD)
-* Klotho
-* Long-term depression (LTD)
-* Long-term potentiation (LTP)
-* Longevity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7473815
-}}
-{{medline-entry
-|title=COX5A Plays a Vital Role in Memory Impairment Associated With Brain Aging [i]via[/i] the BDNF/ERK1/2 Signaling Pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32754029
-|keywords=* BDNF
-* COX5A
-* ERK1/2
-* brain senescence
-* memory impairment
-* mitochondria
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7365906
-}}
-{{medline-entry
-|title=Changes of fat-mass and obesity-associated protein expression in the hippocampus in animal models of high-fat diet-induced obesity and D-galactose-induced aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32647628
-|keywords=* Aging
-* Fto
-* Hippocampus
-* Mice
-* Obesity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7336480
-}}
-{{medline-entry
-|title=Phenylbutyrate ameliorates prefrontal cortex, hippocampus, and nucleus accumbens neural atrophy as well as synaptophysin and GFAP stress in aging mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32531811
-|keywords=* aging
-* dendrites
-* hippocampus
-* memory and learning
-* nucleus accumbens
-* prefrontal cortex
-* sodium phenylbutyrate
-|full-text-url=https://sci-hub.do/10.1002/syn.22177
-}}
-{{medline-entry
-|title=Heterogeneity in brain distribution of activated microglia and astrocytes in a rat ischemic model of Alzheimer's disease after 2 years of survival.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32501292
-|keywords=* Alzheimer’s disease
-* aging
-* brain ischemia
-* glia
-* neuroinflammation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343500
-}}
-{{medline-entry
-|title=Hippocampal Subregion Transcriptomic Profiles Reflect Strategy Selection during Cognitive Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32376783
-|mesh-terms=* Animals
-* Cognitive Aging
-* Dentate Gyrus
-* Hippocampus
-* Maze Learning
-* Rats
-* Rats, Inbred F344
-* Spatial Memory
-* Transcriptome
-|keywords=* aging
-* hippocampus
-* pattern separation
-* reference memory
-* spatial discrimination
-* transcription
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7326352
-}}
-{{medline-entry
-|title=Associations between pattern separation and hippocampal subfield structure and function vary along the lifespan: A 7 T imaging study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32371923
-|mesh-terms=* Adult
-* Age Factors
-* Aged
-* Brain Mapping
-* Female
-* Hippocampus
-* Humans
-* Longevity
-* Magnetic Resonance Imaging
-* Male
-* Middle Aged
-* Young Adult
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7200747
-}}
-{{medline-entry
-|title=Laminarin Pretreatment Provides Neuroprotection against Forebrain Ischemia/Reperfusion Injury by Reducing Oxidative Stress and Neuroinflammation in Aged Gerbils.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32326571
-|keywords=* aging
-* laminarin
-* neuroinflammation
-* neuroprotection
-* oxidative stress
-* transient cerebral ischemia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7230782
-}}
-{{medline-entry
-|title=Age-dependent Alteration in Mitochondrial Dynamics and Autophagy in Hippocampal Neuron of Cannabinoid CB1 Receptor-deficient Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32294520
-|keywords=* Aging
-* CB1 receptor
-* Hippocampus
-* Mitochondria
-* Mitophagy
-|full-text-url=https://sci-hub.do/10.1016/j.brainresbull.2020.03.014
-}}
-{{medline-entry
-|title=Functional Connectivity of Hippocampal CA3 Predicts Neurocognitive Aging via [[CA1]]-Frontal Circuit.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32239141
-|keywords=* aging
-* functional connectivity
-* hippocampus
-* spatial memory
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7325802
-}}
-{{medline-entry
-|title=Integration of qRT-PCR and Immunohistochemical Techniques for mRNA Expression and Localization of m1AChR in the Brain of Aging Rat.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32219760
-|keywords=* Acetylcholine
-* Aging
-* Brain
-* Immunohistochemistry
-* m1AChR
-* qRT-PCR
-|full-text-url=https://sci-hub.do/10.1007/978-1-0716-0471-7_23
-}}
-{{medline-entry
-|title=Role of Eclipta prostrata extract in improving spatial learning and memory deficits in D-galactose-induced aging in rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32186114
-|mesh-terms=* Aging
-* Animals
-* Behavior, Animal
-* CA1 Region, Hippocampal
-* Catalase
-* Dopamine
-* Eclipta
-* Galactose
-* Gene Expression Regulation, Enzymologic
-* Glutathione Peroxidase
-* Glutathione Reductase
-* Male
-* Memory Disorders
-* Nitric Oxide
-* Nitric Oxide Synthase Type II
-* Norepinephrine
-* Plant Extracts
-* RNA, Messenger
-* Rats
-* Rats, Sprague-Dawley
-* Serotonin
-* Spatial Learning
-* Superoxide Dismutase
-|keywords=* Antioxidants
-* Eclipta
-* Galactose
-* Memory disorders
-* Spatial learning
-}}
-{{medline-entry
-|title=Differential annualized rates of hippocampal subfields atrophy in aging and future Alzheimer's clinical syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32107063
-|mesh-terms=* Aged
-* Aging
-* Alzheimer Disease
-* Atrophy
-* Cohort Studies
-* Cross-Sectional Studies
-* Dentate Gyrus
-* Female
-* Hippocampus
-* Humans
-* Magnetic Resonance Imaging
-* Male
-* Neuropsychological Tests
-* Risk
-|keywords=* Aging
-* Alzheimer's disease
-* Hippocampal subfields
-* MRI
-|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.01.011
-}}
-{{medline-entry
-|title=Rectification of radiotherapy-induced cognitive impairments in aged mice by reconstituted Sca-1  stem cells from young donors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32028989
-|mesh-terms=* Animals
-* Behavior, Animal
-* Cognitive Dysfunction
-* Dendritic Spines
-* Hematopoietic Stem Cell Transplantation
-* Hippocampus
-* Humans
-* Long-Term Potentiation
-* Maze Learning
-* Memory
-* Mice
-* Neurons
-* Radiotherapy
-* Recovery of Function
-* Spinocerebellar Ataxias
-* Treatment Outcome
-|keywords=* Aging
-* Bone marrow stem cells
-* Learning and memory
-* Microglia
-* Radiotherapy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7006105
-}}
-{{medline-entry
-|title=Increasing neurogenesis refines hippocampal activity rejuvenating navigational learning strategies and contextual memory throughout life.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31919362
-|mesh-terms=* Aging
-* Animals
-* Cyclin D1
-* Cyclin-Dependent Kinase 4
-* Female
-* Hippocampus
-* Learning
-* Memory
-* Memory Consolidation
-* Mice
-* Mice, Inbred C57BL
-* Neural Stem Cells
-* Neurogenesis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6952376
-}}
-{{medline-entry
-|title=Memory Performance Correlates of Hippocampal Subfield Volume in Mild Cognitive Impairment Subtype.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31849620
-|keywords=* aging
-* hippocampus
-* memory
-* mild cognitive impairment
-* neuroimaging
-* subfields
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6897308
-}}
-{{medline-entry
-|title=Spermidine protects from age-related synaptic alterations at hippocampal mossy fiber-CA3 synapses.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31873156
-|mesh-terms=* Aging
-* Animals
-* CA3 Region, Hippocampal
-* Long-Term Potentiation
-* Mice
-* Mossy Fibers, Hippocampal
-* Spermidine
-* Synaptic Transmission
-* Synaptic Vesicles
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6927957
-}}
-{{medline-entry
-|title=Methylene blue inhibits Caspase-6 activity, and reverses Caspase-6-induced cognitive impairment and neuroinflammation in aged mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31843022
-|mesh-terms=* Aging
-* Animals
-* Caspase 6
-* Caspase Inhibitors
-* Cognitive Dysfunction
-* Female
-* Humans
-* Inflammation
-* Male
-* Methylene Blue
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Mice, Transgenic
-|keywords=* Alzheimer disease
-* Axonal degeneration
-* Caspase-6
-* Caspase-6 inhibitor
-* Hippocampal CA1
-* Hippocampal fibres
-* Methylene blue
-* Synaptic plasticity
-* White matter
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6915996
-}}
-{{medline-entry
-|title=Long-term Memory Upscales Volume of Postsynaptic Densities in the Process that Requires Autophosphorylation of αCaMKII.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31800021
-|keywords=* CA1 area
-* CaMKII
-* IntelliCages
-* aging
-* dendritic spines
-* memory
-* postsynaptic density
-|full-text-url=https://sci-hub.do/10.1093/cercor/bhz261
-}}
-{{medline-entry
-|title=PACAP27 mitigates an age-dependent hippocampal vulnerability to PGJ2-induced spatial learning deficits and neuroinflammation in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31769222
-|keywords=* CA1
-* CA3
-* Fluoro-Jade C
-* aging
-* microglia
-* radial arm maze
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6955932
-}}
-{{medline-entry
-|title=Inhibition of oxidative stress by testosterone improves synaptic plasticity in senescence accelerated mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31746286
-|mesh-terms=* Aging
-* Animals
-* Male
-* Mice
-* Neuronal Plasticity
-* Oxidative Stress
-* Random Allocation
-* Receptors, N-Methyl-D-Aspartate
-* Testosterone
-|keywords=* Alzheimer’s disease
-* N-methyl-D-aspartate receptor-1
-* Senescence accelerated mouse
-* Testosterone
-* oxidative stress
-|full-text-url=https://sci-hub.do/10.1080/15287394.2019.1683988
-}}
-{{medline-entry
-|title=Restored presynaptic synaptophysin and cholinergic inputs contribute to the protective effects of physical running on spatial memory in aged mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31470103
-|mesh-terms=* Aging
-* Animals
-* Cholinergic Neurons
-* Hippocampus
-* Mice
-* Mice, Inbred C57BL
-* Physical Conditioning, Animal
-* Presynaptic Terminals
-* Spatial Memory
-* Synaptophysin
-|keywords=* Aging
-* Cholinergic cells
-* Hippocampus
-* Memory
-* Physical training
-* Presynaptic terminals
-* Synaptophysin
-|full-text-url=https://sci-hub.do/10.1016/j.nbd.2019.104586
-}}
-{{medline-entry
-|title=Senescent neurophysiology: Ca  signaling from the membrane to the nucleus.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31394200
-|mesh-terms=* Aging
-* Animals
-* CA1 Region, Hippocampal
-* Calcium Signaling
-* Cell Nucleus
-* Epigenesis, Genetic
-* Excitatory Postsynaptic Potentials
-* Humans
-* Membrane Potentials
-* Neuronal Plasticity
-* Pyramidal Cells
-* Receptors, N-Methyl-D-Aspartate
-|keywords=* Afterhyperpolarization
-* Aging
-* Epigenetics
-* Hippocampus
-* N-methyl-D-aspartate receptor
-* Synaptic plasticity
-* Transcription
-|full-text-url=https://sci-hub.do/10.1016/j.nlm.2019.107064
-}}
-==CA2==
-{{medline-entry
-|title=Maintaining Aging Hippocampal Function with Safe and Feasible Shaking Exercise in SAMP10 Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32526748
-|keywords=* Aging
-* Behavior analysis
-* Hippocampus
-* Shaking exercise
-* Spatial cognition
-|full-text-url=https://sci-hub.do/10.1159/000507884
-}}
-{{medline-entry
-|title=One-year Follow-up Study of Hippocampal Subfield Atrophy in Alzheimer's Disease and Normal Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32008518
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Alzheimer Disease
-* Atrophy
-* Case-Control Studies
-* Cognitive Dysfunction
-* Disease Progression
-* Female
-* Follow-Up Studies
-* Hippocampus
-* Humans
-* Magnetic Resonance Imaging
-* Male
-* Neuroimaging
-|keywords=* Alzheimer's disease
-* biomarker
-* hippocampal
-* mild cognitive impairment
-* neurodegenerative diseases
-* normal aging
-* radial distance
-* subfield atrophy
-|full-text-url=https://sci-hub.do/10.2174/1573405615666190327102052
-}}
-{{medline-entry
-|title=Maturation of PNN and ErbB4 Signaling in Area [[CA2]] during Adolescence Underlies the Emergence of PV Interneuron Plasticity and Social Memory.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31665627
-|mesh-terms=* Aging
-* Animals
-* Animals, Newborn
-* CA2 Region, Hippocampal
-* Interneurons
-* Long-Term Synaptic Depression
-* Male
-* Memory
-* Mice
-* Mice, Inbred C57BL
-* Neural Inhibition
-* Neuregulin-1
-* Neuronal Plasticity
-* Parvalbumins
-* Receptor, ErbB-4
-* Receptors, Opioid, delta
-* Signal Transduction
-* Social Behavior
-* Synapses
-* gamma-Aminobutyric Acid
-|keywords=* ErbB4
-* adolescence
-* area CA2
-* delta opioid receptors
-* hippocampus
-* long-term depression
-* neuregulin 1
-* parvalbumin interneuron
-* perineuronal net
-* social memory
-|full-text-url=https://sci-hub.do/10.1016/j.celrep.2019.09.044
-}}
-==CA3==
-{{medline-entry
-|title=Features of Postnatal Hippocampal Development in a Rat Model of Sporadic Alzheimer's Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32581685
-|keywords=* Alzheimer’s disease
-* OXYS rats
-* aging
-* hippocampal mossy fibers
-* hippocampus
-* neurogenesis
-* postnatal development
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7289999
-}}
-{{medline-entry
-|title=Age-Related Changes in Synaptic Plasticity Associated with Mossy Fiber Terminal Integration during Adult Neurogenesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32332082
-|keywords=* aging
-* conditional transgenic
-* giant synapse
-* stratum lucidum
-* synaptogenesis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7240290
-}}
-{{medline-entry
-|title=Metabotropic Glutamate Receptors at the Aged Mossy Fiber - [[CA3]] Synapse of the Hippocampus.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31917351
-|keywords=* aging
-* hippocampal area CA3
-* mGluRs
-* mossy fibers
-* synaptic transmission
-|full-text-url=https://sci-hub.do/10.1016/j.neuroscience.2019.12.016
-}}
-==CACNA1S==
-{{medline-entry
-|title=Increased calcium channel in the lamina propria of aging rat.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31682233
-|mesh-terms=* Aging
-* Animals
-* Calcium Channel Blockers
-* Calcium Channels
-* Cell Line
-* Fibroblasts
-* Gene Expression Regulation
-* Humans
-* Larynx
-* Male
-* Mucous Membrane
-* Rats
-* Rats, Sprague-Dawley
-* Verapamil
-|keywords=* aging
-* calcium channel
-* extracellular matrix
-* vocal fold
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834399
-}}
-==CAD==
-{{medline-entry
-|title=Serum soluble Klotho is inversely related to coronary artery calcification assessed by intravascular ultrasound in patients with stable coronary artery disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33303310
-|keywords=* Aging
-* Coronary artery calcification
-* Intravascular ultrasound
-* Klotho
-|full-text-url=https://sci-hub.do/10.1016/j.jjcc.2020.11.014
-}}
-{{medline-entry
-|title=Shear bond strengths of aged and non-aged [[CAD]]/CAM materials after different surface treatments.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33149848
-|keywords=* Bond strength
-* Computer-aided design and computer-aided manufacturing (CAD/CAM)
-* Laser
-* Repair
-* Surface treatment
-* Thermal aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7604239
-}}
-{{medline-entry
-|title=Prediction of Early Postoperative Major Cardiac Events and In-Hospital Mortality in Elderly Hip Fracture Patients: The Role of Different Types of Preoperative Cardiac Abnormalities on Echocardiography Report.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32546993
-|mesh-terms=* Aged
-* Aortic Valve Stenosis
-* Cardiovascular Diseases
-* Comorbidity
-* Echocardiography
-* Female
-* Fracture Fixation
-* Hip Fractures
-* Hospital Mortality
-* Humans
-* Male
-* Postoperative Complications
-* Prognosis
-* Risk Factors
-|keywords=* aging
-* echocardiographic abnormality
-* hip fracture surgery
-* mortality
-* postoperative cardiac complications
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7266334
-}}
-{{medline-entry
-|title=[Polymorbidity in elderly patients needing myocardial revascularization (a review article).]
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31800187
-|mesh-terms=* Aged
-* Cognitive Dysfunction
-* Coronary Artery Disease
-* Humans
-* Myocardial Revascularization
-* Quality of Life
-* Risk
-|keywords=* aging
-* elderly
-* ischemic heart disease
-* myocardial revascularization
-* polymorbidity
-}}
-{{medline-entry
-|title=Fracture force of [[CAD]]/CAM resin composite crowns after in vitro aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31712983
-|mesh-terms=* Ceramics
-* Composite Resins
-* Computer-Aided Design
-* Crowns
-* Dental Porcelain
-* Dental Restoration Failure
-* Dental Stress Analysis
-* Humans
-* Materials Testing
-|keywords=* Aging
-* CAD/CAM
-* CAD/CAM bloc
-* Dental material
-* Fit
-* Preparation
-* Resin composite
-* Resin-based material
-* Storage
-* TCML
-|full-text-url=https://sci-hub.do/10.1007/s00784-019-03099-1
-}}
-{{medline-entry
-|title=Clinical performance of chairside monolithic lithium disilicate glass-ceramic [[CAD]]-CAM crowns.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31565848
-|mesh-terms=* Ceramics
-* Computer-Aided Design
-* Crowns
-* Dental Porcelain
-* Dental Prosthesis Design
-* Humans
-* Materials Testing
-|keywords=* CAD-CAM
-* chairside
-* dental crowns
-* lithium disilicate
-* longevity
-* survival
-|full-text-url=https://sci-hub.do/10.1111/jerd.12531
-}}
-{{medline-entry
-|title=Acute resveratrol supplementation in coronary artery disease: towards patient stratification.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31429599
-|mesh-terms=* Aged
-* Biomarkers
-* Brachial Artery
-* Cardiac Rehabilitation
-* Coronary Artery Bypass
-* Coronary Artery Disease
-* Cross-Over Studies
-* Exercise Therapy
-* Female
-* Humans
-* Kinetics
-* Male
-* Middle Aged
-* Oxygen
-* Oxygen Consumption
-* Percutaneous Coronary Intervention
-* Resveratrol
-* Single-Blind Method
-* Treatment Outcome
-* Vasodilation
-|keywords=* Antioxidant
-* aging
-* endothelial dysfunction
-* oxygen uptake
-|full-text-url=https://sci-hub.do/10.1080/14017431.2019.1657584
-}}
-==CARM1==
-{{medline-entry
-|title=[[CARM1]] regulates senescence during airway epithelial cell injury in COPD pathogenesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31461302
-|mesh-terms=* Aged
-* Animals
-* Apoptosis
-* Cell Differentiation
-* Cell Proliferation
-* Cellular Senescence
-* Epithelial Cells
-* Female
-* Humans
-* Male
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Middle Aged
-* Naphthalenes
-* Protein-Arginine N-Methyltransferases
-* Pulmonary Disease, Chronic Obstructive
-* Respiratory Mucosa
-* Wound Healing
-|keywords=* CARM1
-* COPD
-* airway epithelium
-* senescence
-|full-text-url=https://sci-hub.do/10.1152/ajplung.00441.2018
-}}
-==CASP3==
-{{medline-entry
-|title=Does cartilage ERα overexpression correlate with osteoarthritic chondrosenescence? Indications from [i]Labisia pumila[/i] OA mitigation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31502578
-|mesh-terms=* Aging
-* Animals
-* Bone Development
-* Cartilage
-* Chondrocytes
-* Diclofenac
-* Disease Models, Animal
-* Estrogen Receptor alpha
-* Flavonoids
-* Gallic Acid
-* Gene Expression Regulation
-* Humans
-* Iodoacetates
-* Matrix Metalloproteinase 13
-* Metabolism
-* Osteoarthritis
-* Ovariectomy
-* Plant Extracts
-* Primulaceae
-* Rats
-}}
-==CAT==
-{{medline-entry
-|title=Training improves the handling of inhaler devices and reduces the severity of symptoms in geriatric patients suffering from chronic-obstructive pulmonary disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33036566
-|keywords=* Chronic-obstructive pulmonary disease - Inhaler devices
-* Compliance
-* Geriatrics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7547456
-}}
-{{medline-entry
-|title=7-chloro-4-(phenylselanyl) quinoline co-treatment prevent oxidative stress in diabetic-like phenotype induced by hyperglycidic diet in Drosophila melanogaster.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32931926
-|keywords=* 4-PSQ
-* 7-chloro-4-(phenylselanyl) quinolone
-* Antioxidant effect
-* Diabetic-like phenotype
-* Hyperglycidic diet
-* Longevity
-* Oxidative stress
-|full-text-url=https://sci-hub.do/10.1016/j.cbpc.2020.108892
-}}
-{{medline-entry
-|title=Aging influences in the blood-brain barrier permeability and cerebral oxidative stress in sepsis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32827711
-|keywords=* Aging
-* Blood-brain barrier
-* Brain
-* Oxidative stress
-* Sepsis
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.111063
-}}
-{{medline-entry
-|title=2 -Deoxy - d-glucose at chronic low dose acts as a caloric restriction mimetic through a mitohormetic induction of ROS in the brain of accelerated senescence model of rat.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32559563
-|keywords=* 2-Deoxy- d-glucose
-* Aging
-* Brain
-* CRM
-* Mitohormosis
-* ROS
-|full-text-url=https://sci-hub.do/10.1016/j.archger.2020.104133
-}}
-{{medline-entry
-|title=Ceftriaxone improves senile neurocognition damages induced by D-galactose in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32440324
-|keywords=* Aging
-* Ceftriaxone
-* D-galactose
-* Mice
-* Oxidative stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7229512
-}}
-{{medline-entry
-|title=Ginsenoside Rg1 protects against d-galactose induced fatty liver disease in a mouse model via FOXO1 transcriptional factor.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32437790
-|mesh-terms=* Animals
-* Antioxidants
-* Cellular Senescence
-* Disease Models, Animal
-* Fatty Liver
-* Forkhead Box Protein O1
-* Galactose
-* Ginsenosides
-* Lipid Peroxidation
-* Male
-* Medicine, Chinese Traditional
-* Mice
-* Mice, Inbred C57BL
-* Oxidative Stress
-* Protective Agents
-* Transcription Factors
-|keywords=* D-galactose
-* FOXO1
-* Non-alcoholic fatty liver disease
-* Rg1
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2020.117776
-}}
-{{medline-entry
-|title=Effects of long-term intermittent versus chronic calorie restriction on oxidative stress in a mouse cancer model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31424629
-|mesh-terms=* Aging
-* Animals
-* Antioxidants
-* Caloric Restriction
-* Catalase
-* Erythrocytes
-* Female
-* Glutathione
-* Lipid Peroxidation
-* Malondialdehyde
-* Mammary Neoplasms, Experimental
-* Mice, Inbred C57BL
-* Oxidative Stress
-* Superoxide Dismutase
-|keywords=* MMTV-TGF-α mice
-* breast cancer
-* energy restriction
-* intermittent calorie restriction
-* mammary tumor
-* oxidative stress
-|full-text-url=https://sci-hub.do/10.1002/iub.2145
-}}
-{{medline-entry
-|title=The Toxicity of Nonaged and Aged Coated Silver Nanoparticles to Freshwater Alga Raphidocelis subcapitata.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31403715
-|mesh-terms=* Aquatic Organisms
-* Chlorophyta
-* Fresh Water
-* Hydrodynamics
-* Lipid Peroxidation
-* Metal Nanoparticles
-* Particle Size
-* Reactive Oxygen Species
-* Silver
-* Static Electricity
-* Toxicity Tests
-|keywords=* Aquatic toxicology
-* Ecotoxicology
-* Environmental fate
-* Heavy metals
-* Nanoparticle aging
-* Nanotoxicology
-|full-text-url=https://sci-hub.do/10.1002/etc.4549
-}}
-==CBS==
-{{medline-entry
-|title=Permanent cystathionine-β-Synthase gene knockdown promotes inflammation and oxidative stress in immortalized human adipose-derived mesenchymal stem cells, enhancing their adipogenic capacity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32800520
-|keywords=* Cellular senescence
-* Cystathionine β-synthase
-* Human adipose-derived mesenchymal stem cells
-* Inflammation
-* Oxidative stress and adipogenesis
-|full-text-url=https://sci-hub.do/10.1016/j.redox.2020.101668
-}}
-{{medline-entry
-|title=Cardiovascular phenotype of mice lacking 3-mercaptopyruvate sulfurtransferase.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32027885
-|mesh-terms=* Animals
-* Antioxidants
-* Cardiovascular System
-* Cystathionine beta-Synthase
-* Cystathionine gamma-Lyase
-* Gene Expression Regulation, Enzymologic
-* Hydrogen Sulfide
-* Male
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Myocardial Reperfusion Injury
-* Myocytes, Cardiac
-* Nitric Oxide
-* Phenotype
-* Reactive Oxygen Species
-* Sulfurtransferases
-* Vasodilation
-|keywords=* 3-mercaptopyruvate transferase (3-MST)
-* Aging
-* Blood pressure
-* Myocardial infarction
-* Nitric Oxide (NO)
-* Reactive Oxygen Species (ROS)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7657663
-}}
-==CBX3==
-{{medline-entry
-|title=Biological functions of chromobox (CBX) proteins in stem cell self-renewal, lineage-commitment, cancer and development.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32979540
-|keywords=* Aging
-* Bone
-* CBX1
-* CBX2
-* CBX3
-* CBX4
-* CBX5
-* CBX6
-* CBX7
-* CBX8
-* Cancer
-* Chromatin
-* Development
-* Epigenetics
-* H3K27me3
-* H3K9me3
-* Lineage-commitment
-* Osteoblast
-* Senescence
-* Stem cell
-|full-text-url=https://sci-hub.do/10.1016/j.bone.2020.115659
-}}
-==CCK==
-{{medline-entry
-|title=Senolytic agent Quercetin ameliorates intervertebral disc degeneration via the Nrf2/NF-κB axis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33242601
-|keywords=* Intervertebral disc degeneration
-* NF-κB pathway
-* Nrf2
-* Quercetin
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.joca.2020.11.006
-}}
-{{medline-entry
-|title=Astragalus improve aging bone marrow mesenchymal stem cells (BMSCs) vitality and osteogenesis through VD-FGF23-Klotho axis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32355520
-|keywords=* Astragalus
-* BMSCs
-* VD-FGF23-Klotho axis
-* aging
-* osteogenesis differentiation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191145
-}}
-{{medline-entry
-|title=Effects of Age on Acute Appetite-Related Responses to Whey-Protein Drinks, Including Energy Intake, Gastric Emptying, Blood Glucose, and Plasma Gut Hormone Concentrations-A Randomized Controlled Trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32268554
-|keywords=* aging
-* appetite
-* energy intake
-* gastric emptying
-* glucose
-* gut hormones
-* whey protein
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7231005
-}}
-{{medline-entry
-|title=Lactose induced redox-dependent senescence and activated Nrf2 pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31934025
-|keywords=* Lactose
-* Nrf2
-* ROS
-* cellular senescence
-* oxidative stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6949649
-}}
-{{medline-entry
-|title=Quercetin Suppresses the Progression of Atherosclerosis by Regulating MST1-Mediated Autophagy in ox-LDL-Induced RAW264.7 Macrophage Foam Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31816893
-|mesh-terms=* Adenine
-* Animals
-* Atherosclerosis
-* Autophagy
-* Cell Survival
-* Cellular Senescence
-* Cyclin-Dependent Kinase Inhibitor p16
-* Cyclin-Dependent Kinase Inhibitor p21
-* Disease Progression
-* Foam Cells
-* Hepatocyte Growth Factor
-* Lipid Metabolism
-* Lipoproteins, LDL
-* Mice
-* Proto-Oncogene Proteins
-* Quercetin
-* RAW 264.7 Cells
-* Sirolimus
-* Up-Regulation
-|keywords=* RAW264.7
-* atherosclerosis
-* autophagy
-* quercetin
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6928812
-}}
-{{medline-entry
-|title=LncRNA AW112010 Promotes Mitochondrial Biogenesis and Hair Cell Survival: Implications for Age-Related Hearing Loss.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31781342
-|mesh-terms=* Adenosine Triphosphate
-* Aging
-* Animals
-* Cell Survival
-* DNA-Binding Proteins
-* Gene Silencing
-* Hair Cells, Auditory
-* Hearing Loss
-* Mice
-* Mitochondria
-* Organelle Biogenesis
-* RNA, Long Noncoding
-* Resveratrol
-* Signal Transduction
-* Transcription Factors
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6855056
-}}
-{{medline-entry
-|title=Effects of age on feeding response: Focus on the rostral C1 neuron and its glucoregulatory proteins.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31705967
-|keywords=* Aging
-* Catecholaminergic neurons
-* Feeding response
-* Glucoprivation
-* Rostral ventrolateral medulla
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2019.110779
-}}
-{{medline-entry
-|title=Ser-Tyr and Asn-Ala, vasorelaxing dipeptides found by comprehensive screening, reduce blood pressure via different age-dependent mechanisms.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31685714
-|mesh-terms=* Aging
-* Amino Acid Sequence
-* Animals
-* Antihypertensive Agents
-* Blood Pressure
-* Cholecystokinin
-* Dipeptides
-* Drug Evaluation, Preclinical
-* Hypertension
-* Male
-* Mesenteric Arteries
-* Nitric Oxide
-* Peptide Library
-* Proglumide
-* Rats
-* Rats, Inbred SHR
-* Receptors, Cholecystokinin
-* Vasodilation
-* Vasodilator Agents
-|keywords=* aging
-* dipeptide library
-* nitric oxide
-* structure-activity relationship
-* vasorelaxation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6874431
-}}
-{{medline-entry
-|title=Fisetin, via CKIP-1/REGγ, limits oxidized LDL-induced lipid accumulation and senescence in RAW264.7 macrophage-derived foam cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31655030
-|mesh-terms=* Animals
-* Autoantigens
-* Carrier Proteins
-* Cellular Senescence
-* Flavonoids
-* Foam Cells
-* Lipid Metabolism
-* Lipoproteins, LDL
-* Mice
-* Proteasome Endopeptidase Complex
-* RAW 264.7 Cells
-* Signal Transduction
-|keywords=* CKIP-1/REGγ signaling
-* Fisetin
-* Lipid accumulation
-* RAW264.7
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.ejphar.2019.172748
-}}
-==CCL11==
-{{medline-entry
-|title=CCL-11 or Eotaxin-1: An Immune Marker for Ageing and Accelerated Ageing in Neuro-Psychiatric Disorders.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32887304
-|keywords=* Alzheimer’s disease
-* CCL-11
-* aging
-* behaviour
-* biomarkers
-* brain
-* cytokines
-* eotaxin
-* prevention
-* schizophrenia
-* stroke
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7558796
-}}
-==CCL17==
-{{medline-entry
-|title=Aging and chronic high-fat feeding negatively affects kidney size, function, and gene expression in CTRP1-deficient mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33085906
-|keywords=* aging
-* heart
-* kidney
-* metabolism
-* obesity
-|full-text-url=https://sci-hub.do/10.1152/ajpregu.00139.2020
-}}
-==CCL19==
-{{medline-entry
-|title=Age-Related Gliosis Promotes Central Nervous System Lymphoma through [[CCL19]]-Mediated Tumor Cell Retention.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31526758
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aging
-* Animals
-* Astrocytes
-* Blood-Brain Barrier
-* Cell Line, Tumor
-* Central Nervous System Neoplasms
-* Chemokine CCL19
-* Chemokine CXCL12
-* Disease Models, Animal
-* Female
-* Gliosis
-* Humans
-* Intravital Microscopy
-* Lymphoma
-* Male
-* Mice
-* Mice, Transgenic
-* Microscopy, Fluorescence, Multiphoton
-* Middle Aged
-* NF-kappa B
-* Receptors, CCR7
-* Time-Lapse Imaging
-* Young Adult
-|keywords=* CCL19
-* CNSL
-* CXCL12
-* DLBCL
-* PCNSL
-* SCNSL
-* gliosis
-* lymphoma
-* metastasis
-* neuroinflammation
-|full-text-url=https://sci-hub.do/10.1016/j.ccell.2019.08.001
-}}
-==CCL2==
-{{medline-entry
-|title=β1 Integrin regulates adult lung alveolar epithelial cell inflammation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31873073
-|mesh-terms=* Aging
-* Alveolar Epithelial Cells
-* Animals
-* Cell Adhesion
-* Chemokine CCL2
-* Chemokines
-* Disease Models, Animal
-* Epithelium
-* Integrin beta1
-* Lung
-* Macrophages
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Pneumonia
-* Pulmonary Disease, Chronic Obstructive
-* Receptors, CCR2
-|keywords=* COPD
-* Inflammation
-* Integrins
-* Macrophages
-* Pulmonology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7098727
-}}
-==CCL20==
-{{medline-entry
-|title=p53 and p53-related mediators PAI-1 and IGFBP-3 are downregulated in peripheral blood mononuclear cells of HIV-patients exposed to non-nucleoside reverse transcriptase inhibitors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32272174
-|keywords=* Aging
-* Antiretroviral drugs
-* HIV
-* Inflammation
-* NNRTI
-* Senescence
-* p53
-|full-text-url=https://sci-hub.do/10.1016/j.antiviral.2020.104784
-}}
-==CCL28==
-{{medline-entry
-|title=Age-related chemokine alterations affect IgA secretion and gut immunity in female mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32277312
-|keywords=* Aging
-* CCL25
-* CCL28
-* Gut immunity
-* IgA
-|full-text-url=https://sci-hub.do/10.1007/s10522-020-09877-9
-}}
-==CCN1==
-{{medline-entry
-|title=Sodium tanshinone IIA sulfonate restrains fibrogenesis through induction of senescence in mice with induced deep endometriosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32651107
-|keywords=* Deep endometriosis
-* Fibrogenesis
-* Mouse
-* Senescence
-* Sodium tanshinone IIA sulfonate
-|full-text-url=https://sci-hub.do/10.1016/j.rbmo.2020.04.006
-}}
-{{medline-entry
-|title=Inhibition of cellular communication network factor 1 ([[CCN1]])-driven senescence slows down cartilage inflammaging and osteoarthritis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32622876
-|keywords=* CCN1
-* Cartilage inflammaging
-* Chondrocyte cluster
-* Osteoarthritis
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.bone.2020.115522
-}}
-{{medline-entry
-|title=The senescence-associated matricellular protein [[CCN1]] in plasma of human subjects with idiopathic pulmonary fibrosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31765873
-|mesh-terms=* Aged
-* Cellular Senescence
-* Cysteine-Rich Protein 61
-* Disease Progression
-* Enzyme-Linked Immunosorbent Assay
-* Female
-* Humans
-* Idiopathic Pulmonary Fibrosis
-* Male
-* Middle Aged
-* Outcome Assessment, Health Care
-* Predictive Value of Tests
-* Survival Rate
-|keywords=* CCN1
-* Cellular senescence
-* Idiopathic pulmonary fibrosis
-* Transplant-free survival
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7023981
-}}
-==CCN3==
-{{medline-entry
-|title=[[CCN3]] Signaling Is Differently Regulated in Placental Diseases Preeclampsia and Abnormally Invasive Placenta.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33304321
-|keywords=* CCN3
-* abnormally invasive placenta
-* invasion
-* preeclampsia
-* senescence
-* trophoblast
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7701218
-}}
-{{medline-entry
-|title=[[CCN3]] (NOV) Drives Degradative Changes in Aging Articular Cartilage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33066270
-|keywords=* CCN3
-* NOV
-* SASP
-* aging
-* cellular communication network factor 3
-* oxidative stress
-* p21
-* p53
-* primary chondrocytes
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7593953
-}}
-==CCND1==
-{{medline-entry
-|title=Effects of hydrogen peroxide, doxorubicin and ultraviolet irradiation on senescence of human dental pulp stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32592933
-|mesh-terms=* Cells, Cultured
-* Cellular Senescence
-* Dental Pulp
-* Doxorubicin
-* Humans
-* Hydrogen Peroxide
-* Stem Cells
-* Ultraviolet Rays
-|keywords=* Cell cycle
-* ROS
-* Stress induced senescence
-* Ultraviolet irradiation
-* p21
-|full-text-url=https://sci-hub.do/10.1016/j.archoralbio.2020.104819
-}}
-==CCND3==
-{{medline-entry
-|title=The effect of aging on the biological and immunological characteristics of periodontal ligament stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32727592
-|keywords=* Aging
-* Immunosuppression
-* Osteogenic differentiation
-* Periodontal ligament stem cells
-* Peripheral blood mononuclear cells
-* Tissue engineering
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7392710
-}}
-==CCR2==
-{{medline-entry
-|title=Hip Fracture Leads to Transitory Immune Imprint in Older Patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33072114
-|keywords=* acute stress
-* aging
-* immune response
-* inflammation
-* regulation loop
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7533556
-}}
-{{medline-entry
-|title=The CC-chemokine receptor 2 is involved in the control of ovarian folliculogenesis and fertility lifespan in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32615332
-|keywords=* Aging
-* CCR2
-* Fertility
-* Follicle
-* Ovary
-|full-text-url=https://sci-hub.do/10.1016/j.jri.2020.103174
-}}
-{{medline-entry
-|title=Deficit of resolution receptor magnifies inflammatory leukocyte directed cardiorenal and endothelial dysfunction with signs of cardiomyopathy of obesity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32543720
-|keywords=* inflammatory macrophage
-* kidney function
-* non-resolving inflammation
-* obesogenic aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7704037
-}}
-{{medline-entry
-|title=Tet2-mediated clonal hematopoiesis in nonconditioned mice accelerates age-associated cardiac dysfunction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32154790
-|keywords=* Aging
-* Bone marrow transplantation
-* Cardiology
-* Hematopoietic stem cells
-* Macrophages
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7213793
-}}
-{{medline-entry
-|title=Inflammation and Ectopic Fat Deposition in the Aging Murine Liver Is Influenced by [[CCR2]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31843499
-|mesh-terms=* Aging
-* Animals
-* Body Weight
-* Chemokine CCL2
-* Disease Models, Animal
-* Female
-* Gene Expression Profiling
-* Inflammation
-* Macrophages
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Non-alcoholic Fatty Liver Disease
-* Organ Size
-* Receptors, CCR2
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7013280
-}}
-{{medline-entry
-|title=Klotho-mediated targeting of CCL2 suppresses the induction of colorectal cancer progression by stromal cell senescent microenvironments.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31545552
-|mesh-terms=* Aged
-* Cell Line, Tumor
-* Cell Movement
-* Cell Proliferation
-* Cellular Microenvironment
-* Cellular Senescence
-* Chemokine CCL2
-* Colorectal Neoplasms
-* Disease Progression
-* Down-Regulation
-* Doxorubicin
-* Female
-* Glucuronidase
-* Human Umbilical Vein Endothelial Cells
-* Humans
-* Male
-* Middle Aged
-* NF-kappa B
-* Neoplasm Invasiveness
-* Proportional Hazards Models
-* Signal Transduction
-* Stromal Cells
-|keywords=* CCL2
-* Klotho
-* colorectal cancer
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6822285
-}}
-==CCR3==
-{{medline-entry
-|title=Low Molecular Weight Hyaluronan Induces an Inflammatory Response in Ovarian Stromal Cells and Impairs Gamete Development In Vitro.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32033185
-|mesh-terms=* Aging
-* Animals
-* Extracellular Matrix
-* Female
-* Germ Cells
-* Granulosa Cells
-* Hyaluronan Receptors
-* Hyaluronic Acid
-* Inflammation
-* Mice
-* Mice, Inbred BALB C
-* Mice, Inbred C57BL
-* Molecular Weight
-* Ovary
-* Stromal Cells
-|keywords=* hyaluronan fragments
-* inflammation
-* ovarian biology
-* reproductive aging
-* stroma
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7036885
-}}
-==CCR5==
-{{medline-entry
-|title=[Enhancement can do harm].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31532388
-|mesh-terms=* Adult
-* Aged
-* CRISPR-Cas Systems
-* China
-* Embryo Research
-* Gene Editing
-* Gene Silencing
-* Genetic Enhancement
-* Genome-Wide Association Study
-* HIV Infections
-* HIV-1
-* Humans
-* Longevity
-* Middle Aged
-* Receptors, CCR5
-|full-text-url=https://sci-hub.do/10.1051/medsci/2019136
-}}
-==CCS==
-{{medline-entry
-|title=Frailty Significantly Associated with a Risk for Mid-term Outcomes in Elderly Chronic Coronary Syndrome Patients: a Prospective Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33306315
-|keywords=* Aging
-* Canada
-* Confidence Intervals
-* Death
-* Frail Elderly
-* Frailty
-* Heart
-* Multivariate Analysis
-* Prognosis
-* Risk Factors
-|full-text-url=https://sci-hub.do/10.21470/1678-9741-2019-0484
-}}
-{{medline-entry
-|title=Microbleeds and Medial Temporal Atrophy Determine Cognitive Trajectories in Normal Aging: A Longitudinal PET-MRI Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32925053
-|keywords=* Atrophy
-* cognition
-* imaging markers
-* medial temporal lobe
-* microbleeds
-* normal aging
-|full-text-url=https://sci-hub.do/10.3233/JAD-200559
-}}
-{{medline-entry
-|title=Hippocampal Volume Loss, Brain Amyloid Accumulation, and APOE Status in Cognitively Intact Elderly Subjects.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31846965
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Amyloid beta-Peptides
-* Apolipoprotein E4
-* Brain
-* Cognitive Aging
-* Female
-* Hippocampus
-* Humans
-* Longitudinal Studies
-* Magnetic Resonance Imaging
-* Male
-* Positron-Emission Tomography
-|keywords=* APOE
-* Aging
-* Amyloid
-* Hippocampus
-|full-text-url=https://sci-hub.do/10.1159/000504302
-}}
-{{medline-entry
-|title=Amyloid Load, Hippocampal Volume Loss, and Diffusion Tensor Imaging Changes in Early Phases of Brain Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31803008
-|keywords=* APOE genotyping
-* amyloid deposition
-* magnetic resonance imaging
-* normal aging
-* positron emission tomography
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6872975
-}}
-{{medline-entry
-|title=Lower bone mass is associated with subclinical atherosclerosis, endothelial dysfunction and carotid thickness in the very elderly.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31783200
-|keywords=* Aging
-* Endothelial dysfunction
-* Osteoporosis
-* Subclinical atherosclerosis
-|full-text-url=https://sci-hub.do/10.1016/j.atherosclerosis.2019.11.007
-}}
-==CD14==
-{{medline-entry
-|title=Human innate immune cell crosstalk induces melanoma cell senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32939325
-|keywords=* NK cell
-* cytokines
-* melanoma
-* senescence
-* slanMo
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7470184
-}}
-{{medline-entry
-|title=Fusion Potential of Human Osteoclasts In Vitro Reflects Age, Menopause, and In Vivo Bone Resorption Levels of Their Donors-A Possible Involvement of DC-STAMP.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32887359
-|keywords=* CTX
-* DC-STAMP
-* DNA methylation
-* aging
-* cell fusion
-* epigenetics
-* menopause
-* multinucleation
-* osteoclast
-* osteoclastogenesis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7504560
-}}
-{{medline-entry
-|title=Association of [[CD14]] with incident dementia and markers of brain aging and injury.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31818907
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Atrophy
-* Biomarkers
-* Brain
-* Cognitive Dysfunction
-* Dementia
-* Female
-* Humans
-* Incidence
-* Lipopolysaccharide Receptors
-* Longitudinal Studies
-* Male
-* Middle Aged
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7108812
-}}
-{{medline-entry
-|title=Compromised Bone Healing in Aged Rats Is Associated With Impaired M2 Macrophage Function.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31681320
-|mesh-terms=* Age Factors
-* Aging
-* Animals
-* Antigens, CD
-* Antigens, Differentiation, Myelomonocytic
-* Biomarkers
-* Bone Regeneration
-* Bone and Bones
-* Female
-* Fractures, Bone
-* Gene Expression
-* Lipopolysaccharide Receptors
-* Macrophages
-* Osteotomy
-* Rats, Sprague-Dawley
-* Wound Healing
-|keywords=* CD14+ cells
-* aging
-* angiogenesis
-* bone regeneration
-* compromised healing
-* macrophage
-* monocyte
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6813416
-}}
-==CD19==
-{{medline-entry
-|title=Sequential treatment with aT19 cells generates memory CAR-T cells and prolongs the lifespan of Raji-B-NDG mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31634527
-|mesh-terms=* Animals
-* Antigens, CD19
-* Cell Line, Tumor
-* Combined Modality Therapy
-* Disease-Free Survival
-* HEK293 Cells
-* Healthy Volunteers
-* Humans
-* Immunologic Memory
-* Immunotherapy, Adoptive
-* Longevity
-* Lymphoma, B-Cell
-* Mice
-* Neoplasm Recurrence, Local
-* Receptors, Chimeric Antigen
-* Recombinant Proteins
-* Remission Induction
-* T-Lymphocytes
-* Time Factors
-* Transduction, Genetic
-* Transplantation, Autologous
-* Xenograft Model Antitumor Assays
-|keywords=* Autologous CD19 T cells
-* Chimeric antigen receptor
-* Memory T cells
-* Sequential therapy
-|full-text-url=https://sci-hub.do/10.1016/j.canlet.2019.10.022
-}}
-==CD27==
-{{medline-entry
-|title=The Interplay between [[CD27]]  and [[CD27]]  B Cells Ensures the Flexibility, Stability, and Resilience of Human B Cell Memory.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32130900
-|keywords=* CD27
-* VH repertoire
-* aging
-* germinal center
-* immunodeficiency
-* immunological memory
-* memory B cells
-* pregnancy
-* spleen
-* vaccine
-|full-text-url=https://sci-hub.do/10.1016/j.celrep.2020.02.022
-}}
-{{medline-entry
-|title=CMV-independent increase in [[CD27]]-CD28+ CD8+ EMRA T cells is inversely related to mortality in octogenarians.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31993214
-|keywords=* Biomarkers
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6972903
-}}
-{{medline-entry
-|title=Compartmentalized cytotoxic immune response leads to distinct pathogenic roles of natural killer and senescent CD8  T cells in human cutaneous leishmaniasis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31925782
-|mesh-terms=* CD56 Antigen
-* CD57 Antigens
-* Case-Control Studies
-* Cellular Senescence
-* Cytotoxicity, Immunologic
-* Female
-* Gene Expression Regulation
-* Host-Parasite Interactions
-* Humans
-* Interferon-gamma
-* Killer Cells, Natural
-* Lectins, C-Type
-* Leishmania braziliensis
-* Leishmaniasis, Cutaneous
-* Male
-* Oligosaccharides
-* Receptors, Immunologic
-* Severity of Illness Index
-* Sialyl Lewis X Antigen
-* Signal Transduction
-* Skin
-* T-Lymphocytes, Cytotoxic
-|keywords=*
-Leishmania braziliensis
-* CD8+ T cells
-* cellular senescence
-* cutaneous leishmaniasis
-* immunopathology
-* natural killer cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7078002
-}}
-{{medline-entry
-|title=[[CD27]]- IgD- B cell memory subset associates with inflammation and frailty in elderly individuals but only in males.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31423147
-|keywords=* Aging
-* B cell
-* Frailty
-* Immunosenescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6693136
-}}
-==CD28==
-{{medline-entry
-|title=Premature CD4  T Cells Senescence Induced by Chronic Infection in Patients with Acute Coronary Syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33269101
-|keywords=* CD28null T cells
-* CD4+ T cells
-* acute coronary syndrome
-* immunosenescence
-* infection
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673853
-}}
-{{medline-entry
-|title=The IMMENSE Study: The Interplay Between iMMune and ENdothelial Cells in Mediating Cardiovascular Risk in Systemic Lupus Erythematosus.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33193356
-|keywords=* angiogenic T cells
-* cardiovascular risk
-* endothelial progenitor cells
-* immunosenescence
-* systemic lupus erythematosus
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7658008
-}}
-{{medline-entry
-|title=Emergence of T cell immunosenescence in diabetic chronic kidney disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33088331
-|keywords=* BMI
-* CKD
-* Diabetes
-* Immunosenescence
-* T cell
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7574244
-}}
-{{medline-entry
-|title=The relationship between Chlamydia pneumoniae infection and CD4/CD8 ratio, lymphocyte subsets in middle-aged and elderly individuals.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33068732
-|keywords=* CD4/CD8 ratio
-* Chlamydia pneumoniae
-* Immune profile
-* Immunosenescence
-* Lymphocyte subsets
-|full-text-url=https://sci-hub.do/10.1016/j.micpath.2020.104541
-}}
-{{medline-entry
-|title=Next steps in mechanisms of inflammaging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32960694
-|keywords=* Aging
-* autophagy
-* glutathione
-* membrane potential
-* mitochondria
-* oxidative stress
-|full-text-url=https://sci-hub.do/10.1080/15548627.2020.1822089
-}}
-{{medline-entry
-|title=A randomized pilot trial to evaluate the benefit of the concomitant use of atorvastatin and Raltegravir on immunological markers in protease-inhibitor-treated subjects living with HIV.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32941476
-|mesh-terms=* Adult
-* Anti-HIV Agents
-* Anticholesteremic Agents
-* Atorvastatin
-* CD4-Positive T-Lymphocytes
-* CD8-Positive T-Lymphocytes
-* Female
-* HIV Infections
-* HIV Protease Inhibitors
-* Humans
-* Immunosenescence
-* Inflammation
-* Lymphocyte Activation
-* Male
-* Middle Aged
-* Pilot Projects
-* Raltegravir Potassium
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7498036
-}}
-{{medline-entry
-|title=Aging affects responsiveness of peripheral blood mononuclear cells to immunosuppression of periodontal ligament stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32663414
-|keywords=* Periodontal ligament stem cells
-* T lymphocytes
-* age
-* coculture
-* cytokines
-* immunophenotyping
-* immunosenescence
-* immunosuppression
-* peripheral blood mononuclear cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7364836
-}}
-{{medline-entry
-|title=Comparison of Donepezil, Memantine, Melatonin, and Liuwei Dihuang Decoction on Behavioral and Immune Endocrine Responses of Aged Senescence-Accelerated Mouse Resistant 1 Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32477103
-|keywords=* Liuwei Dihuang decoction
-* aging
-* cognition
-* immune response
-* inflammation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7241684
-}}
-{{medline-entry
-|title=Immunosenescent characteristics of T cells in young patients following haploidentical haematopoietic stem cell transplantation from parental donors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32280463
-|keywords=* CD28− T cells
-* HaploSCT
-* immune monitoring
-* immunosenescence
-* telomere length
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7142179
-}}
-{{medline-entry
-|title=Diagnosis-independent loss of T-cell costimulatory molecules in individuals with cytomegalovirus infection.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32209361
-|keywords=* Biological aging
-* Cytomegalovirus
-* Depression
-* Immunosenescence
-* Major depressive disorder
-* Sex differences
-* T-cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7594105
-}}
-{{medline-entry
-|title=Accelerated immunosenescence in rheumatoid arthritis: impact on clinical progression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32190092
-|keywords=* Ageing
-* Cell senescence
-* Cognitive impairment
-* Immune ageing
-* Rheumatoid arthritis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7068869
-}}
-{{medline-entry
-|title=Accelerated immune aging was correlated with lupus-associated brain fog in reproductive-age systemic lupus erythematosus patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32107852
-|keywords=* immunosenescence
-* lupus-associated brain fog
-* systemic lupus erythematosus
-|full-text-url=https://sci-hub.do/10.1111/1756-185X.13816
-}}
-{{medline-entry
-|title=T cells, aging and senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32092501
-|keywords=* Aging
-* Senescence
-* T cells
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110887
-}}
-{{medline-entry
-|title=Liver fibrosis and accelerated immune dysfunction (immunosenescence) among HIV-infected Russians with heavy alcohol consumption - an observational cross-sectional study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31892306
-|mesh-terms=* Adult
-* Alcoholism
-* CD28 Antigens
-* CD4-Positive T-Lymphocytes
-* CD57 Antigens
-* CD8-Positive T-Lymphocytes
-* Cross-Sectional Studies
-* Female
-* HIV Infections
-* Hepatitis C
-* Humans
-* Immunologic Memory
-* Immunosenescence
-* Leukocyte Common Antigens
-* Linear Models
-* Liver Cirrhosis, Alcoholic
-* Male
-* Phenotype
-* Randomized Controlled Trials as Topic
-* Russia
-* Zinc
-|keywords=* Alcohol
-* HIV
-* Immune senescence
-* Liver fibrosis
-* Russia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6938606
-}}
-{{medline-entry
-|title=Effect of Allogenic Bone Marrow Mesenchymal Stem Cell Transplantation on T Cells of Old Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31895587
-|keywords=* aging
-* cellular senescence
-* memory T cells
-* stem cell
-|full-text-url=https://sci-hub.do/10.1089/cell.2019.0055
-}}
-{{medline-entry
-|title=Peripheral antibody concentrations are associated with highly differentiated T cells and inflammatory processes in the human bone marrow.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31462901
-|keywords=* Aging
-* Antibodies
-* B cells
-* Bone marrow
-* Exhaustion
-* Immunosenescence
-* Inflammation
-* Pro-inflammatory
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6706884
-}}
-==CD33==
-{{medline-entry
-|title=Maximum reproductive lifespan correlates with [[CD33]]rSIGLEC gene number: Implications for NADPH oxidase-derived reactive oxygen species in aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31907986
-|mesh-terms=* Animals
-* Gene Dosage
-* Humans
-* Longevity
-* NADPH Oxidases
-* Neutrophils
-* Reactive Oxygen Species
-* Sialic Acid Binding Ig-like Lectin 3
-* Whale, Killer
-|keywords=*
-CD33rSIGLEC
-* NADPH-oxidase
-* prolonged post-reproductive lifespan
-* reactive oxygen species
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7018541
-}}
-==CD34==
-{{medline-entry
-|title=Comparing the Effect of TGF-β Receptor Inhibition on Human Perivascular Mesenchymal Stromal Cells Derived from Endometrium, Bone Marrow and Adipose Tissues.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33271899
-|keywords=* SUSD2
-* adipose tissue
-* apoptosis
-* bone marrow
-* clonogenicity
-* endometrium
-* menstrual fluid
-* perivascular mesenchymal stromal cells
-* placenta
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7712261
-}}
-{{medline-entry
-|title=ACE2/ACE imbalance and impaired vasoreparative functions of stem/progenitor cells in aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33247425
-|keywords=* ACE2
-* Aging
-* Angiotensin-(1-7)
-* Hematopoietic stem/progenitor cells
-* Ischemia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7694587
-}}
-{{medline-entry
-|title=Innovative Mind-Body Intervention Day Easy Exercise Increases Peripheral Blood [[CD34]]  Cells in Adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32841054
-|keywords=* CD34+ cells
-* aging
-* day easy exercise
-* mind–body intervention
-|full-text-url=https://sci-hub.do/10.1177/0963689720952352
-}}
-{{medline-entry
-|title=Human Thymic Involution and Aging in Humanized Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32733465
-|keywords=* aging
-* human
-* humanized mouse
-* recent thymic emigrants
-* thymus involution
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7358581
-}}
-{{medline-entry
-|title=Coinhibition of activated p38 MAPKα and mTORC1 potentiates stemness maintenance of HSCs from SR1-expanded human cord blood [[CD34]]  cells via inhibition of senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32602209
-|keywords=* HSC stemness maintenance
-* Stem Regenin 1
-* cellular senescence
-* ex vivo expansion
-* human cord blood CD34+ cells
-* mammalian target of rapamycin complex 1
-* p38 mitogen-activated protein kinase α
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7695631
-}}
-{{medline-entry
-|title=Bulk and single-cell gene expression analyses reveal aging human choriocapillaris has pro-inflammatory phenotype.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32531351
-|mesh-terms=* Age Factors
-* Aged
-* Aged, 80 and over
-* Aging
-* Choroid
-* Endothelial Cells
-* Female
-* Gene Expression Regulation
-* Humans
-* Infant
-* Infant, Newborn
-* Inflammation
-* Inflammation Mediators
-* Macular Degeneration
-* Male
-* Middle Aged
-* Phenotype
-* Sequence Analysis, RNA
-* Single-Cell Analysis
-|keywords=* Age-related macular degeneration
-* Choriocapillaris
-* Choroid
-* Infant
-* Pericytes
-* Single-cell
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7396301
-}}
-{{medline-entry
-|title=Mesenchymal stem cells repair bone marrow damage of aging rats and regulate autophagy and aging genes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32432372
-|keywords=* aging
-* autophagy
-* bone marrow injury
-* mesenchymal stem cells
-* repair
-|full-text-url=https://sci-hub.do/10.1002/cbf.3548
-}}
-{{medline-entry
-|title=Immune cell extracellular vesicles and their mitochondrial content decline with ageing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31911808
-|keywords=* Ageing
-* Apoptotic bodies
-* Exosomes
-* Extracellular vesicles
-* Immune cells
-* Immunosenescence
-* Inflammageing
-* Microvesicles
-* Mitochondria
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6942666
-}}
-{{medline-entry
-|title=Young and elderly oral squamous cell carcinoma patients present similar angiogenic profile and predominance of M2 macrophages: Comparative immunohistochemical study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31497915
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Antigens, CD
-* Antigens, Differentiation, Myelomonocytic
-* Carcinoma, Squamous Cell
-* Female
-* Humans
-* Immunohistochemistry
-* Immunosenescence
-* Macrophages
-* Male
-* Middle Aged
-* Mouth Neoplasms
-* Neovascularization, Pathologic
-* Receptors, Cell Surface
-* Tumor Microenvironment
-|keywords=* M1 and M2 macrophages
-* angiogenesis
-* immunohistochemistry
-* immunosenescence
-* oral squamous cell carcinoma
-|full-text-url=https://sci-hub.do/10.1002/hed.25954
-}}
-==CD36==
-{{medline-entry
-|title=Liver osteopontin is required to prevent the progression of age-related nonalcoholic fatty liver disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32638492
-|keywords=* Osteopontin
-* aging
-* lipid metabolism
-* nonalcoholic fatty liver disease
-* p53
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431823
-}}
-{{medline-entry
-|title=Reduction of senescence-associated beta-galactosidase activity by vitamin E in human fibroblasts depends on subjects' age and cell passage number.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32479666
-|keywords=* CD36 scavenger receptor
-* alpha-tocopherol
-* exosomes
-* extracellular vesicles
-* gene expression
-* lysosome
-* senescence
-* signal transduction
-* vitamin E
-|full-text-url=https://sci-hub.do/10.1002/biof.1636
-}}
-{{medline-entry
-|title=Niacin-mediated rejuvenation of macrophage/microglia enhances remyelination of the aging central nervous system.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32030468
-|keywords=* Aging
-* Macrophages
-* Microglia
-* Oligodendrocyte progenitor cells
-* Phagocytosis
-* Remyelination
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7181452
-}}
-==CD38==
-{{medline-entry
-|title=Re-equilibration of imbalanced NAD metabolism ameliorates the impact of telomere dysfunction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32935380
-|keywords=* CD38 NADase
-* NAD metabolism
-* mitochondrial impairment
-* replicative senescence
-* telomere biology disorders
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7604620
-}}
-{{medline-entry
-|title=TNFRSF12A and [[CD38]] Contribute to a Vicious Circle for Chronic Obstructive Pulmonary Disease by Engaging Senescence Pathways.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32537452
-|keywords=* aging
-* chronic inflammation
-* lung
-* network analysis
-* senescence
-* tissue remodeling
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7268922
-}}
-{{medline-entry
-|title=Aging alters acetylation status in skeletal and cardiac muscles.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32300965
-|keywords=* Aging
-* CD38
-* Deacetylation
-* NAD+
-* PARP
-* SIRT
-* Skeletal muscle
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7286993
-}}
-{{medline-entry
-|title=[[CD38]] in Neurodegeneration and Neuroinflammation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32085567
-|keywords=* ALS.
-* Alzheimer’s disease
-* CD38
-* NAD
-* Parkinson’s disease
-* aging
-* neurodegeneration
-* neuroinflammation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072759
-}}
-{{medline-entry
-|title=[[CD38]], a Receptor with Multifunctional Activities: From Modulatory Functions on Regulatory Cell Subsets and Extracellular Vesicles, to a Target for Therapeutic Strategies.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31783629
-|mesh-terms=* ADP-ribosyl Cyclase 1
-* Aging
-* Animals
-* Antibodies, Monoclonal
-* B-Lymphocytes, Regulatory
-* Cell Line
-* Extracellular Vesicles
-* Humans
-* Infections
-* Membrane Glycoproteins
-* Mice
-* Neoplasms
-* T-Lymphocytes, Regulatory
-|keywords=* CD38
-* adenosine
-* immune-modulation
-* regulatory cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6953043
-}}
-{{medline-entry
-|title=[[CD38]] Deficiency Alleviates D-Galactose-Induced Myocardial Cell Senescence Through NAD /Sirt1 Signaling Pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31551807
-|keywords=* CD38
-* D-galactose
-* NAD+
-* heart senescence
-* oxidative stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6735286
-}}
-==CD4==
-{{medline-entry
-|title=Identification of Key Genes and Potential New Biomarkers for Ovarian Aging: A Study Based on RNA-Sequencing Data.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33304387
-|keywords=* GEO database
-* bioinformatics
-* biomarker
-* immune cell infiltration
-* ovarian aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7701310
-}}
-{{medline-entry
-|title=Distinct Age-Related Epigenetic Signatures in [[CD4]] and CD8 T Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33262764
-|keywords=* T-cell
-* T-cell homeostasis
-* aging
-* chromatin accessibility
-* epigenetics
-* ribosomal proteins
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7686576
-}}
-{{medline-entry
-|title=IL-1β-MyD88-mTOR Axis Promotes Immune-Protective IL-17A Foxp3  Cells During Mucosal Infection and Is Dysregulated With Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33240286
-|keywords=* Candida
-* Foxp3
-* IL-1β
-* Treg
-* Treg17
-* aging
-* fungal infection
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7677307
-}}
-{{medline-entry
-|title=Thymus involution sets the clock of declined immunity and repair with aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33248315
-|keywords=* Aging
-* Chronic systemic inflammation
-* Dysregulated CD4 T cells
-* Immune-mediated repair
-* Thymus
-|full-text-url=https://sci-hub.do/10.1016/j.arr.2020.101231
-}}
-{{medline-entry
-|title=Food insecurity and T-cell dysregulation in women living with HIV on antiretroviral therapy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33247896
-|keywords=* HIV
-* exhaustion
-* food insecurity
-* immune activation
-* senescence
-|full-text-url=https://sci-hub.do/10.1093/cid/ciaa1771
-}}
-{{medline-entry
-|title=Rapamycin Eyedrops Increased [[CD4]] Foxp3  Cells and Prevented Goblet Cell Loss in the Aged Ocular Surface.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33255287
-|keywords=* aging
-* dry eye
-* goblet cell
-* inflammation
-* lacrimal gland
-* ocular surface
-* rapamycin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7727717
-}}
-{{medline-entry
-|title=Antioxidants N-Acetylcysteine and Vitamin C Improve T Cell Commitment to Memory and Long-Term Maintenance of Immunological Memory in Old Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33228213
-|keywords=* NAC
-* T cells
-* aging
-* antioxidants
-* immunosenescence
-* vaccination
-* vitamin C
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7699597
-}}
-{{medline-entry
-|title=Evolution of comorbidities in people living with HIV between 2004 and 2014: cross-sectional analyses from ANRS CO3 Aquitaine cohort.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33198667
-|keywords=* Aging
-* Cardiovascular events
-* Chronic kidney disease
-* Comorbidities
-* HIV
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7670698
-}}
-{{medline-entry
-|title=Impact of age on [[CD4]] recovery and viral suppression over time among adults living with HIV who initiated antiretroviral therapy in the African Cohort Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33183355
-|keywords=* Elders on antiretroviral drugs
-* HIV and aging
-* HIV treatment outcomes
-* Sub-saharan Africa
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7664082
-}}
-{{medline-entry
-|title=hPMSCs protects against D-galactose-induced oxidative damage of [[CD4]]  T cells through activating Akt-mediated Nrf2 antioxidant signaling.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33148324
-|keywords=* Aging
-* CD4+ T cells
-* Nrf2
-* Oxidative stress
-* Senescence-associated secretoryphenotype
-* hPMSC
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7641865
-}}
-{{medline-entry
-|title=Substantial gap in primary care: older adults with HIV presenting late to care.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33129258
-|keywords=* Aging population
-* HIV
-* Older adults
-* Risk
-* Stigma
-* Testing
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7603686
-}}
-{{medline-entry
-|title=Quantitative Digitography Measures Fine Motor Disturbances in Chronically Treated HIV Similar to Parkinson's Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33132893
-|keywords=* HIV—human immunodeficiency virus
-* Parkinson’s disease
-* aging
-* fine motor activities
-* motor control
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7575770
-}}
-{{medline-entry
-|title=Monocyte and T Cell Immune Phenotypic Profiles Associated With Age Advancement Differ Between People With HIV, Lifestyle-Comparable Controls and Blood Donors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33123168
-|keywords=* HIV
-* T cell
-* aging
-* immune activation
-* immune dysfunction
-* inflammation
-* monocyte
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7573236
-}}
-{{medline-entry
-|title=HIV and three dimensions of Wisdom: Association with cognitive function and physical and mental well-being: For: Psychiatry Research.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33096437
-|keywords=* Affective
-* Aging
-* Aids
-* Compassion
-* Reflective
-|full-text-url=https://sci-hub.do/10.1016/j.psychres.2020.113510
-}}
-{{medline-entry
-|title=CD8  T cells are present at low levels in the white matter with physiological and pathological aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33049712
-|keywords=* aging
-* neuroscience
-* pathology
-|full-text-url=https://sci-hub.do/10.18632/aging.104043
-}}
-{{medline-entry
-|title=Immunotherapy in older patients with cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33041248
-|keywords=* Ageing
-* Cancer
-* Elderly
-* Immunosenescence
-* Immunotherapy
-* Old people
-* Oncogeriatry
-|full-text-url=https://sci-hub.do/10.1016/j.bj.2020.07.009
-}}
-{{medline-entry
-|title=Multiple genetic programs contribute to [[CD4]] T cell memory differentiation and longevity by maintaining T cell quiescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32987276
-|keywords=* CD4 T cell
-* Cell longevity
-* Gene
-* Genetic programs
-* Memory T cell
-* Memory cell markers
-|full-text-url=https://sci-hub.do/10.1016/j.cellimm.2020.104210
-}}
-{{medline-entry
-|title=Conventional Treatment for Multiple Myeloma Drives Premature Aging Phenotypes and Metabolic Dysfunction in T Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33013907
-|keywords=* T cell
-* aging
-* autologous stem cell transplant
-* metabolism
-* myeloma
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7494758
-}}
-{{medline-entry
-|title=Immunosenescence: the role of age in multiple sclerosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32962809
-|keywords=* Ageing
-* Envejecimiento
-* Esclerosis múltiple
-* Esclerosis múltiple de comienzo tardío
-* Immunosenescence
-* Inmunosenescencia
-* Late-onset multiple sclerosis
-* Multiple sclerosis
-|full-text-url=https://sci-hub.do/10.1016/j.nrl.2020.05.016
-}}
-{{medline-entry
-|title=Umbilical cord mesenchymal stem cells protect thymus structure and function in aged C57 mice by downregulating aging-related genes and upregulating autophagy- and anti-oxidative stress-related genes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32924972
-|keywords=* aged
-* senescence
-* thymus
-* transplantation
-* umbilical cord mesenchymal stem cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7521525
-}}
-{{medline-entry
-|title=Impaired Cytotoxic CD8  T Cell Response in Elderly COVID-19 Patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32948688
-|mesh-terms=* Aged, 80 and over
-* Antigens, CD
-* Betacoronavirus
-* CD4-Positive T-Lymphocytes
-* CD8-Positive T-Lymphocytes
-* COVID-19
-* Coronavirus Infections
-* Cytotoxins
-* Female
-* Humans
-* Immunity, Cellular
-* Male
-* Middle Aged
-* Pandemics
-* Pneumonia, Viral
-* SARS-CoV-2
-* T-Lymphocyte Subsets
-* T-Lymphocytes, Cytotoxic
-|keywords=* CD4+
-* CD8+
-* COVID-19
-* PD-1
-* SARS-CoV-2
-* aging
-* cytotoxic T cells
-* granzyme
-* perforin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7502863
-}}
-{{medline-entry
-|title=What are the roles of antibodies versus a durable, high quality T-cell response in protective immunity against SARS-CoV-2?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32875286
-|keywords=* Antibodies
-* Antibody-dependent enhancement
-* CD8 T-cells
-* COVID-19
-* Durable immunity
-* Protective immunity
-* SARS
-* SARS-CoV-2
-* T cell lifespan
-* T-cell epitopes
-* T-cells
-* Vaccines
-* Yellow Fever Vaccine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7452821
-}}
-{{medline-entry
-|title=Per2 Upregulation in Circulating Hematopoietic Progenitor Cells During Chronic HIV Infection.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32850472
-|keywords=* HIV
-* Sirtuin 1
-* hematopoietic progenitor cells
-* period circadian clock 2
-* senescence
-* telomere length
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7396677
-}}
-{{medline-entry
-|title=COVID-19: age, Interleukin-6, C-reactive protein, and lymphocytes as key clues from a multicentre retrospective study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32802142
-|keywords=* ACE2
-* C-reactive protein
-* COVID-19
-* Immunity
-* Immunosenescence
-* Interleukin-6
-* Lymphocytes
-* Renin-angiotensin system
-* Severe acute respiratory syndrome coronavirus 2
-* Spain
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7426672
-}}
-{{medline-entry
-|title=Immunosenescence profiles are not associated with muscle strength, physical performance and sarcopenia risk in very old adults: The Newcastle 85+ Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32735896
-|keywords=* immunosenescence
-* lymphocyte compartments
-* physical performance
-* sarcopenia
-* very old adults
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2020.111321
-}}
-{{medline-entry
-|title=Homeostasis and the functional roles of [[CD4]]  Treg cells in aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32717201
-|keywords=* Aging
-* Autoimmunity
-* Cancer
-* FOXP3
-* Immune senescence
-* Immune suppression
-* Inflammaging
-* Regulatory T cells
-* T helper 17
-* Treg
-|full-text-url=https://sci-hub.do/10.1016/j.imlet.2020.07.004
-}}
-{{medline-entry
-|title=A Comprehensive Evaluation of the Impact of Bovine Milk Containing Different Beta-Casein Profiles on Gut Health of Ageing Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32707687
-|keywords=* A2 beta-casein
-* SCFAs
-* elderly
-* gut inflammation
-* gut microbiota
-* gut morphology
-* immunosenescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7400800
-}}
-{{medline-entry
-|title=Premature aging of circulating T cells predicts all-cause mortality in hemodialysis patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32660510
-|keywords=* Hemodialysis
-* Inflammation
-* Mortality
-* T cell aging
-* naïve T cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7359274
-}}
-{{medline-entry
-|title=In-depth immune cellular profiling reveals sex-specific associations with frailty.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32582361
-|keywords=* Frailty
-* Healthy aging
-* Immune cellular profiling
-* Immune homeostasis
-* Immunosenescence
-* Sex-specific immune profile
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7310472
-}}
-{{medline-entry
-|title=CD70 contributes to age-associated T cell defects and overwhelming inflammatory responses.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32559178
-|keywords=* CD70
-* T cell aging
-* co-inhibitory molecules
-* immunosenescence
-* overwhelming inflammatory responses
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343466
-}}
-{{medline-entry
-|title=Comparison of Overall and Comorbidity-Free Life Expectancy Between Insured Adults With and Without HIV Infection, 2000-2016.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32539152
-|mesh-terms=* Adult
-* Chronic Disease
-* Cohort Studies
-* Comorbidity
-* Female
-* HIV Infections
-* Humans
-* Insurance, Health
-* Life Expectancy
-* Male
-* Middle Aged
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7296391
-}}
-{{medline-entry
-|title=Comparative Analysis of Age-Related Changes in Lacrimal Glands and Meibomian Glands of a C57BL/6 Male Mouse Model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32545199
-|keywords=* aging
-* dry eye
-* inflammation
-* lacrimal glands
-* meibomian glands
-* oxidative stress
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7313015
-}}
-{{medline-entry
-|title=Thymus aging in mice deficient in either EphB2 or EphB3, two master regulators of thymic epithelium development.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32506584
-|keywords=* senescence
-* thymic epithelial cells
-* thymocytes
-|full-text-url=https://sci-hub.do/10.1002/dvdy.212
-}}
-{{medline-entry
-|title=CD8  T-cell senescence and skewed lymphocyte subsets in young Dyskeratosis Congenita patients with PARN and DKC1 mutations.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32452087
-|keywords=*
-DKC1
-*
-PARN
-* Dyskeratosis Congenita
-* primary immunodeficiency
-* senescence
-* telomere
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7521304
-}}
-{{medline-entry
-|title=Short-Term Environmental Enrichment is a Stronger Modulator of Brain Glial Cells and Cervical Lymph Node T Cell Subtypes than Exercise or Combined Exercise and Enrichment.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32451728
-|keywords=* Aging
-* Astrocytes
-* Environmental enrichment
-* Microglia
-* Physical exercise
-* T cells
-|full-text-url=https://sci-hub.do/10.1007/s10571-020-00862-x
-}}
-{{medline-entry
-|title=Viral and host factors related to the clinical outcome of COVID-19.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32434211
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Animals
-* Asymptomatic Infections
-* Betacoronavirus
-* COVID-19
-* China
-* Cohort Studies
-* Coronavirus Infections
-* Critical Illness
-* Disease Progression
-* Evolution, Molecular
-* Female
-* Genetic Variation
-* Genome, Viral
-* Hospitalization
-* Host-Pathogen Interactions
-* Humans
-* Inflammation Mediators
-* Interleukin-6
-* Interleukin-8
-* Lymphocyte Count
-* Lymphopenia
-* Male
-* Middle Aged
-* Pandemics
-* Phylogeny
-* Pneumonia, Viral
-* Respiratory Distress Syndrome
-* SARS-CoV-2
-* T-Lymphocytes
-* Time Factors
-* Treatment Outcome
-* Virulence
-* Virus Shedding
-* Young Adult
-* Zoonoses
-|full-text-url=https://sci-hub.do/10.1038/s41586-020-2355-0
-}}
-{{medline-entry
-|title=Use of comedications and potential drug-drug interactions in people living with HIV in China.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32354599
-|keywords=* Aging
-* China
-* Co-medication
-* Drug-drug interaction
-* HIV
-|full-text-url=https://sci-hub.do/10.1016/j.jiac.2020.04.003
-}}
-{{medline-entry
-|title=[[CD4]]  T helper 17 cell response of aged mice promotes prostate cancer cell migration and invasion.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32356608
-|mesh-terms=* Aging
-* Animals
-* CD4-Positive T-Lymphocytes
-* Cell Differentiation
-* Cell Line, Tumor
-* Cell Movement
-* Humans
-* Inflammation
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Models, Animal
-* NF-kappa B
-* Neoplasm Invasiveness
-* PC-3 Cells
-* Prostatic Neoplasms
-* Th17 Cells
-|keywords=* CD4+ T cell-secreted factors
-* PCa cells
-* Th17 cytokines
-* aging
-* inflammation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7310589
-}}
-{{medline-entry
-|title=The Rules of Human T Cell Fate [i]in vivo[/i].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32322253
-|keywords=* decision
-* fate
-* half-life
-* labeling
-* lifespan
-* lymphocyte
-* mathematical model
-* proliferation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156550
-}}
-{{medline-entry
-|title=[[CD4]]/CD8 ratio, comorbidities, and aging in treated HIV infected individuals on viral suppression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32314818
-|keywords=* CD4/CD8 ratio
-* HIV
-* aging
-* comorbidities
-|full-text-url=https://sci-hub.do/10.1002/jmv.25911
-}}
-{{medline-entry
-|title=The effects of advanced maternal age on T-cell subsets at the maternal-fetal interface prior to term labor and in the offspring: a mouse study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32279324
-|mesh-terms=* Adult
-* Aging
-* Animals
-* Female
-* Humans
-* Live Birth
-* Mice
-* Mice, Transgenic
-* Placenta
-* Pregnancy
-* T-Lymphocyte Subsets
-|keywords=* birth weight
-* neonate
-* offspring
-* pregnancy
-* preterm labor
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7290081
-}}
-{{medline-entry
-|title=Structural and Functional Changes in the Mesenteric Lymph Nodes in Humans during Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32248450
-|keywords=* age-related involution
-* aging
-* immune system
-* immunomorphology
-* mesenteric lymph nodes
-|full-text-url=https://sci-hub.do/10.1007/s10517-020-04782-0
-}}
-{{medline-entry
-|title=Neurocognitive Functioning is Associated with Self-Reported and Performance-Based Treatment Management Abilities in People Living with HIV with Low Health Literacy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32090235
-|mesh-terms=* Adult
-* Cognition
-* Cross-Sectional Studies
-* HIV Infections
-* Health Literacy
-* Humans
-* Neuropsychological Tests
-* Self Report
-|keywords=* Adherence
-* Aging
-* Cognitive impairment
-* HIV/AIDS
-* Health illiteracy
-* Observational study
-|full-text-url=https://sci-hub.do/10.1093/arclin/acaa005
-}}
-{{medline-entry
-|title=Blockade of Stat3 oncogene addiction induces cellular senescence and reveals a cell-nonautonomous activity suitable for cancer immunotherapy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32064174
-|keywords=* Stat3
-* immune checkpoint blockade
-* immunotherapy
-* oncogene addiction
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996562
-}}
-{{medline-entry
-|title=Age-related changes in T lymphocytes of patients with head and neck squamous cell carcinoma.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32082401
-|keywords=* Aging
-* Head and neck cancer
-* Immune escape
-* Immunosenescence
-* T cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7017629
-}}
-{{medline-entry
-|title=Immunological history governs human stem cell memory [[CD4]] heterogeneity via the Wnt signaling pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32041953
-|mesh-terms=* Aging
-* Animals
-* Antigens, CD
-* CD4-Positive T-Lymphocytes
-* Gene Expression Profiling
-* HIV Infections
-* Humans
-* Immunologic Memory
-* Intercellular Signaling Peptides and Proteins
-* Mice
-* Precursor Cells, T-Lymphoid
-* Thymus Gland
-* Wnt Signaling Pathway
-* beta Catenin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7010798
-}}
-{{medline-entry
-|title=Estimating HIV Management and Comorbidity Costs Among Aging HIV Patients in the United States: A Systematic Review.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32011956
-|mesh-terms=* Anti-HIV Agents
-* CD4 Lymphocyte Count
-* Comorbidity
-* Cost-Benefit Analysis
-* HIV Infections
-* Health Care Costs
-* Humans
-* Life Expectancy
-* United States
-|full-text-url=https://sci-hub.do/10.18553/jmcp.2020.26.2.104
-}}
-{{medline-entry
-|title=Sex Differences in People Aging With HIV.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32032279
-|mesh-terms=* Aged
-* Aging
-* Alcohol Drinking
-* Body Composition
-* CD4 Lymphocyte Count
-* CD4-CD8 Ratio
-* CD4-Positive T-Lymphocytes
-* Cohort Studies
-* Cross-Sectional Studies
-* Female
-* Frailty
-* HIV Infections
-* Humans
-* Male
-* Middle Aged
-* Muscle Strength
-* Prospective Studies
-|full-text-url=https://sci-hub.do/10.1097/QAI.0000000000002259
-}}
-{{medline-entry
-|title=Identification of Differentially Expressed miRNAs in the Response of Spleen [[CD4]]  T Cells to Electroacupuncture in Senescence-Accelerated Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32026263
-|mesh-terms=* Aging
-* Animals
-* Antagomirs
-* CD4-Positive T-Lymphocytes
-* Cell Differentiation
-* Cytokines
-* Down-Regulation
-* Electroacupuncture
-* Female
-* Gene Regulatory Networks
-* High-Throughput Nucleotide Sequencing
-* Male
-* Mice
-* Mice, Inbred C57BL
-* MicroRNAs
-* Sequence Analysis, RNA
-* Spleen
-* Up-Regulation
-|keywords=* CD4+ T cell
-* Deep sequencing
-* Electroacupuncture
-* Immunological aging
-* miRNA
-|full-text-url=https://sci-hub.do/10.1007/s12013-020-00900-x
-}}
-{{medline-entry
-|title=Thymus Involution and Intravenous Drug Abuse.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32000220
-|mesh-terms=* Adolescent
-* Adult
-* Aging
-* Atrophy
-* CD4-Positive T-Lymphocytes
-* CD8-Positive T-Lymphocytes
-* Calcinosis
-* Case-Control Studies
-* Drug Users
-* Female
-* Forensic Pathology
-* Hepatitis C, Chronic
-* Humans
-* Male
-* Middle Aged
-* Substance Abuse, Intravenous
-* Thymus Gland
-* Young Adult
-|full-text-url=https://sci-hub.do/10.1097/PAF.0000000000000530
-}}
-{{medline-entry
-|title=Depletion of [[CD4]] T cells provides therapeutic benefits in aged mice after ischemic stroke.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31954116
-|mesh-terms=* Aging
-* Animals
-* Behavior, Animal
-* Brain Chemistry
-* Brain Ischemia
-* CD4-Positive T-Lymphocytes
-* Chemokines
-* Cytokines
-* Female
-* Infarction, Middle Cerebral Artery
-* Inflammation
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Stroke
-* Treatment Outcome
-|keywords=* Age
-* CD4 T cells
-* CXCL10
-* Inflammation
-* Stroke
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059209
-}}
-{{medline-entry
-|title=Immunological and Virological Responses in Older HIV-Infected Adults Receiving Antiretroviral Therapy: An Evidence-Based Meta-Analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31913990
-|mesh-terms=* Aged
-* Aging
-* Anti-HIV Agents
-* HIV Infections
-* Humans
-* Middle Aged
-|full-text-url=https://sci-hub.do/10.1097/QAI.0000000000002266
-}}
-{{medline-entry
-|title=African Mitochondrial DNA Haplogroup L2 Is Associated With Slower Decline of β-cell Function and Lower Incidence of Diabetes Mellitus in Non-Hispanic, Black Women Living With Human Immunodeficiency Virus.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31927570
-|keywords=* HIV
-* aging
-* diabetes mellitus
-* mitochondrial genetics
-|full-text-url=https://sci-hub.do/10.1093/cid/ciaa026
-}}
-{{medline-entry
-|title=DP1 Activation Reverses Age-Related Hypertension Via NEDD4L-Mediated T-Bet Degradation in T Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31893939
-|mesh-terms=* Aged
-* Aging
-* Animals
-* Antihypertensive Agents
-* CD4-Positive T-Lymphocytes
-* Cyclic AMP-Dependent Protein Kinases
-* Cytokines
-* Humans
-* Hypertension
-* Mice
-* Mice, Inbred C57BL
-* Nedd4 Ubiquitin Protein Ligases
-* Prostaglandin D2
-* Receptors, Prostaglandin
-* Signal Transduction
-* Sp1 Transcription Factor
-* Superoxides
-* T-Box Domain Proteins
-* Th1 Cells
-* Ubiquitination
-|keywords=* D-prostanoid receptor 1
-* aging
-* hypertension
-* lymphocyte
-* prostaglandin (PG) D2
-|full-text-url=https://sci-hub.do/10.1161/CIRCULATIONAHA.119.042532
-}}
-{{medline-entry
-|title=An Emerging Concern-High Rates of Frailty among Middle-aged and Older Individuals Living with HIV.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31885759
-|keywords=* accelerated aging
-* anti-retroviral therapy
-* frailty
-* frailty index
-* geriatric syndrome
-* human immunodeficiency virus (HIV)
-* multimorbidity
-* vulnerability
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6887139
-}}
-{{medline-entry
-|title=Higher Acuity Resource Utilization With Older Age and Poorer HIV Control in Adolescents and Young Adults in the HIV Research Network.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31904706
-|mesh-terms=* Adolescent
-* Adult
-* Aging
-* Anti-Retroviral Agents
-* CD4 Lymphocyte Count
-* Drug Administration Schedule
-* Female
-* HIV Infections
-* HIV-1
-* Humans
-* Male
-* Medication Adherence
-* Viral Load
-* Young Adult
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7055514
-}}
-{{medline-entry
-|title=Mitochondrial DNA Haplogroups and Frailty in Adults Living with HIV.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31822125
-|keywords=* HIV
-* aging
-* frailty
-* haplotypes
-* mitochondria
-* sarcopenia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7133433
-}}
-{{medline-entry
-|title=Gallic acid attenuates thymic involution in the d-galactose induced accelerated aging mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31822433
-|keywords=* Aging
-* FoxN1
-* Gallic acid
-* Thymus
-* d-galactose
-|full-text-url=https://sci-hub.do/10.1016/j.imbio.2019.11.005
-}}
-{{medline-entry
-|title=Mitochondrial mass governs the extent of human T cell senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31788930
-|mesh-terms=* Adenosine Triphosphate
-* Adult
-* CD4-Positive T-Lymphocytes
-* CD8-Positive T-Lymphocytes
-* Cell Movement
-* Cell Proliferation
-* Cellular Senescence
-* Glucose
-* Glycolysis
-* Humans
-* Immunosenescence
-* Leukocyte Common Antigens
-* Microscopy, Electron, Transmission
-* Middle Aged
-* Mitochondria
-* Rotenone
-|keywords=* T cell
-* aging
-* metabolism
-* mitochondria
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996952
-}}
-{{medline-entry
-|title=T cells and immune functions of plasma extracellular vesicles are differentially modulated from adults to centenarians.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31785146
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Extracellular Vesicles
-* Female
-* Humans
-* Immunosenescence
-* Lymphocyte Activation
-* Male
-* Middle Aged
-* T-Lymphocytes
-|keywords=* T cells
-* aging
-* centenarians
-* extracellular vesicles (EVs)
-* immunosenescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6914389
-}}
-{{medline-entry
-|title=Defects in Antiviral T Cell Responses Inflicted by Aging-Associated miR-181a Deficiency.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31747595
-|mesh-terms=* Aging
-* Animals
-* CD4-Positive T-Lymphocytes
-* CD8-Positive T-Lymphocytes
-* Disease Models, Animal
-* Lymphocytic Choriomeningitis
-* Lymphocytic choriomeningitis virus
-* Mice
-* MicroRNAs
-|keywords=* CD8 effector T cell
-* T cell repertoire
-* antiviral response
-* immune aging
-* immunosenescence
-* microRNA
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6957231
-}}
-{{medline-entry
-|title=Increased Prevalence of Neurocognitive Impairment in Aging People Living With Human Immunodeficiency Virus: The ANRS EP58 HAND 55-70 Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31755936
-|keywords=* Frascati criteria
-* HAND
-* HIV
-* aging
-* neurocognitive impairment
-|full-text-url=https://sci-hub.do/10.1093/cid/ciz670
-}}
-{{medline-entry
-|title=Age-associated changes in human [[CD4]]  T cells point to mitochondrial dysfunction consequent to impaired autophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31707363
-|mesh-terms=* Adult
-* Aged
-* CD4-Positive T-Lymphocytes
-* Cell Respiration
-* Humans
-* Immunosenescence
-* Longitudinal Studies
-* Mitochondria
-* Mitophagy
-* Young Adult
-|keywords=* CD4+ T cells
-* aging
-* autophagy
-* mitochondria
-* proteomics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6874450
-}}
-{{medline-entry
-|title=Sex Differences in the Blood Transcriptome Identify Robust Changes in Immune Cell Proportions with Aging and Influenza Infection.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31722210
-|mesh-terms=* Aging
-* CD4-Positive T-Lymphocytes
-* Female
-* Humans
-* Influenza, Human
-* Male
-* Monocytes
-* Sex Characteristics
-* Transcriptome
-|keywords=* CD4(+) T cells
-* aging
-* immune system
-* immunology
-* influenza
-* meta-analysis
-* monocytes
-* multi-cohort analysis
-* sex differences
-* transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6856718
-}}
-{{medline-entry
-|title=Going Beyond Giving Antiretroviral Therapy: Multimorbidity in Older People Aging with HIV in Nigeria.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31711310
-|keywords=* ART
-* PLWH
-* aging
-* multimorbidity
-* quality of life
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7071065
-}}
-{{medline-entry
-|title=Alterations in composition of immune cells and impairment of anti-tumor immune response in aged oral cancer-bearing mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31683168
-|mesh-terms=* Aged
-* Animals
-* Cell Line, Tumor
-* Cell Proliferation
-* Female
-* Humans
-* Immunotherapy
-* Mice
-|keywords=* Aging
-* Immune check-point molecules
-* Immunosenescence
-* Immunotherapy
-* Myeloid derived suppressor cells
-* Oral cancer
-* Regulatory T cells
-|full-text-url=https://sci-hub.do/10.1016/j.oraloncology.2019.104462
-}}
-{{medline-entry
-|title=LTA1 is a safe, intranasal enterotoxin-based adjuvant that improves vaccine protection against influenza in young, old and B-cell-depleted (μMT) mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31641151
-|mesh-terms=* Adjuvants, Immunologic
-* Administration, Intranasal
-* Aging
-* Animals
-* Antibodies
-* Antibody Formation
-* B-Lymphocytes
-* CD4-Positive T-Lymphocytes
-* Dose-Response Relationship, Immunologic
-* Enterotoxins
-* Female
-* Immunity, Mucosal
-* Immunization
-* Inflammation
-* Influenza A Virus, H1N1 Subtype
-* Lung
-* Lymphocyte Activation
-* Lymphocyte Depletion
-* Mast Cells
-* Mice, Inbred C57BL
-* Orthomyxoviridae Infections
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6805908
-}}
-{{medline-entry
-|title=Thymus Imaging Detection and Size Is Inversely Associated With Metabolic Syndrome and Frailty in People With HIV.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31660382
-|keywords=* HIV
-* aging
-* frailty
-* metabolic syndrome
-* thymus
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6809752
-}}
-{{medline-entry
-|title=Alterations in peripheral T cell and B cell subsets in patients with osteoarthritis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31624962
-|mesh-terms=* Aged
-* Aging
-* B-Lymphocyte Subsets
-* Case-Control Studies
-* Female
-* Humans
-* Male
-* Middle Aged
-* Osteoarthritis, Knee
-* T-Lymphocyte Subsets
-|keywords=* B cell
-* Lymphocyte
-* Osteoarthritis
-* T cell
-|full-text-url=https://sci-hub.do/10.1007/s10067-019-04768-y
-}}
-{{medline-entry
-|title=Short Communication: Carotid Intima-Media Thickness Is Not Associated with Neurocognitive Impairment Among People Older than 50 Years With and Without HIV Infection from Thailand.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31588776
-|mesh-terms=* Aging
-* Anti-Retroviral Agents
-* Cardiovascular Diseases
-* Carotid Intima-Media Thickness
-* Cross-Sectional Studies
-* Depression
-* Female
-* HIV Infections
-* Humans
-* Male
-* Middle Aged
-* Neurocognitive Disorders
-* Quality of Life
-* Risk Factors
-* Thailand
-|keywords=* HIV
-* aging
-* carotid intima-media thickness
-* neurocognitive
-|full-text-url=https://sci-hub.do/10.1089/AID.2019.0139
-}}
-{{medline-entry
-|title=Implications of Immune Checkpoint Expression During Aging in HIV-Infected People on Antiretroviral Therapy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31578868
-|mesh-terms=* Adult
-* Aged
-* Aging
-* Anti-HIV Agents
-* Antiretroviral Therapy, Highly Active
-* CD4-Positive T-Lymphocytes
-* CD8-Positive T-Lymphocytes
-* Cytokines
-* Female
-* Flow Cytometry
-* Gene Expression
-* HIV Infections
-* HIV-1
-* Hepatitis A Virus Cellular Receptor 2
-* Humans
-* Leukocytes, Mononuclear
-* Male
-* Middle Aged
-* Young Adult
-* gag Gene Products, Human Immunodeficiency Virus
-|keywords=* aging
-* immune checkpoint molecules
-* virus suppression
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6862963
-}}
-{{medline-entry
-|title=Age-related alterations in human gut [[CD4]] T cell phenotype, T helper cell frequencies, and functional responses to enteric bacteria.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31573727
-|mesh-terms=* Adolescent
-* Adult
-* Age Factors
-* Aged
-* Aged, 80 and over
-* CD4-Positive T-Lymphocytes
-* Female
-* Gastrointestinal Microbiome
-* Humans
-* Interleukin-17
-* Intestinal Mucosa
-* Male
-* Middle Aged
-* Phenotype
-* Th1 Cells
-* Th17 Cells
-* Young Adult
-|keywords=* T helper cells
-* aging
-* gut
-* human
-|full-text-url=https://sci-hub.do/10.1002/JLB.5A0919-177RR
-}}
-{{medline-entry
-|title=Determinants of blood telomere length in antiretroviral treatment-naïve HIV-positive participants enrolled in the NEAT 001/ANRS 143 clinical trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31532902
-|mesh-terms=* Adult
-* Aged
-* Anti-Retroviral Agents
-* Cross-Sectional Studies
-* Darunavir
-* Emtricitabine
-* Female
-* HIV Infections
-* Humans
-* Logistic Models
-* Male
-* Middle Aged
-* RNA, Viral
-* Raltegravir Potassium
-* Ritonavir
-* Telomere
-* Tenofovir
-|keywords=* HIV infection
-* aging
-* immunosenescence
-* telomere length
-* viral load
-|full-text-url=https://sci-hub.do/10.1111/hiv.12791
-}}
-{{medline-entry
-|title=Human T Cell Differentiation Negatively Regulates Telomerase Expression Resulting in Reduced Activation-Induced Proliferation and Survival.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31497023
-|mesh-terms=* Adult
-* Cell Differentiation
-* Cell Proliferation
-* Cell Survival
-* Humans
-* T-Lymphocytes
-* Telomerase
-|keywords=* T cell subsets
-* T lymphocytes
-* aging
-* alternative splicing
-* differentiation
-* hTERT
-* proliferation
-* telomerase
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6712505
-}}
-{{medline-entry
-|title=Short Communication: Getting Older with HIV: Increasing Frequency of Comorbidities and Polypharmacy in Brazilian HIV Patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31452382
-|mesh-terms=* Aged
-* Aging
-* Brazil
-* CD4 Lymphocyte Count
-* Cardiovascular Diseases
-* Comorbidity
-* Diabetes Mellitus
-* Female
-* HIV Infections
-* Humans
-* Life Expectancy
-* Male
-* Middle Aged
-* Neoplasms
-* Polypharmacy
-|keywords=* Brazil
-* HIV
-* aging
-* noncommunicable diseases
-|full-text-url=https://sci-hub.do/10.1089/AID.2019.0069
-}}
-{{medline-entry
-|title=Gait Speed Decline Is Associated with Hemoglobin A1C, Neurocognitive Impairment, and Black Race in Persons with HIV.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31468979
-|mesh-terms=* Adult
-* African Americans
-* Aging
-* CD4 Lymphocyte Count
-* Cohort Studies
-* Female
-* Glycated Hemoglobin A
-* HIV Infections
-* Humans
-* Longitudinal Studies
-* Male
-* Middle Aged
-* Neurocognitive Disorders
-* Odds Ratio
-* RNA, Viral
-* Risk Factors
-* Walking Speed
-|keywords=* aging
-* gait speed
-* hemoglobin A1C
-* neurocognitive impairment
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6862955
-}}
-{{medline-entry
-|title=Noncommunicable Diseases Burden and Risk Factors in a Cohort of HIV+ Elderly Patients in Malawi.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31468993
-|mesh-terms=* Adult
-* Age Factors
-* Aged
-* Anti-HIV Agents
-* Anti-Retroviral Agents
-* CD4 Lymphocyte Count
-* Comorbidity
-* Cost of Illness
-* Cross-Sectional Studies
-* Diabetes Mellitus
-* Female
-* HIV Infections
-* Humans
-* Hypertension
-* Malawi
-* Male
-* Middle Aged
-* Noncommunicable Diseases
-* Odds Ratio
-* Prevalence
-* Retrospective Studies
-* Risk Factors
-|keywords=* HIV infection
-* Malawi
-* aging
-* noncommunicable diseases
-|full-text-url=https://sci-hub.do/10.1089/AID.2019.0125
-}}
-{{medline-entry
-|title=Aging promotes reorganization of the [[CD4]] T cell landscape toward extreme regulatory and effector phenotypes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31457092
-|mesh-terms=* Aging
-* Animals
-* CD4-Positive T-Lymphocytes
-* High-Throughput Nucleotide Sequencing
-* Immunomodulation
-* Mice
-* Phenotype
-* Sequence Analysis, RNA
-* Single-Cell Analysis
-* T-Lymphocyte Subsets
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6703865
-}}
-{{medline-entry
-|title=Prevalence of hypertension and cardiovascular risk factors among long-term AIDS survivors: A report from the field.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31448551
-|mesh-terms=* Acquired Immunodeficiency Syndrome
-* Adult
-* Anti-Retroviral Agents
-* CD4 Lymphocyte Count
-* Cardiovascular Diseases
-* Diabetes Mellitus
-* Diagnostic Screening Programs
-* Female
-* HIV Infections
-* HIV-1
-* Haiti
-* Humans
-* Hypercholesterolemia
-* Hypertension
-* Male
-* Middle Aged
-* Obesity
-* Prevalence
-* Retrospective Studies
-* Risk Factors
-* Smoking
-* Survivors
-|keywords=* HIV
-* aging
-* cardiovascular disease
-* hypertension
-* risk assessment
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6896990
-}}
-==CD44==
-{{medline-entry
-|title=Hyaluronan goes to great length.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32908962
-|keywords=* aging
-* hyaluronan
-* longevity
-* naked mole rat
-* very high molecular weight hyaluronan
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7453635
-}}
-{{medline-entry
-|title=Naked mole-rat very-high-molecular-mass hyaluronan exhibits superior cytoprotective properties.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32398747
-|mesh-terms=* Animals
-* Apoptosis
-* Cell Cycle Checkpoints
-* Cell Line
-* Cytoprotection
-* Gene Expression Regulation
-* Gene Knockout Techniques
-* Humans
-* Hyaluronan Receptors
-* Hyaluronic Acid
-* Longevity
-* Mice
-* Mole Rats
-* Molecular Weight
-* Primary Cell Culture
-* Protein Interaction Maps
-* RNA-Seq
-* Signal Transduction
-* Species Specificity
-* Stress, Physiological
-* Tumor Suppressor Protein p53
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217962
-}}
-{{medline-entry
-|title=Maturity-dependent cartilage cell plasticity and sensitivity to external perturbation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32321631
-|keywords=* Aging
-* Articular cartilage
-* Osteoarthritis
-* Plasticity
-* Progenitor cells
-|full-text-url=https://sci-hub.do/10.1016/j.jmbbm.2020.103732
-}}
-{{medline-entry
-|title=Aged Mice Exhibit Severe Exacerbations of Dry Eye Disease with an Amplified Memory Th17 Cell Response.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32289288
-|mesh-terms=* Aging
-* Animals
-* Dry Eye Syndromes
-* Female
-* Immunologic Memory
-* Mice
-* Mice, Inbred C57BL
-* Th17 Cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7369573
-}}
-{{medline-entry
-|title=Chronic circadian misalignment accelerates immune senescence and abbreviates lifespan in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32054990
-|mesh-terms=* Animals
-* B-Lymphocytes
-* Cellular Senescence
-* Circadian Rhythm
-* Disease Models, Animal
-* Humans
-* Hyaluronan Receptors
-* Inflammation
-* Jet Lag Syndrome
-* Longevity
-* Mice
-* Programmed Cell Death 1 Receptor
-* Sequence Analysis, RNA
-* T-Lymphocytes
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7018741
-}}
-{{medline-entry
-|title=Defective induction of the proteasome associated with T-cell receptor signaling underlies T-cell senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31621149
-|mesh-terms=* Animals
-* CD4-Positive T-Lymphocytes
-* Cell Proliferation
-* Cells, Cultured
-* Cellular Senescence
-* Cytokines
-* Hyaluronan Receptors
-* Mice
-* Mice, Inbred C57BL
-* Phenotype
-* Programmed Cell Death 1 Receptor
-* Proteasome Endopeptidase Complex
-* Receptors, Antigen, T-Cell
-* Signal Transduction
-|keywords=* T cell receptor signal
-* T cell senescence
-* aging
-* proteasome
-|full-text-url=https://sci-hub.do/10.1111/gtc.12728
-}}
-==CD47==
-{{medline-entry
-|title=Aging-associated changes in [[CD47]] arrangement and interaction with thrombospondin-1 on red blood cells visualized by super-resolution imaging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32866348
-|keywords=* CD47
-* aging
-* dSTORM
-* red blood cells
-* thrombospondin-1
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7576236
-}}
-{{medline-entry
-|title=[[CD47]] Promotes Age-Associated Deterioration in Angiogenesis, Blood Flow and Glucose Homeostasis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32679764
-|keywords=* CD47
-* aging
-* angiogenesis
-* blood flow
-* endothelial cells
-* glucose homeostasis
-* metabolism
-* self-renewal
-* thrombospondin-1
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7407670
-}}
-{{medline-entry
-|title=Unique Spatial Immune Profiling in Pancreatic Ductal Adenocarcinoma with Enrichment of Exhausted and Senescent T Cells and Diffused [[CD47]]-SIRPα Expression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32645996
-|keywords=* CD47
-* T cell exhaustion
-* T cell senescence
-* draining lymph nodes
-* macrophage checkpoint
-* neoadjuvant chemotherapy
-* pancreatic ductal adenocarcinoma
-* signal regulatory protein alpha (SIRPα)
-* spatial heterogeneity
-* tumor microenvironment
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7408661
-}}
-==CD5==
-{{medline-entry
-|title=Comparative proteomic analysis identifies biomarkers for renal aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33159023
-|keywords=* NMN
-* biomarkers
-* glutathionylation
-* proteomics
-* renal aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7695359
-}}
-==CD63==
-{{medline-entry
-|title=Cellular senescence contributes to age-dependent changes in circulating extracellular vesicle cargo and function.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31960578
-|keywords=* aging
-* extracellular vesicles
-* microRNA
-* plasma
-* senescence
-* senolytic
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059145
-}}
-==CD68==
-{{medline-entry
-|title=Insulin activates microglia and increases COX-2/IL-1β expression in young but not in aged hippocampus.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32422127
-|keywords=* Aging
-* Hippocampus
-* Insulin
-* Memory
-* Microglia
-* Neuroinflammation
-|full-text-url=https://sci-hub.do/10.1016/j.brainres.2020.146884
-}}
-{{medline-entry
-|title=Epigenetic modulation of macrophage polarization prevents lumbar disc degeneration.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32310825
-|keywords=* DNA methyltransferase 1 (DNMT1)
-* aging
-* lumbar disc degeneration (LDD)
-* macrophage polarization
-* transforming growth factor beta 1 (TGFβ1)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7202517
-}}
-{{medline-entry
-|title=Cellular senescence in recurrent tonsillitis and tonsillar hypertrophy in children.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32200310
-|mesh-terms=* Antigens, CD
-* Antigens, Differentiation, Myelomonocytic
-* Cellular Senescence
-* Child
-* Germinal Center
-* Humans
-* Hypertrophy
-* Macrophages
-* Palatine Tonsil
-* Recurrence
-* Tonsillectomy
-* Tonsillitis
-|keywords=* Cellular senescence
-* Recurrent tonsillitis
-* Tonsillar hypertrophy
-|full-text-url=https://sci-hub.do/10.1016/j.ijporl.2020.110004
-}}
-{{medline-entry
-|title=Ginsenoside Rg1 supplementation clears senescence-associated β-galactosidase in exercising human skeletal muscle.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31695564
-|keywords=* Cellular senescence
-* Endurance
-* Ergogenic aid
-* Inflammation
-* Macrophage
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6823780
-}}
-{{medline-entry
-|title=Histopathological, immunohistochemical, and molecular studies for determination of wound age and vitality in rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31448552
-|mesh-terms=* Actins
-* Animals
-* Antigens, CD
-* Antigens, Differentiation, Myelomonocytic
-* Cell Movement
-* Fibroblasts
-* Granulation Tissue
-* Immunohistochemistry
-* Macrophages
-* Models, Animal
-* Neovascularization, Physiologic
-* RNA, Messenger
-* Rats, Wistar
-* Re-Epithelialization
-* Skin
-* Time Factors
-* Transforming Growth Factor beta1
-* Vascular Endothelial Growth Factor A
-* Wound Healing
-* Wounds and Injuries
-|keywords=* TGFb1
-* VEGF
-* gene expression
-* immunohistochemistry
-* wound aging
-|full-text-url=https://sci-hub.do/10.1111/iwj.13206
-}}
-==CD80==
-{{medline-entry
-|title=The aging common marmoset's immune system: From junior to senior.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32246726
-|mesh-terms=* Aging
-* Animals
-* CD4-CD8 Ratio
-* Callithrix
-* Female
-* Flow Cytometry
-* Immune System
-* Longevity
-* Male
-* Models, Animal
-* Sex Factors
-|keywords=* aging
-* common marmoset
-* immune system
-* immunosenescence
-* innate and adaptive immunity
-* sex
-|full-text-url=https://sci-hub.do/10.1002/ajp.23128
-}}
-==CD81==
-{{medline-entry
-|title=Ovarian aging increases small extracellular vesicle [[CD81]]  release in human follicular fluid and influences miRNA profiles.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32554857
-|keywords=* extracellular vesicles
-* follicular fluid
-* microRNAs
-* reproductive aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343446
-}}
-{{medline-entry
-|title=Older Adults with Physical Frailty and Sarcopenia Show Increased Levels of Circulating Small Extracellular Vesicles with a Specific Mitochondrial Signature.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32326435
-|keywords=* aging
-* biomarkers
-* exosomes
-* mitochondrial dynamics
-* mitochondrial quality control
-* mitochondrial-derived vesicles (MDVs)
-* mitochondrial-lysosomal axis
-* mitophagy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7227017
-}}
-{{medline-entry
-|title=Increased production of functional small extracellular vesicles in senescent endothelial cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32101370
-|keywords=* endothelium
-* exosomes
-* extracellular vesicles
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7176858
-}}
-==CDA==
-{{medline-entry
-|title=Cumulative Dis/Advantage and Health Pattern in Late Life: A Comparison between Genders and Welfare State Regimes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31771483
-|mesh-terms=* Aged
-* Aged, 80 and over
-* China
-* Cross-Sectional Studies
-* England
-* Female
-* Health Behavior
-* Health Status Disparities
-* Humans
-* Longevity
-* Male
-* Mexico
-* Middle Aged
-* Regression Analysis
-* Self Report
-* Sex Factors
-* Social Class
-* Social Welfare
-* United States
-|keywords=* Cumulative dis/advantage
-* cross-national study
-* health retirement study
-* welfare state theory
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7367435
-}}
-{{medline-entry
-|title=Does numerical similarity alter age-related distractibility in working memory?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31483830
-|mesh-terms=* Adult
-* Aged
-* Aging
-* Alpha Rhythm
-* Attention
-* Evoked Potentials
-* Female
-* Healthy Volunteers
-* Humans
-* Male
-* Memory, Short-Term
-* Young Adult
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6726243
-}}
-==CDC20==
-{{medline-entry
-|title=Premature aging syndrome showing random chromosome number instabilities with [[CDC20]] mutation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33094908
-|keywords=* Cdc20 proteins
-* M phase cell cycle checkpoints
-* aging
-* chromosomal instability
-* chromosome segregation
-* genomic instability
-* premature
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7681047
-}}
-==CDC25A==
-{{medline-entry
-|title=Babam2 Regulates Cell Cycle Progression and Pluripotency in Mouse Embryonic Stem Cells as Revealed by Induced DNA Damage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33050379
-|keywords=* Babam2
-* DNA damage
-* cell cycle
-* embryonic stem cells
-* pluripotency
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7600899
-}}
-==CDC42==
-{{medline-entry
-|title=Effects of age-dependent changes in cell size on endothelial cell proliferation and senescence through YAP1.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31487690
-|mesh-terms=* Adaptor Proteins, Signal Transducing
-* Adult
-* Aging
-* Animals
-* Cell Cycle Proteins
-* Cell Size
-* Endothelial Cells
-* Female
-* Humans
-* Male
-* Mice, Inbred C57BL
-* Middle Aged
-* Neovascularization, Physiologic
-* Primary Cell Culture
-* Transcription Factors
-* cdc42 GTP-Binding Protein
-|keywords=* aging
-* angiogenesis
-* cell proliferation
-* cell size
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6756888
-}}
-==CDH1==
-{{medline-entry
-|title=Cdc6 as a novel target in cancer: Oncogenic potential, senescence and subcellular localisation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32010971
-|keywords=* Cdc6
-* cytoplasmic Cdc6
-* pancreatic cancer
-* senescence
-* subcellular localisation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7496346
-}}
-==CDK1==
-{{medline-entry
-|title=MicroRNAomic Transcriptomic Analysis Reveal Deregulation of Clustered Cellular Functions in Human Mesenchymal Stem Cells During in Vitro Passaging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31848878
-|mesh-terms=* CDC2-CDC28 Kinases
-* Cell Differentiation
-* Cell Proliferation
-* Cellular Senescence
-* Cyclin B
-* Gene Expression Regulation, Developmental
-* Humans
-* Mesenchymal Stem Cells
-* MicroRNAs
-* Transcriptome
-* Tumor Suppressor Protein p53
-* Umbilical Cord
-|keywords=* Cell proliferation
-* Cell senescence
-* Cellular ageing
-* Human Mesenchymal stem / stromal cells
-* miRNA-mRNA integration
-|full-text-url=https://sci-hub.do/10.1007/s12015-019-09924-0
-}}
-==CDK2==
-{{medline-entry
-|title=p57  is a master regulator of human adipose derived stem cell quiescence and senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32224418
-|keywords=* Human adipose derived stem cells
-* Quiescence
-* Senescence
-* p57(Kip2)
-|full-text-url=https://sci-hub.do/10.1016/j.scr.2020.101759
-}}
-==CDK4==
-{{medline-entry
-|title=Emerging Roles for the [i]INK4a/ARF[/i] ([i]CDKN2A[/i]) Locus in Adipose Tissue: Implications for Obesity and Type 2 Diabetes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32971832
-|keywords=* adipogenesis
-* inflammation
-* insulin sensitivity
-* obesity
-* oxidative activity
-* senescence
-* type 2 diabetes
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7563355
-}}
-{{medline-entry
-|title=Guilu Erxian Glue () Inhibits Chemotherapy-Induced Bone Marrow Hematopoietic Stem Cell Senescence in Mice May via p16 -Rb Signaling Pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32915425
-|keywords=* Chinese medicine
-* Guilu Erxian Glue
-* bone marrow suppression
-* hematopoietic stem cell senescence
-* p16INK4a
-|full-text-url=https://sci-hub.do/10.1007/s11655-020-3098-3
-}}
-==CDK5==
-{{medline-entry
-|title=Age-related hyperinsulinemia leads to insulin resistance in neurons and cell-cycle-induced senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31636448
-|mesh-terms=* Aging
-* Animals
-* Cell Cycle
-* Cell Death
-* Cellular Senescence
-* Cyclin-Dependent Kinase 5
-* Excitatory Postsynaptic Potentials
-* Gene Expression
-* Glycolysis
-* Hexokinase
-* Hyperinsulinism
-* Inhibitory Postsynaptic Potentials
-* Insulin
-* Insulin Resistance
-* Liraglutide
-* Male
-* Maze Learning
-* Metformin
-* Mice
-* Neurons
-* Phosphotransferases
-* Primary Cell Culture
-* Protein-Serine-Threonine Kinases
-* Ubiquitination
-* beta Catenin
-|full-text-url=https://sci-hub.do/10.1038/s41593-019-0505-1
-}}
-==CDK6==
-{{medline-entry
-|title=Saturated Fatty Acids Promote Hepatocytic Senecence through Regulation of miR-34a/Cyclin-Dependent Kinase 6.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32970940
-|keywords=* cyclin-dependent kinase 6 (CDK6)
-* high-fat diet (HFD)
-* miR-34a
-* palmitate acid (PA)
-* senescence
-|full-text-url=https://sci-hub.do/10.1002/mnfr.202000383
-}}
-{{medline-entry
-|title=Hepatoprotective effects of hydroxysafflor yellow A in D-galactose-treated aging mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32454116
-|keywords=* D-galactose
-* Hydroxysafflor yellow A
-* Oxidative stress
-* Replicative senescence
-* p16
-|full-text-url=https://sci-hub.do/10.1016/j.ejphar.2020.173214
-}}
-{{medline-entry
-|title=Anti-cell growth and anti-cancer stem cell activity of the CDK4/6 inhibitor palbociclib in breast cancer cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31823286
-|keywords=* Breast cancer
-* CDK4
-* Cancer stem cells
-* Palbociclib
-* Senescence
-|full-text-url=https://sci-hub.do/10.1007/s12282-019-01035-5
-}}
-{{medline-entry
-|title=Compromising the constitutive p16  expression sensitizes human neuroblastoma cells to Hsp90 inhibition and promotes premature senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31692039
-|keywords=* 17AAG
-* Hsp90
-* cancer
-* p16INK4a
-* senescence
-* tumor suppressor
-|full-text-url=https://sci-hub.do/10.1002/jcb.29493
-}}
-==CDKN1A==
-{{medline-entry
-|title=Involvement of [[CDKN1A]] (p21) in cellular senescence in response to heat and irradiation stress during preimplantation development.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32253738
-|keywords=* Cdkn1a
-* Heat stress
-* Irradiation
-* Preimplantation
-* Senescence
-* p21
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7193008
-}}
-==CDKN2A==
-{{medline-entry
-|title=Association between Nrf2 and [[CDKN2A]] expression in patients with end-stage renal disease: a pilot study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32661200
-|keywords=* CDKN2A
-* Nrf2
-* aging
-* end-stage renal disease
-* inflammation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7485736
-}}
-==CDKN2B==
-{{medline-entry
-|title=Molecular Genetics and Functional Analysis Implicate [i][[CDKN2B]]AS1-[[CDKN2B]][/i] Involvement in POAG Pathogenesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32825664
-|keywords=* African Americans
-* CDKN2B-AS1
-* Primary open-angle glaucoma (POAG)
-* senescence
-* trabecular meshwork cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7564117
-}}
-==CFI==
-{{medline-entry
-|title=Psychosocial Resources for Hedonic Balance, Life Satisfaction and Happiness in the Elderly: A Path Analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32781590
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Cross-Sectional Studies
-* Female
-* Happiness
-* Health Status
-* Humans
-* Male
-* Personal Satisfaction
-* Quality of Life
-|keywords=* happiness
-* older adults
-* path analysis
-* psychosocial resources
-* subjective well-being
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7459462
-}}
-{{medline-entry
-|title=Validity and Reliability of the Flourishing Scale in a Sample of Older Adults in Iran.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32546985
-|mesh-terms=* Aged
-* Aging
-* Cross-Sectional Studies
-* Female
-* Geriatric Assessment
-* Health Status Disparities
-* Humans
-* Iran
-* Male
-* Mental Health
-* Psychometrics
-* Reproducibility of Results
-* Surveys and Questionnaires
-|keywords=* aging
-* factor analysis
-* flourishing
-* reliability
-* validity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244746
-}}
-{{medline-entry
-|title=The decision about retirement: A scale to describe representations and practices of medical doctors and nurses.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32258559
-|keywords=* Aging
-* Job satisfaction
-* Retirement
-* Scale
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6806742
-}}
-{{medline-entry
-|title=Family versus intimate partners: Estimating who matters more for health in a 20-year longitudinal study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31697103
-|mesh-terms=* Adult
-* Aged
-* Aging
-* Emotions
-* Family Relations
-* Female
-* Health Status
-* Humans
-* Interpersonal Relations
-* Longitudinal Studies
-* Male
-* Middle Aged
-* Sexual Partners
-* United States
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7012715
-}}
-{{medline-entry
-|title=Adapting and validating the Rosenberg Self-Esteem Scale for elderly Spanish population.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31524131
-|keywords=* aging
-* life span
-* self-esteem
-* structural equation model
-* validity
-|full-text-url=https://sci-hub.do/10.1017/S1041610219001170
-}}
-==CFTR==
-{{medline-entry
-|title=Exercise Physiology Across the Lifespan in Cystic Fibrosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31780953
-|keywords=* aging
-* cystic fibrosis
-* exercise capacity
-* exercise prescription
-* pediatric
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6856653
-}}
-{{medline-entry
-|title=Reduced expression of the Ion channel [[CFTR]] contributes to airspace enlargement as a consequence of aging and in response to cigarette smoke in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31477092
-|mesh-terms=* Aging
-* Animals
-* Cystic Fibrosis Transmembrane Conductance Regulator
-* Gene Expression
-* Inhalation Exposure
-* Mice
-* Mice, Knockout
-* Pulmonary Emphysema
-* Tobacco Smoke Pollution
-|keywords=* Aging
-* CFTR
-* Emphysema
-* Smoking
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6720379
-}}
-==CGA==
-{{medline-entry
-|title=Safety and efficacy of preoperative chemoradiotherapy in fit older patients with intermediate or locally advanced rectal cancer evaluated by comprehensive geriatric assessment: A planned interim analysis of a multicenter, phase II trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33160954
-|keywords=* Comprehensive geriatric assessment
-* Geriatrics
-* Preoperative chemoradiotherapy
-* Rectal cancer
-|full-text-url=https://sci-hub.do/10.1016/j.jgo.2020.10.016
-}}
-{{medline-entry
-|title=The Protective Effect of Chlorogenic Acid on Vascular Senescence via the Nrf2/HO-1 Pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32630570
-|keywords=* chlorogenic acid
-* heme oxygenase-1
-* nuclear factor erythroid 2-related factor 2
-* vascular senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7350250
-}}
-{{medline-entry
-|title=Association between comprehensive geriatric assessment and short-term outcomes among older adult patients with stroke: A nationwide retrospective cohort study using propensity score and instrumental variable methods.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32566923
-|keywords=* Comprehensive geriatric assessment
-* Geriatrics
-* Japanese diagnosis procedure combination database
-* Length of stay
-* Mortality
-* Stroke
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7298723
-}}
-{{medline-entry
-|title=Interventions to Improve Clinical Outcomes in Older Adults Admitted to a Surgical Service: A Systematic Review and Meta-analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32417101
-|keywords=* Aging
-* comprehensive geriatric assessment
-* delirium
-* functional status
-* outcomes
-* surgery
-|full-text-url=https://sci-hub.do/10.1016/j.jamda.2020.03.023
-}}
-{{medline-entry
-|title=A Computerized Frailty Assessment Tool at Points-of-Care: Development of a Standalone Electronic Comprehensive Geriatric Assessment/Frailty Index (eFI-[[CGA]]).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32296673
-|keywords=* aging
-* comprehensive geriatric assessment (CGA)
-* electronic assessment tools
-* frailty
-* frailty index
-* healthcare
-* older adults
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7137764
-}}
-{{medline-entry
-|title=Allocating patients to geriatric medicine wards in a tertiary university hospital in England: A service evaluation of the Specialist Advice for the Frail Elderly (SAFE) team.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31942488
-|keywords=* clinical frailty scale
-* frail older adults
-* geriatrics
-* hospital medicine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6880728
-}}
-{{medline-entry
-|title=Role of Frailty on Risk Stratification in Cardiac Surgery and Procedures.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31894551
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Cardiac Surgical Procedures
-* Frail Elderly
-* Frailty
-* Geriatric Assessment
-* Humans
-* Percutaneous Coronary Intervention
-* Risk Assessment
-* Transcatheter Aortic Valve Replacement
-|keywords=* Cardiac surgery
-* Comprehensive geriatric assessment
-* Disability
-* Elderly
-* Frailty
-* Geriatrics
-* Surgical risk scores
-* TAVI
-|full-text-url=https://sci-hub.do/10.1007/978-3-030-33330-0_11
-}}
-{{medline-entry
-|title=Developing an objective structured clinical examination in comprehensive geriatric assessment - A pilot study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31745004
-|mesh-terms=* Aged
-* Clinical Competence
-* Education, Medical, Graduate
-* Educational Measurement
-* Female
-* Geriatric Assessment
-* Geriatrics
-* Humans
-* Male
-* Pilot Projects
-* United Kingdom
-|keywords=* Comprehensive geriatric assessment
-* development
-* entrustable professional capabilities
-* objective structured clinical examination
-* summative assessment
-|full-text-url=https://sci-hub.do/10.4103/efh.EfH_111_18
-}}
-{{medline-entry
-|title=How do doctors choose treatment for older gynecological cancer patients? A Japanese Gynecologic Oncology Group survey of gynecologic oncologists.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31728682
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Comorbidity
-* Female
-* Genital Neoplasms, Female
-* Geriatric Assessment
-* Gynecology
-* Humans
-* Hysterectomy
-* Japan
-* Lymph Node Excision
-* Oncologists
-* Surveys and Questionnaires
-|keywords=* Comprehensive geriatric assessment
-* Elderly
-* Geriatrics
-* Gynecologic cancer
-|full-text-url=https://sci-hub.do/10.1007/s10147-019-01574-z
-}}
-{{medline-entry
-|title=Validation of the Pictorial Fit-Frail Scale in a memory clinic setting.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31524122
-|keywords=* aging
-* dementia
-* frail elderly
-* frailty
-* psychometrics
-|full-text-url=https://sci-hub.do/10.1017/S1041610219000905
-}}
-{{medline-entry
-|title=Impact of Resolution of Hyponatremia on Neurocognitive and Motor Performance in Geriatric Patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31467370
-|mesh-terms=* Activities of Daily Living
-* Aged
-* Aged, 80 and over
-* Aging
-* Cognition
-* Female
-* Geriatrics
-* Humans
-* Hyponatremia
-* Male
-* Mental Status and Dementia Tests
-* Middle Aged
-* Motor Activity
-* Sodium
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6715723
-}}
-{{medline-entry
-|title=Health outcome of older hospitalized patients in internal medicine environments evaluated by Identification of Seniors at Risk (ISAR) screening and geriatric assessment.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31412787
-|mesh-terms=* Accidental Falls
-* Aged
-* Aged, 80 and over
-* Cohort Studies
-* Emergency Service, Hospital
-* Female
-* Geriatric Assessment
-* Health Status
-* Hospitalization
-* Humans
-* Internal Medicine
-* Length of Stay
-* Male
-* Mass Screening
-* Patient Discharge
-* Risk Assessment
-|keywords=* CGA
-* Cutoff
-* Geriatrics
-* ISAR
-* Internal medicine
-* Older in-patients
-* Risk screening
-* Sensitivity
-* Specificity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6694685
-}}
-==CHI3L1==
-{{medline-entry
-|title=Postsynaptic damage and microglial activation in AD patients could be linked CXCR4/CXCL12 expression levels.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32949560
-|keywords=* Aging
-* Alzheimer’s disease
-* Bioinformatics
-* CHI3L1
-* Chitinase
-* NRGN
-|full-text-url=https://sci-hub.do/10.1016/j.brainres.2020.147127
-}}
-==CHRNA7==
-{{medline-entry
-|title=Associations between genetic variations and global motion perception.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31432227
-|mesh-terms=* Adult
-* Differential Threshold
-* Female
-* Genotype
-* Humans
-* Male
-* Motion Perception
-* Polymorphism, Single Nucleotide
-* Receptors, Nicotinic
-* Sensory Thresholds
-* Young Adult
-* alpha7 Nicotinic Acetylcholine Receptor
-|keywords=* Aging
-* CHRNA7
-* Cholinergic system
-* Coherent motion
-* Genetic variations
-|full-text-url=https://sci-hub.do/10.1007/s00221-019-05627-7
-}}
-==CHSY1==
-{{medline-entry
-|title=Loss of Chondroitin Sulfate Modification Causes Inflammation and Neurodegeneration in [i]skt[/i] Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31754016
-|mesh-terms=* Age Factors
-* Animals
-* Apoptosis
-* Chondroitin Sulfates
-* Female
-* Glucuronosyltransferase
-* Inflammation
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Multifunctional Enzymes
-* Mutation
-* N-Acetylgalactosaminyltransferases
-* Neurodegenerative Diseases
-* Neurons
-* Protein Processing, Post-Translational
-* Proteins
-* Retinal Degeneration
-|keywords=* aging
-* chondroitin sulfate synthase
-* hippocampus
-* inflammation
-* mouse
-* myeloid cells
-* neurodegeneration
-* retina
-* retinal pigment epithelium
-* subretinal space
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6944401
-}}
-==CISD2==
-{{medline-entry
-|title=[[CISD2]] Attenuates Inflammation and Regulates Microglia Polarization in EOC Microglial Cells-As a Potential Therapeutic Target for Neurodegenerative Dementia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33005144
-|keywords=* CISD2
-* M1/M2 microglia polarization
-* aging
-* anti-inflammatory effects
-* neurodegenerative disease and dementia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7479185
-}}
-==CIT==
-{{medline-entry
-|title=Effect of sex on aging-related decline of dopamine transporter in healthy subjects.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33052524
-|keywords=* 123I-FP-CIT
-* Aging
-* Dopamine plasma membrane transport proteins
-* SPECT
-* Sex
-|full-text-url=https://sci-hub.do/10.1007/s12149-020-01538-8
-}}
-{{medline-entry
-|title=The Relationship Between the Striatal Dopaminergic Neuronal and Cognitive Function With Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32184717
-|keywords=* SPECT
-* Wechsler Adult Intelligence Scale
-* aging
-* cognitive function
-* dopamine transporter
-* verbal function
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7058549
-}}
-==CLEC3B==
-{{medline-entry
-|title=[[CLEC3B]] p.S106G Mutant in a Caucasian Population of Successful Neurological Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31570938
-|keywords=*
-          APOE
-*
-          CLEC3B
-* Aging
-* Human genetics
-* Human health
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7494029
-}}
-==COL1A1==
-{{medline-entry
-|title=Remodeling process in bone of aged rats in response to resistance training.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32593709
-|mesh-terms=* Age Factors
-* Aging
-* Animals
-* Bone Remodeling
-* Gene Expression Regulation
-* Male
-* Physical Conditioning, Animal
-* RNA, Messenger
-* Random Allocation
-* Rats
-* Rats, Wistar
-* Resistance Training
-|keywords=* Aging
-* Bone homeostasis
-* Function
-* Resistance training
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2020.118008
-}}
-==COL3A1==
-{{medline-entry
-|title=Different expression of Defensin-B gene in the endometrium of mares of different age during the breeding season.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31864349
-|mesh-terms=* Aging
-* Animals
-* Breeding
-* Defensins
-* Endometrium
-* Female
-* Fibrosis
-* Gene Expression
-* Horses
-* Inflammation
-* Reverse Transcriptase Polymerase Chain Reaction
-|keywords=* Defensin-β
-* Endometrium
-* Gene expression
-* Immune-modulation
-* Mare
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6925900
-}}
-==COMT==
-{{medline-entry
-|title=The geriatric pain experience in mice: intact cutaneous thresholds but altered responses to tonic and chronic pain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32008855
-|mesh-terms=* Acetone
-* Aging
-* Animals
-* Behavior
-* Biogenic Monoamines
-* Capsaicin
-* Chronic Pain
-* Disease Models, Animal
-* Male
-* Mice, Inbred C57BL
-* Peripheral Nerve Injuries
-* Physical Stimulation
-* Prefrontal Cortex
-* Sensory Thresholds
-|keywords=* Geriatric pain
-* Healthy aging
-* Mice
-* Sensory thresholds
-* Supraspinal plasticity
-* Tonic and chronic pain response
-|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2019.12.018
-}}
-==COPE==
-{{medline-entry
-|title=Patterns and characteristics of cognitive functioning in older patients approaching end stage kidney disease, the [[COPE]]-study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32272897
-|keywords=* Cognitive function
-* End stage renal disease
-* Geriatric assessment
-* Geriatrics
-* Older patients
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7147053
-}}
-==CORT==
-{{medline-entry
-|title=Sex differences in body composition, metabolism-related hormones, and energy homeostasis during aging in Wistar rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33075214
-|keywords=* aging
-* body composition
-* energy metabolism
-* metabolism-related hormone
-* sex differences
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7571994
-}}
-{{medline-entry
-|title=Effects of age and social isolation on murine hippocampal biochemistry and behavior.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32866520
-|keywords=* Aging
-* Hippocampus
-* Inflammation
-* Memory
-* Serotonin
-* Social isolation
-* Stress
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2020.111337
-}}
-{{medline-entry
-|title=Interleukin 6 reduces allopregnanolone synthesis in the brain and contributes to age-related cognitive decline in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32669383
-|keywords=* Alzheimer’s disease
-* aging
-* cognitive function
-* enzyme regulation
-* inflammation
-* neurosteroid
-* progesterone
-* steroid hormones
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7529050
-}}
-{{medline-entry
-|title=Sex- and age-dependent differences in the hormone and drinking responses to water deprivation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31967852
-|mesh-terms=* Age Factors
-* Animals
-* Arginine Vasopressin
-* Behavior, Animal
-* Dehydration
-* Drinking
-* Female
-* Male
-* Rats, Wistar
-* Sex Factors
-* Sodium Chloride
-* Subfornical Organ
-* Water Deprivation
-|keywords=* aging
-* hormonal response
-* sex differences
-* sodium appetite
-* thirst
-|full-text-url=https://sci-hub.do/10.1152/ajpregu.00303.2019
-}}
-{{medline-entry
-|title=Ontogeny of the adrenocortical response in an extremely altricial bird.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31545013
-|mesh-terms=* Adrenal Glands
-* Aging
-* Animals
-* Corticosterone
-* Female
-* Hypothalamo-Hypophyseal System
-* Male
-* Parrots
-* Restraint, Physical
-* Stress, Physiological
-|keywords=* Venezuela
-* adrenocortical
-* altricial
-* birds
-* corticosterone
-* glucocorticoid
-* hypothalamic-pituitary-adrenal axis
-* ontogeny
-* parrots
-* stress
-|full-text-url=https://sci-hub.do/10.1002/jez.2317
-}}
-==CP==
-{{medline-entry
-|title=A Life Course Perspective on Growing Older With Cerebral Palsy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33213304
-|keywords=* aging
-* cerebral palsy
-* midlife
-* neurological disorders
-* neurology
-* qualitative descriptive
-|full-text-url=https://sci-hub.do/10.1177/1049732320971247
-}}
-{{medline-entry
-|title=The molecular anatomy and functions of the choroid plexus in healthy and diseased brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32750317
-|keywords=* Aging
-* Alzheimer's disease
-* Choroid plexus
-* Development
-* Multiple sclerosis
-* Neuroprotection
-|full-text-url=https://sci-hub.do/10.1016/j.bbamem.2020.183430
-}}
-{{medline-entry
-|title=The effects and mechanism of collagen peptide and elastin peptide on skin aging induced by D-galactose combined with ultraviolet radiation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32717457
-|keywords=* Collagen
-* D-galactose
-* Elastin
-* Skin aging
-* Ultraviolet
-|full-text-url=https://sci-hub.do/10.1016/j.jphotobiol.2020.111964
-}}
-{{medline-entry
-|title=Model based strategies towards protein A resin lifetime optimization and supervision.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32709318
-|mesh-terms=* Algorithms
-* Chromatography
-* Kinetics
-* Least-Squares Analysis
-* Ligands
-* Models, Theoretical
-* Principal Component Analysis
-* Resins, Plant
-* Staphylococcal Protein A
-* Statistics as Topic
-|keywords=* Cleaning procedures
-* Hybrid modeling
-* Multivariate data analysis
-* Protein A chromatography
-* Resin aging
-* Resin lifetime
-|full-text-url=https://sci-hub.do/10.1016/j.chroma.2020.461261
-}}
-{{medline-entry
-|title=The influence of age and environmental conditions on supplement intake by beef cattle winter grazing northern mixed-grass rangelands.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32658282
-|mesh-terms=* Aging
-* Animal Feed
-* Animal Husbandry
-* Animals
-* Cattle
-* Diet
-* Dietary Supplements
-* Ecosystem
-* Female
-* Poaceae
-* Seasons
-* Weather
-|keywords=* beef cattle
-* cow age
-* environment
-* supplement intake
-* winter grazing
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7455287
-}}
-{{medline-entry
-|title=Cyclophosphamide, a cancer chemotherapy drug-induced early onset of reproductive senescence and alterations in reproductive performance and their prevention in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32536211
-|keywords=* Cyclophosphamide
-* Decalepis hamiltonii
-* premature ovarian failure
-* reproductive performance
-* reproductive senescence
-* uterus
-|full-text-url=https://sci-hub.do/10.1080/01480545.2020.1774773
-}}
-{{medline-entry
-|title=Asymptomatic [i]Clostridium perfringens[/i] Inhabitation in Intestine Can Cause Inflammation, Apoptosis, and Disorders in Brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31928429
-|mesh-terms=* Aging
-* Animals
-* Apoptosis
-* Asymptomatic Infections
-* Brain
-* Brain Diseases
-* Clostridium Infections
-* Clostridium perfringens
-* Disease Models, Animal
-* Feces
-* Food Microbiology
-* Gene Expression
-* Humans
-* Inflammation
-* Intestines
-* Liver
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Organ Size
-* Oxidative Stress
-* Risk Factors
-* Spleen
-|keywords=* Clostridium perfringens
-* brain damage
-* brain disorder
-* gut microbiota
-|full-text-url=https://sci-hub.do/10.1089/fpd.2019.2677
-}}
-{{medline-entry
-|title=The Role of the Clinical Pharmacist in the Management of People Living with HIV in the Modern Antiretroviral Era.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31834321
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Anti-Retroviral Agents
-* Disease Management
-* Disease Transmission, Infectious
-* Female
-* HIV Infections
-* Humans
-* Male
-* Medication Adherence
-* Middle Aged
-* Pharmacists
-* Professional Role
-* Treatment Outcome
-|keywords=* Aging
-* Antiretroviral therapy
-* Clinical pharmacist
-* Comorbidities
-* HIV
-|full-text-url=https://sci-hub.do/10.24875/AIDSRev.19000089
-}}
-{{medline-entry
-|title=A clinically feasible method for the assessment and characterization of pain in patients with chronic pancreatitis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31787527
-|mesh-terms=* Adult
-* Aging
-* Case-Control Studies
-* Cross-Sectional Studies
-* Humans
-* Middle Aged
-* Pain
-* Pain Measurement
-* Pancreatitis, Chronic
-* Sex Factors
-|keywords=* Central sensitization
-* Chronic pancreatitis
-* Nociception
-* Pain
-|full-text-url=https://sci-hub.do/10.1016/j.pan.2019.11.007
-}}
-{{medline-entry
-|title=Differences in geometric strength at the contralateral hip between men with hip fracture and non-fractured comparators.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31812699
-|keywords=* Aging
-* DXA
-* Fracture prevention
-* Injury/fracture healing
-* Osteoporosis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7037571
-}}
-{{medline-entry
-|title=Factors associated with the number of clinical pharmacy recommendations: findings from an observational study in geriatric inpatients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31642397
-|keywords=* Clinical pharmacy
-* geriatrics
-* inpatients
-* polypharmacy
-* risk stratification
-|full-text-url=https://sci-hub.do/10.1080/17843286.2019.1683128
-}}
-{{medline-entry
-|title=Protection against oxidative stress and anti-aging effect in Drosophila of royal jelly-collagen peptide.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31622731
-|mesh-terms=* Aging
-* Amino Acids
-* Animals
-* Body Weight
-* Collagen
-* Drosophila
-* Fatty Acids
-* Feeding Behavior
-* Hydrogen Peroxide
-* Longevity
-* Molecular Weight
-* Oxidative Stress
-* Paraquat
-|keywords=* Anti-aging
-* Antioxidant activity
-* Collagen
-* Drosophila
-* Royal jelly
-|full-text-url=https://sci-hub.do/10.1016/j.fct.2019.110881
-}}
-==CPM==
-{{medline-entry
-|title=Test-Retest Instability of Temporal Summation and Conditioned Pain Modulation Measures in Older Adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33083842
-|keywords=* Aging
-* Anxiety
-* Conditioned Pain Modulation
-* Pain Catastrophizing
-* Reliability
-* Temporal Summation of Pain
-|full-text-url=https://sci-hub.do/10.1093/pm/pnaa288
-}}
-{{medline-entry
-|title=Age does not affect sex effect of conditioned pain modulation of pressure and thermal pain across 2 conditioning stimuli.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32072094
-|keywords=* Aging
-* CPM duration
-* Conditioned pain modulation
-* Conditioning stimulus
-* Sex differences
-* Test stimulus
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7004505
-}}
-{{medline-entry
-|title=The Decline of Endogenous Pain Modulation With Aging: A Meta-Analysis of Temporal Summation and Conditioned Pain Modulation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31562994
-|keywords=* Aging
-* conditioned pain modulation
-* meta-analysis
-* pain modulation
-* temporal summation
-|full-text-url=https://sci-hub.do/10.1016/j.jpain.2019.09.005
-}}
-==CPNE1==
-{{medline-entry
-|title=Prevalent intron retention fine-tunes gene expression and contributes to cellular senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33274830
-|keywords=* CPNE1
-* U2AF1
-* intron retention
-* senescence
-* splicing factor
-|full-text-url=https://sci-hub.do/10.1111/acel.13276
-}}
-==CPT1A==
-{{medline-entry
-|title=Alteration of fatty acid oxidation by increased [[CPT1A]] on replicative senescence of placenta-derived mesenchymal stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31900237
-|keywords=* CPT1A
-* Fatty acid
-* Mitochondria
-* Placenta-derived mesenchymal stem cell
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6941254
-}}
-==CPT1C==
-{{medline-entry
-|title=Carnitine palmitoyltransferase 1C reverses cellular senescence of MRC-5 fibroblasts via regulating lipid accumulation and mitochondrial function.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32632982
-|keywords=* MRC-5 fibroblasts
-* carnitine palmitoyltransferase 1C (CPT1C)
-* cellular senescence
-* lipidomics
-* mitochondrial function
-|full-text-url=https://sci-hub.do/10.1002/jcp.29906
-}}
-{{medline-entry
-|title=Carnitine palmitoyltransferase 1C contributes to progressive cellular senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32289751
-|keywords=* carnitine palmitoyltransferase 1C
-* metabolic reprogramming
-* mitochondria
-* senescence
-* stable transfection
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7202531
-}}
-==CPT2==
-{{medline-entry
-|title=The phytochemical epigallocatechin gallate prolongs the lifespan by improving lipid metabolism, reducing inflammation and oxidative stress in high-fat diet-fed obese rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32729662
-|keywords=* EGCG
-* free fatty acid
-* high-fat dietary
-* lifespan
-* proteomics
-* transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7511879
-}}
-==CR1==
-{{medline-entry
-|title=Single Nucleotide Polymorphisms in Alzheimer's Disease Risk Genes Are Associated with Intrinsic Connectivity in Middle Age.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32986668
-|keywords=* Aging
-* Alzheimer’s disease
-* middle aged
-* neuroimaging
-* single nucleotide
-polymorphism
-|full-text-url=https://sci-hub.do/10.3233/JAD-200444
-}}
-{{medline-entry
-|title=The whale shark genome reveals how genomic and physiological properties scale with body size.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32753383
-|mesh-terms=* Adaptation, Physiological
-* Animals
-* Base Sequence
-* Body Size
-* Genome
-* Genomics
-* Longevity
-* Sharks
-* Temperature
-|keywords=* body size
-* lifespan
-* metabolic rate
-* neural genes
-* whale shark
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7456109
-}}
-==CRABP2==
-{{medline-entry
-|title=Preconception resveratrol intake against infertility: Friend or foe?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32273814
-|keywords=* aging
-* assisted reproductive technology
-* infertility
-* resveratrol
-* sirtuin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7138940
-}}
-==CRBN==
-{{medline-entry
-|title=Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32332723
-|mesh-terms=* Adaptor Proteins, Signal Transducing
-* Aging
-* Aniline Compounds
-* Animals
-* Blood Platelets
-* Cell Line
-* Cellular Senescence
-* Female
-* Humans
-* Male
-* Mice
-* Mice, Transgenic
-* Models, Animal
-* Primary Cell Culture
-* Proteolysis
-* Sulfonamides
-* Ubiquitin-Protein Ligases
-* bcl-X Protein
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7181703
-}}
-==CRP==
-{{medline-entry
-|title=Omega-3 supplementation improves isometric strength but not muscle anabolic and catabolic signaling in response to resistance exercise in healthy older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33284965
-|keywords=* Muscle wasting
-* aging
-* anabolic resistance
-* inflammation
-* resistance training
-* sarcopenia
-|full-text-url=https://sci-hub.do/10.1093/gerona/glaa309
-}}
-{{medline-entry
-|title=Circulating angiopoietin-like protein 2 levels and arterial stiffness in patients receiving maintenance hemodialysis: A cross-sectional study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33197687
-|keywords=* Angiopoietin-like protein (ANGPTL) 2
-* Cardio-ankle vascular index (CAVI)
-* Chronic inflammation
-* Hemodialysis
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.atherosclerosis.2020.10.890
-}}
-{{medline-entry
-|title=Cardiovascular rehabilitation in patients aged 70-year-old or older: benefits on functional capacity, physical activity and metabolic profile in younger [i]vs[/i]. older patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33117418
-|keywords=* Aging
-* Cardiovascular prevention
-* Exercise-based cardiac rehabilitation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7568038
-}}
-{{medline-entry
-|title=rRT-PCR Results of a Covid-19 Diagnosed Geriatric Patient.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33103060
-|keywords=* COVID-19
-* False negative reactions
-* Geriatrics
-* Mass screening
-* Reverse transcriptase polymerase chain reaction
-* SARS-CoV-2
-* Tomography
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7567648
-}}
-{{medline-entry
-|title=The Association of Aging Biomarkers, Interstitial Lung Abnormalities, and Mortality.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33080140
-|keywords=* aging
-* growth differentiation factor 15
-* idiopathic pulmonary fibrosis
-* interstitial lung abnormalities
-* mortality
-|full-text-url=https://sci-hub.do/10.1164/rccm.202007-2993OC
-}}
-{{medline-entry
-|title=A Novel Fortified Dairy Product and Sarcopenia Measures in Sarcopenic Older Adults: A Double-Blind Randomized Controlled Trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33067129
-|keywords=* Functional food
-* aging
-* beta-hydroxy beta-methylbutyrate
-* muscle strength
-* sarcopenia
-* vitamin D
-|full-text-url=https://sci-hub.do/10.1016/j.jamda.2020.08.035
-}}
-{{medline-entry
-|title=Age-Related Colonic Mucosal Microbiome Community Shifts in Monkeys.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33021628
-|keywords=* Aging
-* Microbial co-occurrences
-* Mucosal microbiome
-* Systemic inflammation
-|full-text-url=https://sci-hub.do/10.1093/gerona/glaa256
-}}
-{{medline-entry
-|title=The relationship between frailty and serum alpha klotho levels in geriatric patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32905907
-|keywords=* Aging
-* Biomarkers
-* Frailty syndrome
-* Geriatric syndrome
-* Sarcopenia
-|full-text-url=https://sci-hub.do/10.1016/j.archger.2020.104225
-}}
-{{medline-entry
-|title=ZMPSTE24 Is Associated with Elevated Inflammation and Progerin mRNA.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32872320
-|keywords=* ZMPSTE24
-* aging
-* inflammation
-* lamin A/C
-* progerin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7563344
-}}
-{{medline-entry
-|title=Cultural and life style practices associated with low inflammatory physiology in Japanese adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32805392
-|keywords=* Aging
-* Bathing
-* C-reactive protein
-* Diet
-* Inflammation
-* Interleukin-6
-* Japan
-* Tea
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7544652
-}}
-{{medline-entry
-|title=Moderate- to high intensity aerobic and resistance exercise reduces peripheral blood regulatory cell populations in older adults with rheumatoid arthritis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32467712
-|keywords=* Aging
-* Breg cells
-* Exercise
-* IL-10
-* Rheumatoid arthritis
-* T cells
-* Treg cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7229606
-}}
-{{medline-entry
-|title=PTSD and the klotho longevity gene: Evaluation of longitudinal effects on inflammation via DNA methylation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32438247
-|keywords=* Accelerated aging
-* Inflammation
-* Klotho
-* Methylation
-* PTSD
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7293549
-}}
-{{medline-entry
-|title=Bereavement is associated with reduced systemic inflammation: C-reactive protein before and after widowhood.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32283288
-|keywords=* Aging
-* Bereavement
-* C-reactive protein
-* Health
-* Inflammation
-* Widowhood
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7415735
-}}
-{{medline-entry
-|title=The Impact of Age on the Prevalence of Sarcopenic Obesity in Bariatric Surgery Candidates.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32249368
-|keywords=* Aging
-* Bariatric surgery
-* Elderly
-* Obesity
-* Sarcopenia
-|full-text-url=https://sci-hub.do/10.1007/s11695-019-04198-4
-}}
-{{medline-entry
-|title=Intake of dietary advanced glycation end products influences inflammatory markers, immune phenotypes, and antiradical capacity of healthy elderly in a little-studied population.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32148813
-|keywords=* CRP
-* advanced glycationed end products
-* aging
-* dAGE
-* immunity
-* inflammation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7020308
-}}
-{{medline-entry
-|title=Intentional Switching Between Bimanual Coordination Patterns in Older Adults: Is It Mediated by Inhibition Processes?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32132919
-|keywords=* Stroop task
-* aging
-* bimanual coordination
-* inhibition
-* mediation analysis
-* switching
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7041435
-}}
-{{medline-entry
-|title=Shorter Telomere Length in Peripheral Blood Leukocytes Is Associated with Post-Traumatic Chronic Osteomyelitis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32125944
-|keywords=* aging
-* post-traumatic chronic osteomyelitis
-* telomere
-|full-text-url=https://sci-hub.do/10.1089/sur.2019.326
-}}
-{{medline-entry
-|title=Risk Factors of Progression to Frailty: Findings from the Singapore Longitudinal Ageing Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31886815
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Disease Progression
-* Female
-* Frail Elderly
-* Frailty
-* Geriatric Assessment
-* Humans
-* Independent Living
-* Longitudinal Studies
-* Male
-* Nutrition Assessment
-* Nutritional Status
-* Physical Examination
-* Risk Factors
-* Singapore
-* Socioeconomic Factors
-|keywords=* Frailty
-* longitudinal
-* risk factors
-* transition
-|full-text-url=https://sci-hub.do/10.1007/s12603-019-1277-8
-}}
-{{medline-entry
-|title=Physical Function and Strength in Relation to Inflammation in Older Adults with Obesity and Increased Cardiometabolic Risk.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31781724
-|mesh-terms=* Aged
-* Aging
-* Cardiovascular Diseases
-* Female
-* Humans
-* Inflammation
-* Male
-* Muscle Strength
-* Obesity
-* Physical Exertion
-|keywords=* Inflammation
-* cardiovascular disease risk factors
-* obesity
-* physical activity
-* physical function
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996491
-}}
-{{medline-entry
-|title=Key diagnostic characteristics of fever of unknown origin in Japanese patients: a prospective multicentre study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31748308
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Female
-* Fever of Unknown Origin
-* Humans
-* Japan
-* Male
-* Middle Aged
-* Prospective Studies
-* Young Adult
-|keywords=* Japan
-* aging population
-* elderly
-* erythrocyte sedimentation rate
-* fever of unknown origin
-* prospective studies
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6886908
-}}
-{{medline-entry
-|title=Decrease in Serum Vitamin D Level of Older Patients with Fatigue.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31635199
-|mesh-terms=* Aged
-* Cohort Studies
-* Fatigue
-* Female
-* Humans
-* Male
-* Middle Aged
-* Vitamin D
-* Vitamin D Deficiency
-|keywords=* aging
-* mental fatigue
-* older
-* physical fatigue
-* sex differences
-* vitamin D
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6836014
-}}
-{{medline-entry
-|title=The Association between Frailty Indicators and Blood-Based Biomarkers in Early-Old Community Dwellers of Thailand.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31533354
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Biomarkers
-* C-Reactive Protein
-* CD4-CD8 Ratio
-* Cross-Sectional Studies
-* Female
-* Frail Elderly
-* Frailty
-* Humans
-* Independent Living
-* Interleukin-6
-* Male
-* Middle Aged
-* Thailand
-|keywords=* C-reactive protein
-* Thailand
-* aging
-* cross-sectional study
-* frailty
-* frailty biomarkers
-* fried’s phenotypes
-* interleukin-6
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6765843
-}}
-{{medline-entry
-|title=Associations of C-reactive protein and homocysteine concentrations with the impairment of intrinsic capacity domains over a 5-year follow-up among community-dwelling older adults at risk of cognitive decline (MAPT Study).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31493520
-|mesh-terms=* Activities of Daily Living
-* Aged
-* Biomarkers
-* Body Mass Index
-* C-Reactive Protein
-* Cognitive Dysfunction
-* Depression
-* Female
-* Follow-Up Studies
-* Geriatric Assessment
-* Hand Strength
-* Homocysteine
-* Humans
-* Independent Living
-* Inflammation
-* Male
-* Mobility Limitation
-* Neuropsychological Tests
-* Prospective Studies
-* Risk Factors
-* Time Factors
-|keywords=* Aging
-* C-reactive protein
-* Homocysteine
-* Inflammation
-* Intrinsic capacity
-* Older adults
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2019.110716
-}}
-{{medline-entry
-|title=Longitudinal analysis of loneliness and inflammation at older ages: English longitudinal study of ageing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31494341
-|mesh-terms=* Age Factors
-* Aged
-* Aged, 80 and over
-* Aging
-* C-Reactive Protein
-* England
-* Female
-* Ferritins
-* Fibrinogen
-* Humans
-* Inflammation
-* Loneliness
-* Longitudinal Studies
-* Male
-* Middle Aged
-|keywords=* C-reactive protein
-* Ferritin
-* Fibrinogen
-* Inflammation
-* Loneliness
-|full-text-url=https://sci-hub.do/10.1016/j.psyneuen.2019.104421
-}}
-{{medline-entry
-|title=The cortisol burden in elderly subjects with metabolic syndrome and its association with low-grade inflammation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31471891
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Echocardiography
-* Female
-* Humans
-* Hydrocortisone
-* Inflammation
-* Male
-* Metabolic Syndrome
-|keywords=* Aging
-* Cortisol
-* Inflammation
-* Metabolic syndrome
-|full-text-url=https://sci-hub.do/10.1007/s40520-019-01322-3
-}}
-{{medline-entry
-|title=Recurrent circadian fasting (RCF) improves blood pressure, biomarkers of cardiometabolic risk and regulates inflammation in men.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31426866
-|mesh-terms=* Adult
-* Biomarkers
-* Blood Pressure
-* C-Reactive Protein
-* Cardiovascular Diseases
-* Circadian Rhythm
-* Diet
-* Energy Intake
-* Fasting
-* Heart Rate
-* Humans
-* Inflammation
-* Male
-* Metabolic Diseases
-* Middle Aged
-* Nutritional Physiological Phenomena
-* Regression Analysis
-* Risk Factors
-* Young Adult
-|keywords=* Aging
-* Health benefits
-* Inflammation
-* Recurrent fasting
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6700786
-}}
-{{medline-entry
-|title=Characteristics of patients with rheumatoid arthritis undergoing primary total joint replacement: A 14-year trend analysis (2004-2017).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31393198
-|mesh-terms=* Adult
-* Aged
-* Antirheumatic Agents
-* Arthritis, Rheumatoid
-* Arthroplasty, Replacement
-* Arthroplasty, Replacement, Knee
-* Biological Products
-* Drug Utilization
-* Female
-* Humans
-* Japan
-* Male
-* Middle Aged
-* Postoperative Complications
-|keywords=* C-reactive protein
-* Rheumatoid arthritis
-* aging
-* arthroplasty
-* drug therapy
-|full-text-url=https://sci-hub.do/10.1080/14397595.2019.1649111
-}}
-==CS==
-{{medline-entry
-|title=Acute effect of bodyweight-based strength training on blood pressure of hypertensive older adults: A randomized crossover clinical trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33198514
-|keywords=* Exercise
-* aging
-* hypertension
-* hypotension
-* resistance training
-|full-text-url=https://sci-hub.do/10.1080/10641963.2020.1847130
-}}
-{{medline-entry
-|title=Particle growth with photochemical age from new particle formation to haze in the winter of Beijing, China.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33207435
-|keywords=* Condensation sink
-* Haze
-* New particle formation
-* Photochemical aging
-* Pollution evolution
-|full-text-url=https://sci-hub.do/10.1016/j.scitotenv.2020.142207
-}}
-{{medline-entry
-|title=Effect of aging on stabilization of Cd and Ni by biochars and enzyme activities in a historically contaminated alkaline agricultural soil simulated with wet-dry and freeze-thaw cycling.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33143976
-|keywords=* Accelerated aging
-* Biochar
-* Cadmium
-* Enzyme activity
-* Heavy metal stabilization
-* Soil remediation
-|full-text-url=https://sci-hub.do/10.1016/j.envpol.2020.115846
-}}
-{{medline-entry
-|title=Cockayne syndrome proteins [[CS]]A and [[CS]]B maintain mitochondrial homeostasis through NAD  signaling.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33166073
-|keywords=* AMPK
-* Cockayne syndrome
-* NAD+
-* accelerated ageing
-* aging
-* mitochondrial maintenance
-* mitophagy
-|full-text-url=https://sci-hub.do/10.1111/acel.13268
-}}
-{{medline-entry
-|title=Vision Impairment and Participation in Cognitively Stimulating Activities: The Health ABC Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32710546
-|keywords=* Cognition
-* Cognitive Aging
-* Sensory
-* Vision loss
-|full-text-url=https://sci-hub.do/10.1093/gerona/glaa184
-}}
-{{medline-entry
-|title=Suspension training vs. traditional resistance training: effects on muscle mass, strength and functional performance in older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32700098
-|keywords=* Aging
-* Functionality
-* Instability resistance training
-* Muscle hypertrophy
-* TRX training
-|full-text-url=https://sci-hub.do/10.1007/s00421-020-04446-x
-}}
-{{medline-entry
-|title=Generational Differences in the 10-year Incidence of Impaired Contrast Sensitivity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32693658
-|keywords=* Aging
-* Birth Cohort Effect
-* Contrast Sensitivity
-* Epidemiology
-* Visual Function
-|full-text-url=https://sci-hub.do/10.1080/09286586.2020.1791909
-}}
-{{medline-entry
-|title=Inducible aging in Hydra oligactis implicates sexual reproduction, loss of stem cells, and genome maintenance as major pathways.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32578072
-|keywords=* Aging
-* Cold-sensitive
-* DNA repair
-* Gametogenesis
-* Hydra oligactis
-* Transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7394996
-}}
-{{medline-entry
-|title=Noradrenergic Responsiveness Supports Selective Attention across the Adult Lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32317388
-|mesh-terms=* Adult
-* Aged
-* Aging
-* Attention
-* Brain Waves
-* Cortical Synchronization
-* Humans
-* Male
-* Norepinephrine
-* Reflex, Pupillary
-|keywords=* cognitive aging
-* locus coeruleus
-* noradrenaline
-* norepinephrine
-* rhythmic neural activity
-* selective attention
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7252473
-}}
-{{medline-entry
-|title=Cellular senescence: from anti-cancer weapon to anti-aging target.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32060861
-|mesh-terms=* Aging
-* Animals
-* Antineoplastic Agents
-* Breast Neoplasms
-* Cell Proliferation
-* Cell Transformation, Neoplastic
-* Cellular Senescence
-* Cyclin-Dependent Kinases
-* Drug Discovery
-* Female
-* Humans
-* Piperazines
-* Protein Kinase Inhibitors
-* Pyridines
-|keywords=* cancer
-* cellular senescence
-* healthy aging
-* pro-senescence cancer therapy
-* senolytic therapies
-|full-text-url=https://sci-hub.do/10.1007/s11427-019-1629-6
-}}
-{{medline-entry
-|title=Extra-mitochondrial citrate synthase initiates calcium oscillation and suppresses age-dependent sperm dysfunction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31857692
-|mesh-terms=* Aging
-* Animals
-* Calcium Signaling
-* Citrate (si)-Synthase
-* Citric Acid Cycle
-* Female
-* Infertility, Male
-* Male
-* Metabolome
-* Mice
-* Ovum
-* Spermatozoa
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7096335
-}}
-{{medline-entry
-|title=Pathogenesis of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31737341
-|keywords=* Airway inflammation
-* autophagy
-* cellular senescence
-* chronic obstructive pulmonary disease (COPD)
-* necroptosis
-* oxidative stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6831915
-}}
-{{medline-entry
-|title=Possible Role of Amyloid Cross-Seeding in Evolvability and Neurodegenerative Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31524179
-|mesh-terms=* Aging
-* Amyloidogenic Proteins
-* Animals
-* Biological Evolution
-* Brain
-* Female
-* Humans
-* Inheritance Patterns
-* Models, Neurological
-* Neurodegenerative Diseases
-* Pregnancy
-* Stress, Physiological
-|keywords=* Alzheimer’s disease
-* Parkinson’s disease
-* amyloid cascade hypothesis
-* amyloidogenic proteins
-* antimicrobial protection model
-* cross-seeding
-* evolvability hypothesis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6839461
-}}
-{{medline-entry
-|title=Targeting p16-induced senescence prevents cigarette smoke-induced emphysema by promoting IGF1/Akt1 signaling in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31428695
-|mesh-terms=* Alveolar Epithelial Cells
-* Animals
-* Cell Proliferation
-* Cellular Senescence
-* Cyclin-Dependent Kinase Inhibitor p16
-* Cytokines
-* Emphysema
-* Insulin-Like Growth Factor I
-* Lung
-* Mice, Inbred C57BL
-* Models, Biological
-* Promoter Regions, Genetic
-* Proto-Oncogene Proteins c-akt
-* Pulmonary Disease, Chronic Obstructive
-* RNA, Messenger
-* Signal Transduction
-* Smoking
-|keywords=* Molecular biology
-* Senescence
-* Stem cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6689060
-}}
-==CSF1R==
-{{medline-entry
-|title=[[CSF1R]] inhibitor PLX5622 and environmental enrichment additively improve metabolic outcomes in middle-aged female mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32007953
-|keywords=* CSF1R
-* adipose
-* aging
-* environmental enrichment
-* microglia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7041757
-}}
-{{medline-entry
-|title=Modulation of Microglia by Voluntary Exercise or [[CSF1R]] Inhibition Prevents Age-Related Loss of Functional Motor Units.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31693894
-|mesh-terms=* Aging
-* Animals
-* Cell Line
-* Databases, Genetic
-* Humans
-* Induced Pluripotent Stem Cells
-* Macrophages
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Microglia
-* Motor Neurons
-* Muscle, Skeletal
-* Neuromuscular Junction
-* Neuronal Plasticity
-* Physical Conditioning, Animal
-* RNA-Seq
-* Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
-* Spinal Cord
-|keywords=* CSF1R inhibition
-* aging
-* exercise
-* innervation
-* microglia
-* motor unit
-* neuroinflammation
-* neuromuscular junction
-* neuromuscular system
-* spinal cord
-|full-text-url=https://sci-hub.do/10.1016/j.celrep.2019.10.003
-}}
-==CTCF==
-{{medline-entry
-|title=New targeted approaches for epigenetic age predictions.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32580727
-|keywords=* Aging
-* Amplicon sequencing
-* Blood
-* Buccal swabs
-* CTCF
-* DNA methylation
-* Droplet digital PCR
-* Epigenetic
-* Human
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7315536
-}}
-==CTH==
-{{medline-entry
-|title=Anterior Cingulate Structure and Perfusion is Associated with Cerebrospinal Fluid Tau among Cognitively Normal Older Adult APOEɛ4 Carriers.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31743999
-|keywords=* APOE
-* Aging
-* Alzheimer’s disease
-* cerebral blood flow
-* cognition
-* cognitive decline
-* grey matter
-* magnetic resonance imaging
-* tau proteins
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7310575
-}}
-==CTLA4==
-{{medline-entry
-|title=Horticultural Therapy Reduces Biomarkers of Immunosenescence and Inflammaging in Community-Dwelling Older Adults: A Feasibility Pilot Randomized Controlled Trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33070170
-|keywords=* CTLA-4
-* Geroscience
-* IL-6
-* Immunosenescence
-* Inflammaging
-|full-text-url=https://sci-hub.do/10.1093/gerona/glaa271
-}}
-==CTRL==
-{{medline-entry
-|title=Aging reduces the maximal level of peripheral fatigue tolerable and impairs exercise capacity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32966120
-|keywords=* aging
-* critical torque
-* exercise performance
-* group III/IV muscle afferents
-* neuromuscular fatigue
-|full-text-url=https://sci-hub.do/10.1152/ajpregu.00151.2020
-}}
-{{medline-entry
-|title=miR-146a Plasma Levels Are Not Altered in Alzheimer's Disease but Correlate With Age and Illness Severity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32009940
-|keywords=* Alzheimer’s disease
-* aging
-* blood
-* miR-146a
-* microRNA
-* plasma
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6978630
-}}
-{{medline-entry
-|title=Centrally-mediated regulation of peripheral fatigue during knee extensor exercise and consequences on the force-duration relationship in older men.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31397211
-|keywords=* Aging
-* critical torque
-* group III/IV muscle afferents
-|full-text-url=https://sci-hub.do/10.1080/17461391.2019.1655099
-}}
-==CTSA==
-{{medline-entry
-|title=A [[CTSA]]-based consultation service to advance research on special and underserved populations.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33244406
-|keywords=* faculty development
-* geriatrics
-* grant review
-* grant studio
-* pediatrics
-* peer review
-* research consultation service
-* special populations
-* underrepresented minorities
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7681147
-}}
-==CTSB==
-{{medline-entry
-|title=Myocardial cathepsin D is downregulated in sudden cardiac death.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32176724
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Cathepsin D
-* Death, Sudden, Cardiac
-* Down-Regulation
-* Female
-* Humans
-* Male
-* Middle Aged
-* Myocardium
-* Substrate Specificity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7075574
-}}
-==CX3CL1==
-{{medline-entry
-|title=Two forms of [[CX3CL1]] display differential activity and rescue cognitive deficits in [[CX3CL1]] knockout mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32410624
-|keywords=* Aging
-* CX3CL1
-* Cognition
-* Fractalkine
-* Long-term potentiation
-* Microglia
-* Neurodegeneration
-* Neurogenesis
-* Neuroinflammation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7227354
-}}
-==CX3CR1==
-{{medline-entry
-|title=Monocytes present age-related changes in phospholipid concentration and decreased energy metabolism.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32107839
-|keywords=* DNA methylation
-* aging
-* glucose metabolism
-* monocytes
-* phosphatidylcholines
-* transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189998
-}}
-{{medline-entry
-|title=Muscle Injury Induces Postoperative Cognitive Dysfunction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32066806
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Brain-Derived Neurotrophic Factor
-* CX3C Chemokine Receptor 1
-* Cytokines
-* Disease Models, Animal
-* Hippocampus
-* Humans
-* Male
-* Mice
-* Microglia
-* Muscle, Skeletal
-* Nerve Growth Factor
-* Postoperative Cognitive Complications
-* Postoperative Complications
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7026159
-}}
-==CXCL1==
-{{medline-entry
-|title=Contusion spinal cord injury upregulates p53 protein expression in rat soleus muscle at multiple timepoints but not key senescence cytokines.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32026570
-|keywords=* SASP
-* cytokines
-* inflammation
-* paralysis
-* senescence
-* spinal cord injury
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7002538
-}}
-{{medline-entry
-|title=Systemic Inflammation and the Increased Risk of Inflamm-Aging and Age-Associated Diseases in People Living With HIV on Long Term Suppressive Antiretroviral Therapy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31507593
-|mesh-terms=* Adult
-* Aging
-* Anti-HIV Agents
-* Antiretroviral Therapy, Highly Active
-* Biomarkers
-* CD4 Lymphocyte Count
-* Computational Biology
-* Cross-Sectional Studies
-* Disease Susceptibility
-* Duration of Therapy
-* Female
-* HIV Infections
-* Humans
-* Inflammation
-* Male
-* Metabolome
-* Metabolomics
-* Middle Aged
-* Proteomics
-* Telomere Homeostasis
-* Viral Load
-|keywords=* HIV
-* India
-* LMIC (lower middle income country)
-* inflammation markers
-* long term antiretroviral therapy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6718454
-}}
-==CXCL10==
-{{medline-entry
-|title=Age-related decline of interferon-gamma responses in macrophage impairs satellite cell proliferation and regeneration.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32725722
-|keywords=* Aging
-* CXCL10
-* IFN-γ
-* Macrophage
-* Muscle regeneration
-* Single-cell RNA sequence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7567146
-}}
-==CXCL11==
-{{medline-entry
-|title=Endothelial cells under therapy-induced senescence secrete [[CXCL11]], which increases aggressiveness of breast cancer cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32659248
-|keywords=* CXCL11
-* Endothelial cells
-* Therapy-induced senescence
-* Tumor microenvironment
-|full-text-url=https://sci-hub.do/10.1016/j.canlet.2020.06.019
-}}
-==CXCL12==
-{{medline-entry
-|title=Co-option of Neutrophil Fates by Tissue Environments.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33098771
-|keywords=* angiogenesis
-* immune heterogeneity
-* immune niche
-* innate immunity
-* neutrophil lifespan
-* neutrophils
-* single-cell analysis
-* tissue-resident cells
-|full-text-url=https://sci-hub.do/10.1016/j.cell.2020.10.003
-}}
-{{medline-entry
-|title=Heme oxygenase-1 deficiency triggers exhaustion of hematopoietic stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31885181
-|keywords=* aging
-* bone marrow
-* cxcl12-abudant reticular cells
-* endothelial cells
-* niche
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7001511
-}}
-{{medline-entry
-|title=Global Transcriptomic Profiling of the Bone Marrow Stromal Microenvironment during Postnatal Development, Aging, and Inflammation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31801092
-|mesh-terms=* Aging
-* Animals
-* Bone Marrow
-* Bone Marrow Cells
-* Cell Differentiation
-* Cells, Cultured
-* Cellular Microenvironment
-* Chemokine CXCL12
-* Embryonic Development
-* Endothelial Cells
-* Gene Expression Profiling
-* Hematopoiesis
-* Hematopoietic Stem Cells
-* Inflammation
-* Male
-* Mesenchymal Stem Cells
-* Mice
-* Mice, Inbred C57BL
-* Stem Cell Niche
-* Transcriptome
-|keywords=* aging
-* bone marrow microenvironment
-* hematopoietic stem cells
-* inflammation
-* niches
-* stromal cells
-* transcriptomics
-|full-text-url=https://sci-hub.do/10.1016/j.celrep.2019.11.004
-}}
-==CXCL13==
-{{medline-entry
-|title=RNA-seq data from C-X-C chemokine receptor type 5 (CXCR5) gene knockout aged mice with retinal degeneration phenotype.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32642521
-|keywords=* CXCR5
-* FastQC
-* RNA-Seq
-* aging
-* choroid
-* mice
-* retina
-* retinal degeneration
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7334305
-}}
-==CXCL14==
-{{medline-entry
-|title=Identification of genes associated with endometrial cell aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33258951
-|keywords=* CXCL12
-* CXCL14
-* IL17RB
-* endometrial cell aging
-* infertility
-* quantitative
-immunohistochemistry
-|full-text-url=https://sci-hub.do/10.1093/molehr/gaaa078
-}}
-==CXCL8==
-{{medline-entry
-|title=Cerebrovascular Senescence Is Associated With Tau Pathology in Alzheimer's Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33041998
-|keywords=* Alzheimer's disease
-* endothelial senescence
-* gene expression
-* neurofibrillary tangles
-* plasma biomarkers
-* tau pathology
-* vascular dysfunction
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7525127
-}}
-==CXCL9==
-{{medline-entry
-|title=[[CXCL9]] and CXCL10 display an age-dependent profile in Chagas patients: a cohort study of aging in Bambui, Brazil.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32393333
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Biomarkers
-* Brazil
-* Chagas Disease
-* Chemokine CXCL10
-* Chemokine CXCL9
-* Cohort Studies
-* Electrocardiography
-* Female
-* Humans
-* Male
-* Middle Aged
-* Trypanosoma cruzi
-|keywords=* Chagas disease
-* Chemokines
-* Cohort
-* Cytokines
-* Immune biomarkers
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7216412
-}}
-==CXCR2==
-{{medline-entry
-|title=CXCL5-[[CXCR2]] signaling is a senescence-associated secretory phenotype in preimplantation embryos.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32959976
-|keywords=* CXCL5
-* CXCR2
-* SASP
-* aging
-* infertility
-* preimplantation embryo
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7576282
-}}
-{{medline-entry
-|title=Senescence in Wound Repair: Emerging Strategies to Target Chronic Healing Wounds.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32850866
-|keywords=* ageing
-* diabetes
-* senescence
-* senolytics
-* wound healing
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431694
-}}
-==CXCR3==
-{{medline-entry
-|title=Senescent hepatocytes enhance natural killer cell activity via the CXCL-10/[[CXCR3]] axis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31616512
-|keywords=* chemokine
-* hepatocyte
-* natural killer cell
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6781833
-}}
-==CXCR4==
-{{medline-entry
-|title=Aging-Related Reduced Expression of [[CXCR4]] on Bone Marrow Mesenchymal Stromal Cells Contributes to Hematopoietic Stem and Progenitor Cell Defects.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32418119
-|keywords=* Aging
-* CXCR4 and ROS
-* HSPC
-* MSC
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7395885
-}}
-{{medline-entry
-|title=Transfer of a human gene variant associated with exceptional longevity improves cardiac function in obese type 2 diabetic mice through induction of the SDF-1/[[CXCR4]] signalling pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32384208
-|keywords=* BPIFB4
-* Cardiomyopathy
-* Diabetes
-* Gene therapy
-* Longevity
-|full-text-url=https://sci-hub.do/10.1002/ejhf.1840
-}}
-{{medline-entry
-|title=Stromal Cell-Derived Factor 1 Protects Brain Vascular Endothelial Cells from Radiation-Induced Brain Damage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31658727
-|mesh-terms=* Animals
-* Blood Vessels
-* Brain
-* Cell Line
-* Cellular Senescence
-* Chemokine CXCL12
-* Cranial Irradiation
-* Disease Models, Animal
-* Down-Regulation
-* Endothelial Cells
-* Female
-* Gene Expression Regulation
-* Humans
-* Lipopeptides
-* Mice
-* Receptors, CXCR4
-* Signal Transduction
-|keywords=* CXCR4
-* SDF-1
-* brain disorder
-* endothelial dysfunction
-* ionizing radiation
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6830118
-}}
-==CYP11B1==
-{{medline-entry
-|title=Intratumoral heterogeneity of the tumor cells based on in situ cortisol excess in cortisol-producing adenomas; ∼An association among morphometry, genotype and cellular senescence∼.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33002589
-|keywords=* CYP11B1
-* CYP17A
-* Cellular senescence
-* Compact and clear cells
-* Cortisol-producing adenoma
-* PRKACA
-|full-text-url=https://sci-hub.do/10.1016/j.jsbmb.2020.105764
-}}
-==CYP1A1==
-{{medline-entry
-|title=Genome-wide scan identified genetic variants associated with skin aging in a Chinese female population.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31522824
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Asian Continental Ancestry Group
-* Cheek
-* Cohort Studies
-* Cytochrome P-450 CYP1A1
-* European Continental Ancestry Group
-* Female
-* Genome-Wide Association Study
-* Humans
-* Middle Aged
-* Polymorphism, Single Nucleotide
-* Risk Factors
-* Skin Aging
-* Skin Pigmentation
-|keywords=* Candidate SNPs
-* Chinese Han females
-* GWAS
-* Skin aging
-|full-text-url=https://sci-hub.do/10.1016/j.jdermsci.2019.08.010
-}}
-==CYP26B1==
-{{medline-entry
-|title=Increased Retinoic Acid Catabolism in Olfactory Sensory Neurons Activates Dormant Tissue-Specific Stem Cells and Accelerates Age-Related Metaplasia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32385093
-|mesh-terms=* Aging
-* Animals
-* Female
-* Isotretinoin
-* Male
-* Metaplasia
-* Mice
-* Neural Stem Cells
-* Neurogenesis
-* Olfactory Mucosa
-* Olfactory Receptor Neurons
-* Retinoic Acid 4-Hydroxylase
-|keywords=* aging
-* inositol-1,4,5-triphosphate
-* metaplasia
-* olfactory epithelium
-* retinoic acid
-* stem cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244205
-}}
-==CYP2C19==
-{{medline-entry
-|title=Physiologically Based Pharmacokinetic Approach Can Successfully Predict Pharmacokinetics of Citalopram in Different Patient Populations.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31750550
-|keywords=* citalopram
-* genetic polymorphism
-* geriatrics
-* physiologically based pharmacokinetic modeling
-|full-text-url=https://sci-hub.do/10.1002/jcph.1541
-}}
-{{medline-entry
-|title=Longitudinal exposure of English primary care patients to pharmacogenomic drugs: An analysis to inform design of pre-emptive pharmacogenomic testing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31454087
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Cytochrome P-450 CYP2C19
-* Cytochrome P-450 CYP2D6
-* Drug Prescriptions
-* Female
-* Humans
-* Liver-Specific Organic Anion Transporter 1
-* Longitudinal Studies
-* Male
-* Middle Aged
-* Pharmaceutical Preparations
-* Pharmacogenomic Testing
-* Precision Medicine
-* Primary Health Care
-* United Kingdom
-|keywords=* clinical pharmacology
-* general practice
-* pharmacogenomics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6955399
-}}
-==CYP2E1==
-{{medline-entry
-|title=DNA methylation and histone acetylation changes to cytochrome P450 2E1 regulation in normal aging and impact on rates of drug metabolism in the liver.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32221779
-|keywords=* Aging
-* Cyp2e1
-* DNA methylation
-* Drug metabolism
-* Histone acetylation
-* Pharmacokinetics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7287002
-}}
-==CYP7A1==
-{{medline-entry
-|title=Age-associated changes of cytochrome P450 and related phase-2 gene/proteins in livers of rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31396457
-|keywords=* Aging
-* Cytochrome P450’s
-* Nuclear receptors
-* Ontogeny
-* Rat liver
-* mRNA/protein expression
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6681801
-}}
-==DBI==
-{{medline-entry
-|title=Quantifying cumulative anticholinergic and sedative drug load among US Medicare Beneficiaries.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33000867
-|keywords=* aging
-* cholinergic antagonists
-* drug burden index
-* drug utilization
-* hypnotics and sedatives
-* inappropriate prescribing
-* pharmacoepidemiology
-|full-text-url=https://sci-hub.do/10.1002/pds.5144
-}}
-{{medline-entry
-|title=Drug Burden Index and Cognitive and Physical Function in Aged Care Residents: A Longitudinal Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32736845
-|keywords=* Cognitive function
-* anti-muscarinics
-* benzodiazepines
-* geriatrics
-* longitudinal
-* mobility impairment
-* physical function
-* polypharmacy
-|full-text-url=https://sci-hub.do/10.1016/j.jamda.2020.05.037
-}}
-{{medline-entry
-|title=Using the Drug Burden Index to identify older adults at highest risk for medication-related falls.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32532276
-|keywords=* Accidental falls
-* Aging
-* Health services
-* Medication
-* Medication therapy management
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7291506
-}}
-{{medline-entry
-|title=Impact of STEADI-Rx: A Community Pharmacy-Based Fall Prevention Intervention.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32315461
-|keywords=* aging
-* community pharmacy
-* falls
-* health services
-* medication
-|full-text-url=https://sci-hub.do/10.1111/jgs.16459
-}}
-==DBP==
-{{medline-entry
-|title=Do baseline blood pressure and type of exercise influence level of reduction induced by training in hypertensive older adults? A meta-analysis of controlled trials.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32795629
-|keywords=* Aged
-* Aging
-* Exercise
-* Exercise therapy
-* High blood pressure
-* Hypertension
-* Resistance training
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.111052
-}}
-{{medline-entry
-|title=Attenuated aortic blood pressure responses to metaboreflex activation in older adults with dynapenia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32502600
-|keywords=* Aging
-* Diastolic pressure
-* Handgrip strength
-* Post-exercise muscle ischemia
-* Walking performance
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110984
-}}
-{{medline-entry
-|title=The Effect of Blood Pressure on Cognitive Performance. An 8-Year Follow-Up of the Tromsø Study, Comprising People Aged 45-74 Years.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32373010
-|keywords=* aging
-* blood pressure
-* cognitive performance
-* dementia
-* sex differences
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7186429
-}}
-{{medline-entry
-|title=Low Diastolic Blood Pressure and Cognitive Decline in Korean Elderly People: The Korean Longitudinal Study on Cognitive Aging and Dementia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31995969
-|keywords=* Cognition
-* Diastolic blood pressure
-* Senility
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6992855
-}}
-{{medline-entry
-|title=Diastolic Blood Pressure Is Associated With Regional White Matter Lesion Load: The Northern Manhattan Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31910743
-|mesh-terms=* Aged
-* Arterial Pressure
-* Blood Pressure
-* Brain
-* Cohort Studies
-* Diastole
-* Female
-* Frontal Lobe
-* Humans
-* Hypertension
-* Linear Models
-* Magnetic Resonance Imaging
-* Male
-* Middle Aged
-* Organ Size
-* Parietal Lobe
-* Prospective Studies
-* Systole
-* Temporal Lobe
-* White Matter
-|keywords=* American Heart Association
-* blood pressure
-* cerebrovascular disease
-* cognitive aging
-* white matter
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7219602
-}}
-{{medline-entry
-|title=Orthostatic Hypotension and Novel Blood Pressure Associated Gene Variants in Older Adults: Data From the TILDA Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31821404
-|keywords=* Aging
-* Blood pressure
-* Cardiovascular
-* Genetics
-* Single-nucleotide polymorphism
-|full-text-url=https://sci-hub.do/10.1093/gerona/glz286
-}}
-{{medline-entry
-|title=Blood pressure and hypertension prevalence among oldest-old in China for 16 year: based on CLHLS.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31500574
-|mesh-terms=* Aged, 80 and over
-* Blood Pressure
-* Blood Pressure Determination
-* China
-* Female
-* Health Surveys
-* Humans
-* Hypertension
-* Longevity
-* Longitudinal Studies
-* Male
-* Prevalence
-|keywords=* Blood pressure
-* Epidemiology
-* Hypertension
-* Oldest-old
-* Prevalence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6734230
-}}
-{{medline-entry
-|title=The age-related blood pressure trajectories from young-old adults to centenarians: A cohort study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31443986
-|mesh-terms=* Age Factors
-* Aged
-* Aged, 80 and over
-* Aging
-* Blood Pressure
-* Cohort Studies
-* Female
-* Humans
-* Male
-* Middle Aged
-|keywords=* Antihypertensive therapy
-* Birth cohort effect
-* Blood pressure
-* Cohort study
-* Heart disease
-* Survival
-|full-text-url=https://sci-hub.do/10.1016/j.ijcard.2019.08.011
-}}
-==DCC==
-{{medline-entry
-|title=X Chromosome Domain Architecture Regulates Caenorhabditis elegans Lifespan but Not Dosage Compensation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31495695
-|mesh-terms=* Adenosine Triphosphatases
-* Animals
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* DNA-Binding Proteins
-* Dosage Compensation, Genetic
-* Gene Expression Regulation
-* Longevity
-* Multiprotein Complexes
-* X Chromosome
-|keywords=* X chromosome dosage compensation
-* aging
-* condensin
-* gene expression
-* higher-order chromosome structure
-* lifespan
-* proteotoxic stress
-* topologically associating domains
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6810858
-}}
-==DCN==
-{{medline-entry
-|title=Decorin inhibits the insulin-like growth factor I signaling in bone marrow mesenchymal stem cells of aged humans.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33257596
-|keywords=* IGF-I
-* aging
-* bone marrow mesenchymal stem cell
-* osteoporosis
-* small leucine-rich proteoglycan
-|full-text-url=https://sci-hub.do/10.18632/aging.202166
-}}
-==DCX==
-{{medline-entry
-|title=GSK-3β activation accelerates early-stage consumption of Hippocampal Neurogenesis in senescent mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32863953
-|keywords=* Adult hippocampal neurogenesis
-* Glycogen synthase kinase-3β
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7449917
-}}
-{{medline-entry
-|title=Doublecortin and IGF-1R protein levels are reduced in spite of unchanged DNA methylation in the hippocampus of aged rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32236698
-|keywords=* Aging
-* DNA methylation
-* Doublecortin
-* Hippocampus
-* IGF-1R
-* mGluR5
-|full-text-url=https://sci-hub.do/10.1007/s00726-020-02834-3
-}}
-==DDB1==
-{{medline-entry
-|title=DCAF1 regulates Treg senescence via the ROS axis during immunological aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32730228
-|keywords=* Aging
-* Cellular senescence
-* Immunology
-* Inflammatory bowel disease
-* T cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7598062
-}}
-==DDC==
-{{medline-entry
-|title=N-Acetyl Cysteine Attenuates the Sarcopenia and Muscle Apoptosis Induced by Chronic Liver Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31530262
-|mesh-terms=* Acetylcysteine
-* Aging
-* Animals
-* Apoptosis
-* Disease Models, Animal
-* End Stage Liver Disease
-* Humans
-* Mice
-* Muscle Fibers, Skeletal
-* Muscular Atrophy
-* Oxidative Stress
-* Pyridines
-* Sarcopenia
-|keywords=* Sarcopenia
-* UPP oxidative stress
-* apoptosis
-* chronic liver disease
-* hepatotoxin.
-|full-text-url=https://sci-hub.do/10.2174/1566524019666190917124636
-}}
-==DDO==
-{{medline-entry
-|title=New insights on the influence of free d-aspartate metabolism in the mammalian brain during prenatal and postnatal life.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32561430
-|keywords=* Brain aging
-* Cell death
-* L-Glutamate
-* NMDA receptors
-* d-Aspartate
-* d-Aspartate oxidase
-|full-text-url=https://sci-hub.do/10.1016/j.bbapap.2020.140471
-}}
-==DDT==
-{{medline-entry
-|title=Prognostic Value of a Test of Central Auditory Function in Conversion from Mild Cognitive Impairment to Dementia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32388503
-|keywords=* Aging
-* Alzheimer’s disease
-* Auditory processing
-* Cognition
-* Dichotic Digits Test
-|full-text-url=https://sci-hub.do/10.1159/000506621
-}}
-{{medline-entry
-|title=Uptake kinetics of four hydrophobic organic pollutants in the earthworm Eisenia andrei in aged laboratory-contaminated natural soils.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32061977
-|mesh-terms=* Animals
-* DDT
-* Hexachlorocyclohexane
-* Hydrophobic and Hydrophilic Interactions
-* Kinetics
-* Oligochaeta
-* Polychlorinated Biphenyls
-* Pyrenes
-* Soil Pollutants
-|keywords=* Aging
-* BAFs
-* Bioaccumulation
-* HOCs
-* Laboratory-contaminated soils
-|full-text-url=https://sci-hub.do/10.1016/j.ecoenv.2020.110317
-}}
-{{medline-entry
-|title=Adult exposure to insecticides causes persistent behavioral and neurochemical alterations in zebrafish.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31911208
-|keywords=* Aging
-* Anxiety-related behavior
-* DDT
-* Neurobehavioral toxicology
-* Zebrafish
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7061078
-}}
-{{medline-entry
-|title=Second generation effects of larval metal pollutant exposure on reproduction, longevity and insecticide tolerance in the major malaria vector Anopheles arabiensis (Diptera: Culicidae).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31910892
-|mesh-terms=* Animals
-* Anopheles
-* Drug Resistance
-* Female
-* Fertility
-* Insecticides
-* Larva
-* Male
-* Metals
-* Reproduction
-* Water Pollutants
-|keywords=* Anopheles arabiensis
-* Insecticide resistance
-* Longevity
-* Transgenerational effects
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6947826
-}}
-{{medline-entry
-|title=Protective effect of Pedro-Ximénez must against p,p'-DDE-induced liver damages in aged Mus spretus mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31765701
-|mesh-terms=* Aging
-* Animals
-* Antioxidants
-* Chemical and Drug Induced Liver Injury
-* Dichlorodiphenyl Dichloroethylene
-* Down-Regulation
-* Liver
-* Male
-* Mice
-* Oxidative Stress
-* Pesticides
-* Plant Extracts
-* Polyphenols
-* Transcriptome
-* Up-Regulation
-* Vitis
-|keywords=* Aging
-* Hepatoprotection
-* Mus spretus
-* Organochlorine
-* Oxidative damage
-* Pedro-ximénez grape must
-* Transcriptional analysis
-* p,p'-DDE
-|full-text-url=https://sci-hub.do/10.1016/j.fct.2019.110984
-}}
-{{medline-entry
-|title=Low-dose endosulfan inhibits proliferation and induces senescence and pro-inflammatory cytokine production in human lymphocytes, preferentially impacting cytotoxic cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31589084
-|mesh-terms=* Adult
-* B-Lymphocytes
-* Cell Proliferation
-* Cells, Cultured
-* Cellular Senescence
-* Cytokines
-* Dose-Response Relationship, Drug
-* Endosulfan
-* Female
-* Healthy Volunteers
-* Humans
-* Inflammation Mediators
-* Insecticides
-* Killer Cells, Natural
-* Male
-* Primary Cell Culture
-* T-Lymphocytes, Cytotoxic
-* Young Adult
-|keywords=* Endosulfan
-* Immunosenescence
-* NK cells
-* PBMC
-* cytotoxic cells
-* interferon
-* organochlorine pesticide
-* senescence
-|full-text-url=https://sci-hub.do/10.1080/1547691X.2019.1668513
-}}
-==DKC1==
-{{medline-entry
-|title=Successful liver transplantation in short telomere syndromes without bone marrow failure due to [[DKC1]] mutation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32166868
-|keywords=* DKC1
-* cell death: senescence
-* cirrhosis
-* hepatopulmonary syndrome
-* liver transplantation
-* short telomere syndromes
-|full-text-url=https://sci-hub.do/10.1111/petr.13695
-}}
-==DLD==
-{{medline-entry
-|title=A preliminary study of cerebral blood flow, aging and dementia in people with Down syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32996650
-|keywords=* Alzheimer's disease
-* Down syndrome
-* aging
-* cerebral blood flow
-* neuroimaging
-|full-text-url=https://sci-hub.do/10.1111/jir.12784
-}}
-==DLGAP2==
-{{medline-entry
-|title=Cross-Species Analyses Identify Dlgap2 as a Regulator of Age-Related Cognitive Decline and Alzheimer's Dementia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32877673
-|keywords=* Alzheimer’s
-* Diversity Outbred
-* Dlgap2
-* GWAS
-* aging
-* cognition
-* genetic diversity
-* resilience
-* spines
-* susceptibility
-* translational
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7502175
-}}
-==DLX5==
-{{medline-entry
-|title=Inhibition of microRNA-27b-3p relieves osteoarthritis pain via regulation of KDM4B-dependent [[DLX5]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32856377
-|keywords=* adipogenic differentiation
-* cell senescence
-* distal-less homeobox 5
-* lysine demethylase 4B
-* mesenchymal stem cells
-* microRNA-27b-3p
-* osteoarthritis pain
-* osteogenic differentiation
-|full-text-url=https://sci-hub.do/10.1002/biof.1670
-}}
-==DMD==
-{{medline-entry
-|title=Aldehyde dehydrogenases contribute to skeletal muscle homeostasis in healthy, aging, and Duchenne muscular dystrophy patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32157826
-|keywords=* Aging
-* Aldehyde dehydrogenase
-* Dog model
-* Duchenne muscular dystrophy
-* Human
-* Myogenic
-* Non-human primate
-* Skeletal muscle
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432589
-}}
-{{medline-entry
-|title=Life expectancy at birth in Duchenne muscular dystrophy: a systematic review and meta-analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32107739
-|mesh-terms=* Female
-* Humans
-* Life Expectancy
-* Male
-* Muscular Dystrophy, Duchenne
-* Parturition
-* Pregnancy
-* Prognosis
-* Quality of Life
-* Respiration, Artificial
-* Survival
-|keywords=* Mechanical ventilation
-* Mortality
-* Prognosis
-* Survival
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7387367
-}}
-{{medline-entry
-|title=Renal dysfunction can occur in advanced-stage Duchenne muscular dystrophy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31725904
-|mesh-terms=* Adolescent
-* Adult
-* Aging
-* Child
-* Child, Preschool
-* Cystatin C
-* Disease Progression
-* Female
-* Heart Diseases
-* Heart Function Tests
-* Humans
-* Kidney Diseases
-* Kidney Function Tests
-* Male
-* Muscular Dystrophy, Duchenne
-* Risk Factors
-* Young Adult
-|keywords=* Duchenne muscular dystrophy
-* advanced stage
-* cystatin C
-* ejection fraction
-* fractional shortening
-* renal dysfunction
-|full-text-url=https://sci-hub.do/10.1002/mus.26757
-}}
-==DNAJB9==
-{{medline-entry
-|title=[[DNAJB9]] Inhibits p53-Dependent Oncogene-Induced Senescence and Induces Cell Transformation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32264658
-|keywords=* DNAJB9
-* RAS
-* p53
-* senescence
-* transformation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191047
-}}
-==DNMT1==
-{{medline-entry
-|title=DNA Methyltransferase 1 ([[DNMT1]]) Function Is Implicated in the Age-Related Loss of Cortical Interneurons.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32793592
-|keywords=* DNA methylation
-* GABA
-* aging
-* cerebral cortex
-* inhibitory interneurons
-* proteostasis
-* synapse
-* transcriptional control
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7387673
-}}
-==DNMT3A==
-{{medline-entry
-|title=Epigenetic regulation of miR-29a/miR-30c/[[DNMT3A]] axis controls SOD2 and mitochondrial oxidative stress in human mesenchymal stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32961441
-|keywords=* Cellular senescence
-* DNMT3A
-* Human mesenchymal stem cells
-* Mitochondrial oxidative stress
-* SOD2
-* microRNAs
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7509080
-}}
-{{medline-entry
-|title=Collagens and DNA methyltransferases in mare endometrosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31512314
-|mesh-terms=* Aging
-* Animals
-* Collagen
-* DNA (Cytosine-5-)-Methyltransferases
-* DNA Methylation
-* Endometritis
-* Endometrium
-* Female
-* Fibrosis
-* Horse Diseases
-* Horses
-* RNA, Messenger
-|keywords=* DNA methylation
-* collagen
-* endometrium
-* epigenetic
-* fibrosis
-* mare
-|full-text-url=https://sci-hub.do/10.1111/rda.13515
-}}
-{{medline-entry
-|title=Age-related clonal haemopoiesis is associated with increased epigenetic age.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31430471
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Epigenesis, Genetic
-* Female
-* Hematopoiesis
-* Humans
-* Longitudinal Studies
-* Male
-* Risk Factors
-* Scotland
-|full-text-url=https://sci-hub.do/10.1016/j.cub.2019.07.011
-}}
-==DNMT3L==
-{{medline-entry
-|title=Transient [[DNMT3L]] Expression Reinforces Chromatin Surveillance to Halt Senescence Progression in Mouse Embryonic Fibroblast.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32195249
-|keywords=* DNA methyltransferase 3-like (DNMT3L)
-* chromatin surveillance
-* epigenetics
-* polycomb repressive complex 2 (PRC2)
-* senescence
-* transposable element (TE)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064442
-}}
-==DOCK11==
-{{medline-entry
-|title=[Immunosenescence: The Forefront of Infection and Trophic Control].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115558
-|mesh-terms=* Aging
-* Animals
-* B-Lymphocytes
-* Cytokinesis
-* Gene Expression
-* Guanine Nucleotide Exchange Factors
-* Humans
-* Immunoglobulin M
-* Immunosenescence
-* Mice
-* Nutritional Status
-* Streptococcus pneumoniae
-|keywords=* B-1a B cell
-* dedicator of cytokinesis 11
-* immunosenescence
-|full-text-url=https://sci-hub.do/10.1248/yakushi.19-00193-3
-}}
-==DPP4==
-{{medline-entry
-|title=Age-Dependent Assessment of Genes Involved in Cellular Senescence, Telomere, and Mitochondrial Pathways in Human Lung Tissue of Smokers, COPD, and IPF: Associations With SARS-CoV-2 COVID-19 ACE2-TMPRSS2-Furin-[[DPP4]] Axis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33013423
-|keywords=* DNA damage
-* aging
-* cellular senescence
-* chronic obstructive pulmonary diseases
-* idiopathic pulmonary fibrosis
-* mitochondria
-* smokers
-* telomere
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7510459
-}}
-{{medline-entry
-|title=Dipeptidyl peptidase-4 inhibition improves endothelial senescence by activating AMPK/SIRT1/Nrf2 signaling pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32251672
-|keywords=* Aging
-* Dipeptidyl peptidase-4
-* Endothelium
-* Oxidative stress
-* Vascular
-|full-text-url=https://sci-hub.do/10.1016/j.bcp.2020.113951
-}}
-{{medline-entry
-|title=Molecular crosstalk between Y5 receptor and neuropeptide Y drives liver cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31999643
-|keywords=* Aging
-* Cancer
-* Hepatology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7190991
-}}
-==DPP6==
-{{medline-entry
-|title=A novel structure associated with aging is augmented in the [[DPP6]]-KO mouse brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33225987
-|keywords=* Aging dementia
-* Alzheimer’s disease
-* DPP6
-* Presynaptic terminals
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7682109
-}}
-==DPYSL2==
-{{medline-entry
-|title=Alcohol drinking exacerbates neural and behavioral pathology in the 3xTg-AD mouse model of Alzheimer's disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31733664
-|mesh-terms=* Alcohol Drinking
-* Alzheimer Disease
-* Amyloid beta-Protein Precursor
-* Animals
-* Behavior, Animal
-* Brain
-* Disease Models, Animal
-* Mice, Transgenic
-* tau Proteins
-|keywords=* Aging
-* Amyloid beta
-* Ethanol
-* GSK
-* Immunohistochemistry
-* Morris Water Maze
-* Prepulse inhibition
-* Self-administration
-* Tau pathology
-* Transgenic mouse model
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6939615
-}}
-==DRD1==
-{{medline-entry
-|title=Impact of dopamine-related genetic variants on physical activity in old age - a cohort study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32448293
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Cohort Studies
-* Exercise
-* Humans
-* Receptors, Dopamine
-* Sedentary Behavior
-* Sweden
-|keywords=* Accelerometery
-* Aging
-* Dopamine
-* Genes
-* Physical activity
-* Sedentary behaviour
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7245799
-}}
-==DRD2==
-{{medline-entry
-|title=Cortical thickness mediates the relationship between [[DRD2]] C957T polymorphism and executive function across the adult lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33179159
-|keywords=* Aging
-* Cortical thickness
-* DRD2
-* Dopamine
-* Executive function
-|full-text-url=https://sci-hub.do/10.1007/s00429-020-02169-5
-}}
-{{medline-entry
-|title=The relationship of age and [[DRD2]] polymorphisms to frontostriatal brain activity and working memory performance.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31629117
-|mesh-terms=* Aging
-* Brain
-* Humans
-* Memory, Short-Term
-* Polymorphism, Genetic
-* Receptors, Dopamine D2
-|keywords=* Aging
-* C957T
-* DRD2
-* Dopamine
-* Working memory
-* fMRI
-|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2019.08.022
-}}
-==DSPP==
-{{medline-entry
-|title=Effects of [i]p[/i]-Cresol on Senescence, Survival, Inflammation, and Odontoblast Differentiation in Canine Dental Pulp Stem Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32967298
-|keywords=* aged teeth
-* apoptosis
-* dental pulp stem cells
-* differentiation
-* pulp regeneration
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7555360
-}}
-==DST==
-{{medline-entry
-|title=Ancestral germen/soma distinction in microbes: Expanding the disposable soma theory of aging to all unicellular lineages.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32268207
-|mesh-terms=* Aging
-* Animals
-* Biological Evolution
-* DNA Replication
-* Humans
-* Phylogeny
-|keywords=* Aging
-* Asymmetric cell division
-* DNA replication
-* Disposable Soma Theory
-* Epigenetics
-* Evolution
-* Germen/Soma
-* Prokaryotes
-* Protists
-* Rejuvenation
-* Unicellular
-|full-text-url=https://sci-hub.do/10.1016/j.arr.2020.101064
-}}
-==DUSP1==
-{{medline-entry
-|title=miR-1468-3p Promotes Aging-Related Cardiac Fibrosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32348937
-|keywords=* aging
-* cardiac fibrosis
-* dual-specificity phosphatases
-* extracellular matrix
-* miR-1468-3p
-* microRNA
-* p38
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191129
-}}
-==DUSP8==
-{{medline-entry
-|title=MiR-21-5p/dual-specificity phosphatase 8 signalling mediates the anti-inflammatory effect of haem oxygenase-1 in aged intracerebral haemorrhage rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31400088
-|mesh-terms=* Aging
-* Animals
-* Antagomirs
-* Anti-Inflammatory Agents
-* Cells, Cultured
-* Cerebral Hemorrhage
-* Dual-Specificity Phosphatases
-* HEK293 Cells
-* Heme Oxygenase-1
-* Hemin
-* Humans
-* Male
-* MicroRNAs
-* Rats
-* Rats, Sprague-Dawley
-* Signal Transduction
-|keywords=* aging
-* dual-specificity phosphatase 8
-* haem oxygenase-1
-* intracerebral haemorrhage
-* microRNA
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826124
-}}
-==DUT==
-{{medline-entry
-|title=Simultaneous liquefaction, saccharification, and fermentation of L-lactic acid using aging paddy rice with hull by an isolated thermotolerant Enterococcus faecalis [[DUT]]1805.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32388689
-|keywords=* Aging paddy rice with hull (APRH)
-* Corn steep liquor powder (CSLP)
-* High-thermotolerance
-* Lactic acid
-* Saccharification and fermentation (SLSF)
-* Simultaneous liquification
-|full-text-url=https://sci-hub.do/10.1007/s00449-020-02364-y
-}}
-==DYRK1A==
-{{medline-entry
-|title=Altered age-linked regulation of plasma [[DYRK1A]] in elderly cognitive complainers (INSIGHT-preAD study) with high brain amyloid load.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32642550
-|keywords=* Alzheimer's disease
-* aging
-* blood marker
-* immunometric test
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7331462
-}}
-==E2F1==
-{{medline-entry
-|title=Regulation of [[E2F1]] activity via PKA-mediated phosphorylations.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33110360
-|keywords=* E2F1
-* PKA
-* cell cycle
-* forskolin
-* proliferation
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7585165
-}}
-{{medline-entry
-|title=Astragaloside IV ameliorates radiation-induced senescence via antioxidative mechanism.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32412100
-|keywords=* cell signal pathway
-* nerve cells
-* radiation
-* senescence
-|full-text-url=https://sci-hub.do/10.1111/jphp.13284
-}}
-==ECD==
-{{medline-entry
-|title=Outcome of Descemet Membrane Endothelial Keratoplasty Using Corneas from Donors ≥80 Years of Age.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31837315
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Cell Count
-* Cornea
-* Descemet Stripping Endothelial Keratoplasty
-* Donor Selection
-* Endothelium, Corneal
-* Female
-* Fuchs' Endothelial Dystrophy
-* Humans
-* Male
-* Middle Aged
-* Retrospective Studies
-* Tissue Donors
-* Treatment Outcome
-* Visual Acuity
-* Young Adult
-|full-text-url=https://sci-hub.do/10.1016/j.ajo.2019.12.001
-}}
-==EDA==
-{{medline-entry
-|title=Interplay between aging, lung inflammation/remodeling, and fibronectin [[EDA]] in lung cancer progression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33222614
-|keywords=* Lung cancer
-* aging
-* fibronectin EDA
-* fibrosis
-* inflammation
-* lewis lung carcinoma
-* metastasis
-|full-text-url=https://sci-hub.do/10.1080/15384047.2020.1831372
-}}
-{{medline-entry
-|title=Arousal Detection in Elderly People from Electrodermal Activity Using Musical Stimuli.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32854302
-|keywords=* aging adults
-* arousal
-* electrodermal activity
-* musical genres
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7506973
-}}
-{{medline-entry
-|title=The structure of agricultural microplastics (PT, PU and UF) and their sorption capacities for PAHs and PHE derivates under various salinity and oxidation treatments.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31761592
-|mesh-terms=* Adsorption
-* Agriculture
-* Ecosystem
-* Environmental Pollutants
-* Hydrogen Peroxide
-* Microplastics
-* Models, Chemical
-* Naphthalenes
-* Organic Chemicals
-* Phenanthrenes
-* Plastics
-* Polycyclic Aromatic Hydrocarbons
-* Polyethylene
-* Polypropylenes
-* Polyurethanes
-* Polyuria
-* Pyrenes
-* Salinity
-|keywords=* Aging
-* Microplastics
-* Polycyclic aromatic hydrocarbons
-* Salinity
-* Sorption
-|full-text-url=https://sci-hub.do/10.1016/j.envpol.2019.113525
-}}
-==EDARADD==
-{{medline-entry
-|title=Age prediction in living: Forensic epigenetic age estimation based on blood samples.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32721866
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aging
-* Child
-* Child, Preschool
-* CpG Islands
-* Cyclic Nucleotide Phosphodiesterases, Type 4
-* DNA Methylation
-* Edar-Associated Death Domain Protein
-* Fatty Acid Elongases
-* Female
-* Forensic Genetics
-* Humans
-* Infant
-* LIM-Homeodomain Proteins
-* Male
-* Middle Aged
-* Muscle Proteins
-* Polymerase Chain Reaction
-* Transcription Factors
-* Young Adult
-|keywords=* Age the living
-* CpGs
-* DNA methylation age
-* Forensic epigenetics
-* Forensic sciences
-|full-text-url=https://sci-hub.do/10.1016/j.legalmed.2020.101763
-}}
-==EDF1==
-{{medline-entry
-|title=Silencing of FOREVER YOUNG FLOWER Like Genes from Phalaenopsis Orchids Promotes Flower Senescence and Abscission.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33237274
-|keywords=*
-          FOREVER YOUNG FLOWER
-*
-          Phalaenopsis orchids
-* Abscission
-* Ethylene responses
-* MADS-box gene
-* Senescence
-|full-text-url=https://sci-hub.do/10.1093/pcp/pcaa145
-}}
-==EFS==
-{{medline-entry
-|title=The aging bladder phenotype is not the direct consequence of bladder aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31452236
-|mesh-terms=* Adrenergic beta-Agonists
-* Aging
-* Animals
-* Carbachol
-* Cholinergic Agonists
-* Electric Stimulation
-* Female
-* Isoproterenol
-* Male
-* Mice
-* Mucous Membrane
-* Muscle Contraction
-* Myography
-* Phenotype
-* Receptor, Muscarinic M3
-* Receptors, Adrenergic, beta-2
-* Urinary Bladder
-* Urination
-|keywords=* aging
-* control physiology
-* resilience
-* urinary dysfunction
-|full-text-url=https://sci-hub.do/10.1002/nau.24149
-}}
-==EGF==
-{{medline-entry
-|title=Acute, exercise-induced alterations in cytokines and chemokines in the blood distinguish physically active and sedentary aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33289019
-|keywords=* growth factors
-* human aging
-* inflammation
-* physical activity
-|full-text-url=https://sci-hub.do/10.1093/gerona/glaa310
-}}
-{{medline-entry
-|title=Proinflammation, profibrosis, and arterial aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33103036
-|keywords=* aging
-* artery
-* collagen
-* profibrosis
-* proinflammation
-* stiffening
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7574637
-}}
-{{medline-entry
-|title=Hinokitiol induces cell death and inhibits epidermal growth factor-induced cell migration and signaling pathways in human cervical adenocarcinoma.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32917321
-|keywords=* Autophagy
-* Epidermal growth factor
-* Hinokitiol
-* Senescence
-* c-Jun N-Terminal kinase
-|full-text-url=https://sci-hub.do/10.1016/j.tjog.2020.07.013
-}}
-{{medline-entry
-|title=Activation of epidermal growth factor receptor signaling mediates cellular senescence induced by certain pro-inflammatory cytokines.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32323422
-|keywords=* EGFR
-* HUVEC
-* IMR90
-* Ras signaling
-* pro-inflammatory cytokine
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7253070
-}}
-{{medline-entry
-|title=Insulin Signaling in Intestinal Stem and Progenitor Cells as an Important Determinant of Physiological and Metabolic Traits in [i]Drosophila[/i].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32225024
-|keywords=* ISC
-* fruit fly
-* insulin signaling pathway
-* lifespan
-* metabolism
-* midgut
-* progenitor cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7226132
-}}
-{{medline-entry
-|title=Different cellular properties and loss of nuclear signalling of porcine epidermal growth factor receptor with aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32001323
-|mesh-terms=* Animals
-* ErbB Receptors
-* Signal Transduction
-* Swine
-|keywords=* Aging
-* Cell behaviour
-* EGF
-* EGFR
-* Signalling pathway
-|full-text-url=https://sci-hub.do/10.1016/j.ygcen.2020.113415
-}}
-==EGFR==
-{{medline-entry
-|title=Type I Collagen Aging Increases Expression and Activation of [[EGFR]] and Induces Resistance to Erlotinib in Lung Carcinoma in 3D Matrix Model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33014812
-|keywords=* EGFR
-* Erlotinib
-* Type I collagen
-* aging
-* resistance
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7511549
-}}
-{{medline-entry
-|title=Comparative effectiveness and cost-effectiveness of three first-line [[EGFR]]-tyrosine kinase inhibitors: Analysis of real-world data in a tertiary hospital in Taiwan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32267879
-|mesh-terms=* Afatinib
-* Aged
-* Carcinoma, Non-Small-Cell Lung
-* Cost-Benefit Analysis
-* Erlotinib Hydrochloride
-* Female
-* Gefitinib
-* Humans
-* Life Expectancy
-* Lung Neoplasms
-* Male
-* Propensity Score
-* Protein Kinase Inhibitors
-* Quality of Life
-* Survival Rate
-* Taiwan
-* Tertiary Care Centers
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7141611
-}}
-{{medline-entry
-|title=An Optogenetic Method to Study Signal Transduction in Intestinal Stem Cell Homeostasis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32201167
-|mesh-terms=* Animals
-* Cell Communication
-* Cell Proliferation
-* Cells, Cultured
-* Drosophila Proteins
-* Drosophila melanogaster
-* Gene Expression Regulation
-* Gene Regulatory Networks
-* Homeostasis
-* Intestinal Mucosa
-* Light
-* Longevity
-* Optogenetics
-* Signal Transduction
-* Stem Cells
-|keywords=* Drosophila
-* EGFR
-* Toll
-* optogenetics
-* stem cells
-|full-text-url=https://sci-hub.do/10.1016/j.jmb.2020.03.019
-}}
-{{medline-entry
-|title=Treatment-Induced Tumor Dormancy through YAP-Mediated Transcriptional Reprogramming of the Apoptotic Pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31935369
-|mesh-terms=* Adaptor Proteins, Signal Transducing
-* Animals
-* Apoptosis
-* Cell Cycle Proteins
-* Cell Line, Tumor
-* Cell Proliferation
-* Cell Survival
-* Cellular Senescence
-* Drug Resistance, Neoplasm
-* ErbB Receptors
-* Female
-* Gene Deletion
-* Gene Expression Regulation, Neoplastic
-* Humans
-* Lung Neoplasms
-* MAP Kinase Kinase 1
-* Male
-* Mice
-* Mice, Knockout
-* Mutation
-* Signal Transduction
-* Transcription Factors
-* Transcription, Genetic
-|keywords=* YAP
-* dormancy
-* drug resistance
-* drug tolerance
-* epidermal growth factor receptor
-* lung cancer
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7146079
-}}
-{{medline-entry
-|title=Association between [[EGFR]] mutation and ageing, history of pneumonia and gastroesophageal reflux disease among patients with advanced lung cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31634646
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Case-Control Studies
-* ErbB Receptors
-* Female
-* Gastroesophageal Reflux
-* Humans
-* Lung Neoplasms
-* Male
-* Middle Aged
-* Mutation
-* Pneumonia
-* Republic of Korea
-* Retrospective Studies
-* Risk Factors
-* Young Adult
-|keywords=* Ageing
-* EGFR mutation
-* GERD
-* Lung cancer
-* Pneumonia
-* Risk factors
-|full-text-url=https://sci-hub.do/10.1016/j.ejca.2019.09.010
-}}
-==EHF==
-{{medline-entry
-|title=Extended high frequency hearing and speech perception implications in adults and children.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32111404
-|keywords=* Aging
-* Development
-* Extended high frequency audiometry
-* Otitis media
-* Ototoxicity
-* Speech in noise
-* Speech perception
-* Tinnitus
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431381
-}}
-==EIF4E==
-{{medline-entry
-|title=Transcriptomic evidence that insulin signalling pathway regulates the ageing of subterranean termite castes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32424344
-|mesh-terms=* Aging
-* Animals
-* Insulin
-* Isoptera
-* Molecular Sequence Annotation
-* Signal Transduction
-* Transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7235038
-}}
-==ELF3==
-{{medline-entry
-|title=High Ambient Temperature Accelerates Leaf Senescence via PHYTOCHROME-INTERACTING FACTOR 4 and 5 in [i]Arabidopsis[/i].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32732458
-|keywords=* Arabidopsis
-* PIF4
-* phytochrome
-* senescence
-* temperature
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7398796
-}}
-==ELOVL2==
-{{medline-entry
-|title=[[ELOVL2]]: Not just a biomarker of aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33043173
-|keywords=* Aging
-* Macular degeneration
-* Membrane structure
-* Polyunsaturated fatty acids
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7544151
-}}
-{{medline-entry
-|title=The lipid elongation enzyme [[ELOVL2]] is a molecular regulator of aging in the retina.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31943697
-|mesh-terms=* Aging
-* Animals
-* Cell Line
-* DNA Methylation
-* Decitabine
-* Down-Regulation
-* Fatty Acid Elongases
-* Fatty Acids, Unsaturated
-* Female
-* Humans
-* Macular Degeneration
-* Male
-* Mice
-* Mice, Transgenic
-* Point Mutation
-* Promoter Regions, Genetic
-* Retina
-* Retinal Pigment Epithelium
-|keywords=* DNA methylation
-* ELOVL2
-* PUFA
-* age-related macular degeneration
-* aging
-* retina
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996962
-}}
-==EN1==
-{{medline-entry
-|title=Electrochemically detecting DNA methylation in the [[EN1]] gene promoter: implications for understanding ageing and disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33135722
-|keywords=* Aging
-* biosensor
-* electrochemistry
-* methylation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7670582
-}}
-==ENO1==
-{{medline-entry
-|title=Reduced expression of enolase-1 correlates with high intracellular glucose levels and increased senescence in cisplatin-resistant ovarian cancer cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32355541
-|keywords=* ENO1
-* Enolase
-* beta-Gal
-* cisplatin resistance
-* glucose
-* ovarian cancer
-* p21
-* p53
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191177
-}}
-==ENTPD7==
-{{medline-entry
-|title=Inhibition of lung cancer cells and Ras/Raf/MEK/ERK signal transduction by ectonucleoside triphosphate phosphohydrolase-7 ([[ENTPD7]]).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31443651
-|mesh-terms=* Adult
-* Aged
-* Animals
-* Apoptosis
-* Apyrase
-* Biomarkers
-* Cell Line, Tumor
-* Cell Proliferation
-* Cells, Cultured
-* Female
-* Gene Expression Regulation, Neoplastic
-* Gene Silencing
-* Humans
-* Lung Neoplasms
-* MAP Kinase Signaling System
-* Male
-* Mice
-* Mice, Inbred BALB C
-* Mice, Nude
-* Middle Aged
-* Mitogen-Activated Protein Kinases
-* Plasmids
-* Signal Transduction
-* Survival Analysis
-* raf Kinases
-* ras Proteins
-|keywords=* Ectonucleoside triphosphate phosphohydrolase-7
-* Lung cancer
-* Proliferation
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6708200
-}}
-==EPO==
-{{medline-entry
-|title=Regulation of muscle and metabolic physiology by hypothalamic erythropoietin independently of its peripheral action.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32029230
-|keywords=* Aging
-* Brain
-* Erythropoietin
-* Glucose tolerance
-* Hypothalamus
-* Metabolism
-* Muscle
-* Obesity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6938905
-}}
-{{medline-entry
-|title=Red Blood Cell Lifespan Shortening in Patients with Early-Stage Chronic Kidney Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31550724
-|mesh-terms=* Anemia
-* Erythrocytes
-* Female
-* Humans
-* Male
-* Middle Aged
-* Renal Insufficiency, Chronic
-|keywords=* Chronic kidney disease
-* Erythropoietin
-* Levitt’s CO breath test
-* Red blood cell lifespan
-* Renal anemia
-|full-text-url=https://sci-hub.do/10.1159/000502525
-}}
-==ERCC1==
-{{medline-entry
-|title=Chronic Sildenafil Treatment Improves Vasomotor Function in a Mouse Model of Accelerated Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32630010
-|keywords=* aging
-* cGMP
-* guanylate cyclase
-* hypertension
-* nitric oxide
-* phosphodiesterase
-* sildenafil
-* vascular dysfunction
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7369923
-}}
-{{medline-entry
-|title=Local endothelial DNA repair deficiency causes aging-resembling endothelial-specific dysfunction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32202295
-|mesh-terms=* Age Factors
-* Aging
-* Animals
-* Capillary Permeability
-* Cellular Senescence
-* Cyclin-Dependent Kinase Inhibitor p21
-* DNA Damage
-* DNA Repair
-* DNA-Binding Proteins
-* Endonucleases
-* Endothelial Cells
-* Endothelium, Vascular
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Nitric Oxide
-* Nitric Oxide Synthase Type III
-* Superoxides
-* Vascular Stiffness
-* Vasodilation
-|keywords=* DNA damage
-* aging
-* endothelial dysfunction
-* endothelium-dependent dilation
-* nitric oxide
-|full-text-url=https://sci-hub.do/10.1042/CS20190124
-}}
-{{medline-entry
-|title=Tissue specificity of senescent cell accumulation during physiologic and accelerated aging of mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31981461
-|keywords=* DNA repair
-* ERCC1-XPF
-* aging
-* cellular senescence
-* endogenous DNA damage
-* progeria
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059165
-}}
-{{medline-entry
-|title=Deficiency in the DNA repair protein [[ERCC1]] triggers a link between senescence and apoptosis in human fibroblasts and mouse skin.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31737985
-|keywords=* DNA damage repair
-* aging
-* cell death
-* senescence-associated secretory phenotype
-* tumor necrosis factor α
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059167
-}}
-==ERF==
-{{medline-entry
-|title=Angiotensin-Converting Enzyme Gene D/I Polymorphism in Relation to Endothelial Function and Endothelial-Released Factors in Chinese Women.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33041838
-|keywords=* ACE D/I gene polymorphism
-* Chinese women
-* aging
-* endothelial function
-* endothelial-released factors
-* menopause
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7526498
-}}
-{{medline-entry
-|title=Projections of Ambient Temperature- and Air Pollution-Related Mortality Burden Under Combined Climate Change and Population Aging Scenarios: a Review.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32542573
-|keywords=* Air pollution
-* Climate change
-* Mortality
-* Population aging
-* Projection
-* Temperature
-|full-text-url=https://sci-hub.do/10.1007/s40572-020-00281-6
-}}
-{{medline-entry
-|title=Exome Sequencing Analysis Identifies Rare Variants in [i]ATM[/i] and [i]RPL8[/i] That Are Associated With Shorter Telomere Length.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32425970
-|keywords=* ATM
-* RPL8
-* aging
-* meta-analysis
-* telomere
-* whole exome sequencing
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7204400
-}}
-==ERG==
-{{medline-entry
-|title=Effect of age and sex on neurodevelopment and neurodegeneration in the healthy eye: Longitudinal functional and structural study in the Long-Evans rat.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32882213
-|keywords=* Aging
-* Electroretinography
-* Neurodegeneration
-* Neurodevelopment
-* Optical coherence tomography
-* Retina
-* Sex
-|full-text-url=https://sci-hub.do/10.1016/j.exer.2020.108208
-}}
-{{medline-entry
-|title=Mice With a Combined Deficiency of Superoxide Dismutase 1 (Sod1), DJ-1 (Park7), and Parkin (Prkn) Develop Spontaneous Retinal Degeneration With Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31487745
-|mesh-terms=* Aging
-* Animals
-* Biomarkers
-* Electroretinography
-* Enzyme-Linked Immunosorbent Assay
-* Immunohistochemistry
-* Malondialdehyde
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Microscopy, Electron, Transmission
-* Mitochondria
-* Oxidative Stress
-* Protein Deglycase DJ-1
-* Retina
-* Retinal Degeneration
-* Retinal Pigment Epithelium
-* Superoxide Dismutase-1
-* Tomography, Optical Coherence
-* Ubiquitin-Protein Ligases
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6733419
-}}
-==ESPL1==
-{{medline-entry
-|title=Identification and genomic analysis of pedigrees with exceptional longevity identifies candidate rare variants.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32574725
-|keywords=* Genomics
-* Longevity
-* Pedigree
-* Rare variant sharing
-* Utah population database
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7461696
-}}
-==ETS1==
-{{medline-entry
-|title=The transcription factor [[ETS1]] promotes apoptosis resistance of senescent cholangiocytes by epigenetically up-regulating the apoptosis suppressor BCL2L1.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31659122
-|mesh-terms=* ATP Binding Cassette Transporter, Subfamily B
-* Animals
-* Apoptosis
-* Cellular Senescence
-* Hepatocytes
-* Humans
-* Lipopolysaccharides
-* Liver
-* Mice
-* Proto-Oncogene Protein c-ets-1
-* Transcription Factors
-* bcl-X Protein
-|keywords=* BCL2 like 1 (BCL2L1)
-* apoptosis
-* cholangiocyte
-* chromatin modification
-* epigenetics
-* gene expression
-* primary sclerosing cholangitis (PSC)
-* senescence
-* transcription factor
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6901313
-}}
-==EVL==
-{{medline-entry
-|title=Health Years in Total: A New Health Objective Function for Cost-Effectiveness Analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31952678
-|mesh-terms=* Cost-Benefit Analysis
-* Health Care Costs
-* Health Status
-* Health Status Indicators
-* Humans
-* Life Expectancy
-* Quality of Life
-* Quality-Adjusted Life Years
-* Time Factors
-|keywords=* cost-effectiveness
-* equal value of life
-* health years in total
-* quality-adjusted life-year
-* thresholds
-|full-text-url=https://sci-hub.do/10.1016/j.jval.2019.10.014
-}}
-==EZH2==
-{{medline-entry
-|title=Linking gene expression and phenotypic changes in the developmental and evolutionary origins of osteosclerosis in the ribs of bowhead whales (Balaena mysticetus).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32729176
-|keywords=* Cetacea
-* aging
-* bone
-* hyperostosis
-* osteoblasts
-* whales
-|full-text-url=https://sci-hub.do/10.1002/jez.b.22990
-}}
-{{medline-entry
-|title=[[EZH2]] is involved in vulnerability to neuroinflammation and depression-like behaviors induced by chronic stress in different aged mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32553389
-|keywords=* Aging
-* CUMS
-* Cytokines
-* Depresion
-* EZH2
-* Microglia
-|full-text-url=https://sci-hub.do/10.1016/j.jad.2020.03.154
-}}
-{{medline-entry
-|title=A positive feedback loop between [[EZH2]] and NOX4 regulates nucleus pulposus cell senescence in age-related intervertebral disc degeneration.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32025238
-|keywords=* Epigenetic histone modification
-* Intervertebral disc degeneration
-* Nucleus pulposus cell senescence
-* Wnt/β-catenin signaling pathway
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6995653
-}}
-{{medline-entry
-|title=Perinatal exposure to bisphenol A impacts in the mammary gland morphology of adult Mongolian gerbils.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31917966
-|mesh-terms=* Actins
-* Aging
-* Animals
-* Benzhydryl Compounds
-* Cell Proliferation
-* Collagen
-* Enhancer of Zeste Homolog 2 Protein
-* Female
-* Gerbillinae
-* Histones
-* Mammary Glands, Animal
-* Phenols
-* Pregnancy
-* Prenatal Exposure Delayed Effects
-|keywords=* BPA
-* EZH2
-* Environment pollutant
-* Estrogen
-* Morphologic alterations
-* Phospho-histone-h3
-|full-text-url=https://sci-hub.do/10.1016/j.yexmp.2020.104374
-}}
-==F2==
-{{medline-entry
-|title=Environmental risk assessment of glufosinate-resistant soybean by pollen-mediated gene flow under field conditions in the region of the genetic origin.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33189381
-|keywords=* Glufosinate resistance
-* Relative fitness
-* Seed longevity
-* Transgene flow
-* Weed risk
-|full-text-url=https://sci-hub.do/10.1016/j.scitotenv.2020.143073
-}}
-{{medline-entry
-|title=Gestational arsenite exposure augments hepatic tumors of C3H mice by promoting senescence in F1 and [[F2]] offspring via different pathways.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33010264
-|keywords=* Arsenic
-* Liver
-* Multigenerational Effect
-* SASP
-* Senescence
-* Tumor
-|full-text-url=https://sci-hub.do/10.1016/j.taap.2020.115259
-}}
-{{medline-entry
-|title=Familial Longevity is Associated with an Attenuated Thyroidal Response to Recombinant Human Thyroid Stimulating Hormone.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32303766
-|keywords=* Thyroid
-* longevity
-* recombinant human TSH
-* responsivity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7239378
-}}
-{{medline-entry
-|title=Conclusions from a behavioral aging study on male and female [[F2]] hybrid mice on age-related behavior, buoyancy in water-based tests, and an ethical method to assess lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31509518
-|mesh-terms=* Adiposity
-* Aging
-* Animals
-* Exploratory Behavior
-* Female
-* Male
-* Memory
-* Mice, Inbred BALB C
-* Mice, Inbred C57BL
-* Swimming
-|keywords=* F2 hybrid mice
-* aging
-* exploratory activity
-* sex comparison
-* water-based behavioral tests
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6756906
-}}
-{{medline-entry
-|title=In utero exposure to acetaminophen and ibuprofen leads to intergenerational accelerated reproductive aging in female mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31428698
-|mesh-terms=* Acetaminophen
-* Aging
-* Animals
-* Animals, Newborn
-* Cell Proliferation
-* Female
-* Fertility
-* Forkhead Box Protein O3
-* Germ Cells
-* Ibuprofen
-* Luteolysis
-* Mice
-* Ovary
-* Pregnancy
-* Prenatal Exposure Delayed Effects
-* Proto-Oncogene Proteins c-akt
-* Reproduction
-* Signal Transduction
-|keywords=* Infertility
-* Oogenesis
-* Risk factors
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6692356
-}}
-==F3==
-{{medline-entry
-|title=A Comprehensive Analysis of Age and Gender Effects in European Portuguese Oral Vowels.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33293174
-|keywords=* Acoustic
-* Aging voice
-* European Portuguese
-* Oral vowel
-|full-text-url=https://sci-hub.do/10.1016/j.jvoice.2020.10.021
-}}
-{{medline-entry
-|title=Prenatal exposure to an environmentally relevant phthalate mixture accelerates biomarkers of reproductive aging in a multiple and transgenerational manner in female mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33129917
-|keywords=* cyclicity
-* hormone
-* mixture
-* ovary
-* phthalates
-* reproductive aging
-* transgenerational
-|full-text-url=https://sci-hub.do/10.1016/j.reprotox.2020.10.009
-}}
-{{medline-entry
-|title=Combining Frontal Transcranial Direct Current Stimulation With Walking Rehabilitation to Enhance Mobility and Executive Function: A Pilot Clinical Trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32808403
-|keywords=* Aging
-* cognition
-* rehabilitation
-* transcranial direct current stimulation
-* walking
-|full-text-url=https://sci-hub.do/10.1111/ner.13250
-}}
-{{medline-entry
-|title=Multigenerational exposure to TiO  nanoparticles in soil stimulates stress resistance and longevity of survived C. elegans via activating insulin/IGF-like signaling.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32203849
-|mesh-terms=* Animals
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* Insulin
-* Longevity
-* Nanoparticles
-* Oxidative Stress
-* Soil
-* Titanium
-|keywords=* Insulin/IGF-like signaling
-* Longevity
-* Multigenerational toxicity
-* Nanomaterial
-* Soil nematode
-|full-text-url=https://sci-hub.do/10.1016/j.envpol.2020.114376
-}}
-{{medline-entry
-|title=Co-expression network analysis identified hub genes critical to triglyceride and free fatty acid metabolism as key regulators of age-related vascular dysfunction in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31514170
-|mesh-terms=* Aging
-* Animals
-* Fatty Acids, Nonesterified
-* Gene Expression Profiling
-* Gene Expression Regulation
-* Gene Regulatory Networks
-* Lipid Metabolism
-* Mice
-* Microarray Analysis
-* Signal Transduction
-* Triglycerides
-* Vascular Diseases
-|keywords=* aging
-* co-expression network
-* hub gene
-* module
-* mouse
-* vascular dysfunction
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6781998
-}}
-==F5==
-{{medline-entry
-|title=Methylation signatures in peripheral blood are associated with marked age acceleration and disease progression in patients with primary sclerosing cholangitis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32039401
-|keywords=* ALP, alkaline phosphatase
-* ALT, alanine aminotransferase
-* Aging
-* BMI, body mass index
-* DNAm, DNA methylation
-* ELF, enhanced liver fibrosis
-* FDR, false discovery rate
-* GGT, gamma-glutamyltransferase
-* IBD, inflammatory bowel disease
-* IL, interleukin
-* LOXL2, lysyl oxidase-like-2
-* NASH, non-alcoholic steatohepatitis
-* PSC, primary sclerosing cholangitis
-* SMA, smooth muscle actin
-* UDCA, ursodeoxycholic acid
-* biomarker
-* inflammatory bowel disease
-* primary sclerosing cholangitis
-* prognosis
-* ursodeoxycholic acid
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7005566
-}}
-{{medline-entry
-|title=Fermentation of Blackberry with [i]L. plantarum[/i] JBMI [[F5]] Enhance the Protection Effect on UVB-Mediated Photoaging in Human Foreskin Fibroblast and Hairless Mice through Regulation of MAPK/NF-κB Signaling.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31614689
-|mesh-terms=* Animals
-* Cell Line
-* Cell Survival
-* Female
-* Fermentation
-* Fibroblasts
-* Foreskin
-* Fruit
-* Lactobacillus plantarum
-* Male
-* Mice
-* Mice, Hairless
-* Plant Extracts
-* Rubus
-* Skin Aging
-* Ultraviolet Rays
-|keywords=* Lactobacillus plantarum
-* MMPs
-* fermented blackberry
-* photoaging
-* skin aging
-* type I procollagen
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6835613
-}}
-==F7==
-{{medline-entry
-|title=The Pattern of Mu Rhythm Modulation During Emotional Destination Memory: Comparison Between Mild Cognitive Impairment Patients and Healthy Controls.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31524160
-|mesh-terms=* Aged
-* Aging
-* Cognitive Dysfunction
-* Electroencephalography
-* Emotions
-* Female
-* Frontal Lobe
-* Humans
-* Male
-* Memory
-* Neurophysiological Monitoring
-* Neuropsychological Tests
-* Task Performance and Analysis
-* Temporal Lobe
-|keywords=* Emotional destination memory
-* Mu suppression
-* fronto-temporal
-* mild cognitive impairment
-* mirror neurons
-|full-text-url=https://sci-hub.do/10.3233/JAD-190311
-}}
-==FAAH==
-{{medline-entry
-|title=Endocannabinoid genetic variation enhances vulnerability to THC reward in adolescent female mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32095523
-|mesh-terms=* Aging
-* Amidohydrolases
-* Animals
-* Axons
-* Choice Behavior
-* Dronabinol
-* Endocannabinoids
-* Female
-* Genetic Variation
-* Male
-* Mice, Inbred C57BL
-* Nerve Net
-* Nucleus Accumbens
-* Polymorphism, Single Nucleotide
-* Receptor, Cannabinoid, CB1
-* Reward
-* Tyrosine 3-Monooxygenase
-* Ventral Tegmental Area
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7015690
-}}
-==FABP3==
-{{medline-entry
-|title=[[FABP3]]-mediated membrane lipid saturation alters fluidity and induces ER stress in skeletal muscle with aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33168829
-|mesh-terms=* Aging
-* Animals
-* Cell Line
-* Endoplasmic Reticulum Stress
-* Eukaryotic Initiation Factor-2
-* Fatty Acid Binding Protein 3
-* Female
-* Gene Knockdown Techniques
-* Lipidomics
-* Membrane Fluidity
-* Membrane Lipids
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Muscle, Skeletal
-* Myoblasts
-* Phospholipids
-* Protein-Serine-Threonine Kinases
-* Sarcopenia
-* Up-Regulation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7653047
-}}
-{{medline-entry
-|title=Autophagy receptor OPTN (optineurin) regulates mesenchymal stem cell fate and bone-fat balance during aging by clearing [[FABP3]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33143524
-|keywords=* Adipogenesis
-* autophagy
-* bone metabolism
-* fabp3
-* mesenchymal stem cell
-* optineurin
-* osteogenesis
-* osteoporosis
-* senescence
-|full-text-url=https://sci-hub.do/10.1080/15548627.2020.1839286
-}}
-{{medline-entry
-|title=Myokines as biomarkers of frailty and cardiovascular disease risk in females.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32017952
-|keywords=* Aging
-* Biomarkers
-* Cardiovascular disease
-* Females
-* Frailty
-* Myokines
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110859
-}}
-==FADS1==
-{{medline-entry
-|title=Aging and [[FADS1]] polymorphisms decrease the biosynthetic capacity of long-chain PUFAs: A human trial using [U- C]linoleic acid.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31492428
-|mesh-terms=* Adult
-* Age Factors
-* Aged
-* Aging
-* Alleles
-* Arachidonic Acid
-* Area Under Curve
-* Fatty Acid Desaturases
-* Fatty Acids, Unsaturated
-* Female
-* Healthy Volunteers
-* Humans
-* Linoleic Acid
-* Male
-* Polymorphism, Single Nucleotide
-|keywords=* Aging
-* Arachidonic acid
-* Fatty acid conversion
-* Linoleic acid
-* Lipid metabolism
-* Long-chain polyunsaturated fatty acid
-|full-text-url=https://sci-hub.do/10.1016/j.plefa.2019.07.003
-}}
-==FANCD2==
-{{medline-entry
-|title=TFG-maintaining stability of overlooked [[FANCD2]] confers early DNA-damage response.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33099537
-|keywords=* DNA damage response
-* FANCD2
-* TFG
-* aging and cancer
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7655164
-}}
-==FAP==
-{{medline-entry
-|title=Rapamycin Extends Life Span in Apc  Colon Cancer [[FAP]] Model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33132009
-|keywords=* Aging
-* Crypt stem cells
-* eEF2K
-* mTORC1
-* rpS6
-|full-text-url=https://sci-hub.do/10.1016/j.clcc.2020.08.006
-}}
-{{medline-entry
-|title=Exercise enhances skeletal muscle regeneration by promoting senescence in fibro-adipogenic progenitors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32060352
-|mesh-terms=* Aging
-* Animals
-* Apoptosis
-* Exercise Therapy
-* Female
-* Humans
-* Mesenchymal Stem Cells
-* Mice
-* Mice, Inbred BALB C
-* Mice, Inbred C57BL
-* Muscle, Skeletal
-* Muscular Diseases
-* Regeneration
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7021787
-}}
-{{medline-entry
-|title=Control of Muscle Fibro-Adipogenic Progenitors by Myogenic Lineage is Altered in Aging and Duchenne Muscular Dystrophy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31865646
-|mesh-terms=* Adipogenesis
-* Adolescent
-* Adult
-* Adult Stem Cells
-* Aged
-* Aging
-* Cells, Cultured
-* Child
-* Child, Preschool
-* Female
-* Humans
-* Infant
-* Male
-* Middle Aged
-* Muscle Development
-* Muscular Dystrophy, Duchenne
-* Myoblasts
-* Young Adult
-|keywords=Adipocytes; Myofibroblasts; Muscle progenitors; Myopathies
-|full-text-url=https://sci-hub.do/10.33594/000000196
-}}
-==FAS==
-{{medline-entry
-|title=Five-year change in maximum tongue pressure and physical function in community-dwelling elderly adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32952883
-|keywords=* Aging
-* Biological age
-* Elderly
-* Physical function
-* Tongue pressure
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7486543
-}}
-{{medline-entry
-|title=Inhibition of USP7 activity selectively eliminates senescent cells in part via restoration of p53 activity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32064756
-|keywords=* MDM2
-* Senescence
-* USP7
-* apoptosis
-* p53
-* senolytics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059172
-}}
-==FES==
-{{medline-entry
-|title=An outpatient Tai Chi program: Effects on veterans' functional outcomes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33241873
-|keywords=* Tai Chi
-* balance
-* exercise
-* gait
-* geriatrics
-|full-text-url=https://sci-hub.do/10.1111/nuf.12532
-}}
-{{medline-entry
-|title=Gait Function in Adults Aged 50 Years and Older With Spina Bifida.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33166524
-|keywords=* Adult
-* Aging
-* Gait analysis
-* Myelomeningocele
-* Rehabilitation
-|full-text-url=https://sci-hub.do/10.1016/j.apmr.2020.10.118
-}}
-{{medline-entry
-|title=A Single Question as a Screening Tool to Assess Fear of Falling in Young-Old Community-Dwelling Persons.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32165062
-|keywords=* FES-I
-* elderly
-* fear of falling
-* healthy aging
-* older adults
-|full-text-url=https://sci-hub.do/10.1016/j.jamda.2020.01.101
-}}
-{{medline-entry
-|title=Fall-related efficacy is a useful and independent index to detect fall risk in Japanese community-dwelling older people: a 1-year longitudinal study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31664911
-|mesh-terms=* Accidental Falls
-* Activities of Daily Living
-* Aged
-* Aging
-* Female
-* Geriatric Assessment
-* Humans
-* Independent Living
-* Japan
-* Longitudinal Studies
-* Male
-* Physical Functional Performance
-* Postural Balance
-* Risk Factors
-* Walking Speed
-|keywords=* Accidental falls
-* Aged
-* Fall-related efficacy
-* Japanese
-* Physical performance
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6820944
-}}
-{{medline-entry
-|title=Investigating Changes in Real-time Conscious Postural Processing by Older Adults during Different Stance Positions Using Electroencephalography Coherence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31514583
-|mesh-terms=* Accidental Falls
-* Aged
-* Aging
-* Brain
-* Electroencephalography
-* Fear
-* Female
-* Humans
-* Male
-* Movement
-* Postural Balance
-* Posture
-|full-text-url=https://sci-hub.do/10.1080/0361073X.2019.1664450
-}}
-==FEV==
-{{medline-entry
-|title=Prediction of Lung Function in Adolescence Using Epigenetic Aging: A Machine Learning Approach.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33182250
-|keywords=* epigenetic aging
-* feature selection
-* hyperparameter tuning
-* lung function
-* machine learning
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7712054
-}}
-{{medline-entry
-|title=Effect of Age on the Efficacy and Safety of Once-Daily Single-Inhaler Triple Therapy Fluticasone Furoate/Umeclidinium/Vilanterol in Patients With Chronic Obstructive Pulmonary Disease: A Post Hoc Analysis of the IMPACT Trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33031829
-|keywords=* COPD
-* aging
-* exacerbations
-* safety
-* single-inhaler triple therapy
-|full-text-url=https://sci-hub.do/10.1016/j.chest.2020.09.253
-}}
-{{medline-entry
-|title=A comprehensive analysis of factors related to lung function in older adults: Cross-sectional findings from the Canadian Longitudinal Study on Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33010732
-|keywords=* Aging
-* Determinants
-* Lung function
-* Sex
-* Spirometry
-|full-text-url=https://sci-hub.do/10.1016/j.rmed.2020.106157
-}}
-{{medline-entry
-|title=Risk factors associated with the detection of pulmonary emphysema in older asymptomatic respiratory subjects.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32517728
-|keywords=* Aging
-* COPD
-* Klotho
-* Pulmonary emphysema
-* Risk factors
-* Telomere length
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7285611
-}}
-{{medline-entry
-|title=Tiotropium Respimat Efficacy and Safety in Asthma: Relationship to Age.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32320797
-|keywords=* Aging
-* Asthma
-* Long-acting muscarinic antagonist
-* Long-acting β(2)-agonists
-* Pharmacotherapy
-|full-text-url=https://sci-hub.do/10.1016/j.jaip.2020.04.013
-}}
-{{medline-entry
-|title=Current Bronchodilator Responsiveness Criteria Underestimate Asthma in Older Adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32071132
-|keywords=* aging
-* albuterol
-* asthma
-* bronchodilator effect
-* lung diseases
-* older adult
-* spirometry
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7538007
-}}
-{{medline-entry
-|title=Physical performances show conflicting associations in aged manual workers.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32042126
-|mesh-terms=* Aged
-* Aging
-* Body Composition
-* Body Mass Index
-* Cardiorespiratory Fitness
-* Cross-Sectional Studies
-* Hand Strength
-* Humans
-* Lung
-* Male
-* Middle Aged
-* Physical Functional Performance
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7010773
-}}
-{{medline-entry
-|title=[[FEV]]  as a Standalone Spirometric Predictor and the Attributable Fraction for Death in Older Persons.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31662447
-|keywords=* aging
-* average attributable fraction
-* death
-* relative risk
-* spirometry
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7055488
-}}
-{{medline-entry
-|title=An Individualized Prediction Model for Long-term Lung Function Trajectory and Risk of COPD in the General Population.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31542453
-|mesh-terms=* Adult
-* Age Factors
-* Aging
-* Alcohol Drinking
-* Algorithms
-* Alkaline Phosphatase
-* Body Height
-* Bronchodilator Agents
-* Cigarette Smoking
-* Cohort Studies
-* Cough
-* Dyspnea
-* Electrocardiography
-* Female
-* Forced Expiratory Volume
-* Hematocrit
-* Humans
-* Leukocyte Count
-* Longitudinal Studies
-* Lung
-* Machine Learning
-* Male
-* Middle Aged
-* Pulmonary Disease, Chronic Obstructive
-* Risk Assessment
-* Serum Albumin
-* Serum Globulins
-* Sex Factors
-* Spirometry
-* Triglycerides
-* Vital Capacity
-|keywords=* COPD
-* FEV(1)
-* FEV(1)/FVC
-* airflow limitation
-* lung function
-* predictive modeling
-|full-text-url=https://sci-hub.do/10.1016/j.chest.2019.09.003
-}}
-{{medline-entry
-|title=Telomere length and lung function in a population-based cohort of children and mid-life adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31456360
-|mesh-terms=* Aged
-* Asthma
-* Body Mass Index
-* Child
-* Cohort Studies
-* Cross-Sectional Studies
-* Exercise
-* Female
-* Forced Expiratory Volume
-* Humans
-* Lung
-* Male
-* Respiratory Function Tests
-* Risk Factors
-* Smoking
-* Spirometry
-* Telomere
-* Vital Capacity
-|keywords=* aging
-* cell senescence
-* life course
-* national cohort
-* spirometry
-|full-text-url=https://sci-hub.do/10.1002/ppul.24489
-}}
-==FGA==
-{{medline-entry
-|title=Goal Pursuit, Goal Adjustment, and Pain in Middle-Aged Adults Aging With Physical Disability.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31718416
-|mesh-terms=* Adaptation, Psychological
-* Aged
-* Aging
-* Depression
-* Disabled Persons
-* Female
-* Goals
-* Humans
-* Male
-* Middle Aged
-* Multiple Sclerosis
-* Muscular Dystrophies
-* Pain
-* Postpoliomyelitis Syndrome
-* Spinal Cord Injuries
-|keywords=* aging
-* disability
-* goal management
-* pain
-* psychological adaptation
-|full-text-url=https://sci-hub.do/10.1177/0898264319827142
-}}
-{{medline-entry
-|title=Tenacious Goal Pursuit, Flexible Goal Adjustment, and Life Satisfaction Among Chinese Older Adult Couples.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31547780
-|keywords=* flexible goal adjustment
-* life satisfaction
-* older couples
-* self-perceptions of aging
-* tenacious goal pursuit
-|full-text-url=https://sci-hub.do/10.1177/0164027519876125
-}}
-==FGF19==
-{{medline-entry
-|title=Bile acid receptor agonists in primary biliary cholangitis: Regulation of the cholangiocyte secretome and downstream T cell differentiation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32123836
-|keywords=* FGF19
-* FXR
-* TGR5
-* autoimmunity
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996327
-}}
-==FGF2==
-{{medline-entry
-|title=The influence of fibroblast growth factor 2 on the senescence of human adipose-derived mesenchymal stem cells during long-term culture.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31840944
-|keywords=* cell proliferation
-* cellular senescence
-* fibroblast growth factor 2
-* long-term culture
-* mesenchymal stem cell
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7103622
-}}
-==FGF21==
-{{medline-entry
-|title=Differential effects of sulfur amino acid-restricted and low-calorie diets on gut microbiome profile and bile acid composition in male C57BL6/J mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33106871
-|keywords=* Clostridales
-* firmicutes
-* lifespan
-* methionine restriction
-* sulfur metabolism
-|full-text-url=https://sci-hub.do/10.1093/gerona/glaa270
-}}
-{{medline-entry
-|title=Relationship between physical activity and circulating fibroblast growth factor 21 in middle-aged and older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32911033
-|keywords=* Accelerometer
-* Activity intensity
-* Aging
-* FGF21
-* Physical activity
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.111081
-}}
-{{medline-entry
-|title=Exercise and dietary intervention ameliorate high-fat diet-induced NAFLD and liver aging by inducing lipophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32863214
-|keywords=* Aging
-* Exercise
-* FGF21
-* Lipophagy
-* Nonalcoholic fatty liver disease (NAFLD)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7365984
-}}
-{{medline-entry
-|title=Mitochondria, immunosenescence and inflammaging: a role for mitokines?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32757036
-|keywords=* Human ageing
-* Immunosenescence
-* Inflammaging
-* Mitochondrial metabolism
-* Mitokines
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7666292
-}}
-{{medline-entry
-|title=Age-at-onset-dependent effects of sulfur amino acid restriction on markers of growth and stress in male F344 rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32573078
-|keywords=* ER stress
-* cysteine
-* glutathione
-* hormesis
-* lifespan
-* methionine
-* trade-offs
-* translational
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7426777
-}}
-{{medline-entry
-|title=Fibroblast growth factor 21 prolongs lifespan and improves stress tolerance in the silkworm, [i]Bombyx mori[/i].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32309367
-|keywords=* Bombyx mori
-* fibroblast growth factor 21 (FGF21)
-* lifespan
-* oxidation resistance
-* stress tolerance
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7154471
-}}
-{{medline-entry
-|title=Neurogenesis and prolongevity signaling in young germ-free mice transplanted with the gut microbiota of old mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31723038
-|mesh-terms=* Animals
-* Butyrates
-* Fecal Microbiota Transplantation
-* Fibroblast Growth Factors
-* Gastrointestinal Microbiome
-* Germ-Free Life
-* Hippocampus
-* Intestines
-* Liver
-* Longevity
-* Male
-* Metabolome
-* Mice, Inbred C57BL
-* Microtubule-Associated Proteins
-* Neurogenesis
-* Neurons
-* Neuropeptides
-* Phenotype
-* Proton Magnetic Resonance Spectroscopy
-|full-text-url=https://sci-hub.do/10.1126/scitranslmed.aau4760
-}}
-{{medline-entry
-|title=Fibroblast Growth Factor 21 Mediates the Associations between Exercise, Aging, and Glucose Regulation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31490857
-|mesh-terms=* Adiponectin
-* Adult
-* Aging
-* Blood Glucose
-* Blood Pressure
-* Body Mass Index
-* Diabetes Mellitus, Type 2
-* Exercise
-* Female
-* Fibroblast Growth Factors
-* Glucose Tolerance Test
-* Humans
-* Insulin
-* Lipids
-* Male
-* Middle Aged
-* Risk Factors
-|full-text-url=https://sci-hub.do/10.1249/MSS.0000000000002150
-}}
-{{medline-entry
-|title=Effects of Moderate Chronic Food Restriction on the Development of Postprandial Dyslipidemia with Ageing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31405194
-|mesh-terms=* Adiposity
-* Aging
-* Animals
-* Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
-* Blood Glucose
-* Diet, Fat-Restricted
-* Dietary Fats
-* Disease Models, Animal
-* Dyslipidemias
-* Glucagon
-* Insulin
-* Lipids
-* Liver
-* Metabolic Syndrome
-* Postprandial Period
-* Rats
-* Rats, Wistar
-* Triglycerides
-|keywords=* ChREBP
-* adipose tissue
-* ageing
-* oral lipid loading test
-* postprandial hypertrigliceridemia
-* postprandial thermogenesis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6723802
-}}
-==FGF23==
-{{medline-entry
-|title=Phosphate as a Pathogen of Arteriosclerosis and Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33028781
-|keywords=* Aging
-* Calciprotein particles (CPPs)
-* Fibroblast growth factor-23 (FGF23)
-* Inflammation
-* Klotho
-* Phosphate
-* Vascular calcification
-|full-text-url=https://sci-hub.do/10.5551/jat.RV17045
-}}
-{{medline-entry
-|title=Plasma Soluble αKlotho, Serum Fibroblast Growth Factor 23, and Mobility Disability in Community-Dwelling Older Adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32405607
-|keywords=* aging
-* chronic kidney disease
-* fibroblast growth factor 23
-* mobility disability
-* αKlotho
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7209777
-}}
-{{medline-entry
-|title=Protective effect of Polygonatum sibiricum Polysaccharide on D-galactose-induced aging rats model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32042011
-|mesh-terms=* Aging
-* Animals
-* Calcium
-* Dietary Carbohydrates
-* Fibroblast Growth Factors
-* Galactose
-* Glucuronidase
-* Male
-* Oxidative Stress
-* Phosphorus
-* Phytochemicals
-* Polygonatum
-* Polysaccharides
-* Protective Agents
-* Rats
-* Rats, Sprague-Dawley
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7010663
-}}
-{{medline-entry
-|title=[[FGF23]] expression is stimulated in transgenic α-Klotho longevity mouse model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31801907
-|mesh-terms=* Aldosterone
-* Animals
-* Bone and Bones
-* Cardiovascular Diseases
-* Disease Models, Animal
-* Female
-* Fibroblast Growth Factors
-* Gene Knockout Techniques
-* Glucuronidase
-* Kidney
-* Longevity
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Mice, Transgenic
-* Osteoblasts
-* Protein Isoforms
-* Transcriptome
-|keywords=* Bone Biology
-* Cardiovascular disease
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6962016
-}}
-{{medline-entry
-|title=Fibroblast growth factor 23 and symmetric dimethylarginine concentrations in geriatric cats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31568615
-|mesh-terms=* Aging
-* Animals
-* Arginine
-* Biomarkers
-* Cats
-* Cross-Sectional Studies
-* Female
-* Fibroblast Growth Factors
-* Male
-* Reference Values
-* Retrospective Moral Judgment
-|keywords=* azotemia
-* feline
-* phosphate
-* renal
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6872607
-}}
-==FGFR1==
-{{medline-entry
-|title=Alignment of Alzheimer's disease amyloid β-peptide and klotho.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32999998
-|keywords=* Alzheimer’s disease
-* HSV-1
-* aging
-* alignment
-* klotho
-* neurodegeneration
-* neuroinflammation
-* protein
-* ubiquitin
-* β-amyloid
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7521834
-}}
-{{medline-entry
-|title=Satellite cell-specific ablation of Cdon impairs integrin activation, FGF signalling, and muscle regeneration.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32103583
-|keywords=* Cdon
-* Cellular senescence
-* FGFR
-* Growth factor signalling
-* Muscle regeneration
-* Satellite cell
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432598
-}}
-==FGFR4==
-{{medline-entry
-|title=[[FGFR4]] Inhibitor BLU9931 Attenuates Pancreatic Cancer Cell Proliferation and Invasion While Inducing Senescence: Evidence for Senolytic Therapy Potential in Pancreatic Cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33066597
-|keywords=* FGFR4
-* FGFR4 inhibitor
-* growth
-* invasion
-* pancreatic cancer
-* senescence
-* senolytic therapy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7602396
-}}
-==FGR==
-{{medline-entry
-|title=Aurora kinase mRNA expression is reduced with increasing gestational age and in severe early onset fetal growth restriction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32452402
-|keywords=* Aurora kinase
-* Cellular senescence
-* FGR
-* Preeclampsia
-|full-text-url=https://sci-hub.do/10.1016/j.placenta.2020.04.012
-}}
-==FH==
-{{medline-entry
-|title=Genetic Factors of Alzheimer's Disease Modulate How Diet is Associated with Long-Term Cognitive Trajectories: A UK Biobank Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33252089
-|keywords=* APOE4
-* Aging
-* Mediterranean diet
-* cognitive decline
-* functional food
-* lamb
-* nutrition policy
-* preventive medicine
-* red wine
-* salt
-|full-text-url=https://sci-hub.do/10.3233/JAD-201058
-}}
-{{medline-entry
-|title=Volumetric alterations in the hippocampal subfields of subjects at increased risk of dementia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32311609
-|mesh-terms=* Adult
-* Aging
-* Alzheimer Disease
-* Apolipoproteins E
-* Atrophy
-* Dementia
-* Diffusion Magnetic Resonance Imaging
-* Educational Status
-* Female
-* Genotype
-* Hippocampus
-* Humans
-* Male
-* Middle Aged
-* Organ Size
-* Risk
-|keywords=* Alzheimer's disease
-* Dementia
-* Hippocampal subfields
-* Hippocampus
-* Preclinical dementia
-|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.03.006
-}}
-{{medline-entry
-|title=Macroscopic hematuria as a risk factor for hypertension in ageing people with hemophilia and a family history of hypertension.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32118768
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Cross-Sectional Studies
-* Female
-* Hematuria
-* Hemophilia A
-* Humans
-* Hypertension
-* Israel
-* Logistic Models
-* Male
-* Middle Aged
-* Risk Factors
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7478422
-}}
-{{medline-entry
-|title=LDL Receptor Deficiency Does not Alter Brain Amyloid-β Levels but Causes an Exacerbation of Apoptosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31815695
-|mesh-terms=* Aging
-* Amyloid beta-Protein Precursor
-* Animals
-* Apoptosis
-* Brain Chemistry
-* Caspase 3
-* Cholesterol
-* Gene Expression
-* Hippocampus
-* Male
-* Maze Learning
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Prefrontal Cortex
-* Receptors, LDL
-|keywords=* Familial hypercholesterolemia
-* LDLr-/- mice
-* amyloid-β
-* apoptosis
-* memory impairment
-|full-text-url=https://sci-hub.do/10.3233/JAD-190742
-}}
-==FNDC5==
-{{medline-entry
-|title=Irisin Correlates Positively With BMD in a Cohort of Older Adult Patients and Downregulates the Senescent Marker p21 in Osteoblasts.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33053231
-|keywords=* BONE-MUSCLE INTERACTIONS
-* IRISIN
-* OSTEOPOROSIS
-* SARCOPENIA
-* SENESCENCE
-|full-text-url=https://sci-hub.do/10.1002/jbmr.4192
-}}
-{{medline-entry
-|title=[Investigation of signal molecules in saliva: prospects of application for diagnostics of myocardial infarction and the aging rate of different age people.]
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31512422
-|mesh-terms=* Aged
-* Aging
-* Biomarkers
-* Cytokines
-* Humans
-* Middle Aged
-* Myocardial Infarction
-* Saliva
-* Tumor Necrosis Factor-alpha
-|keywords=* aging
-* diagnosis
-* myocardial infarction
-* saliva
-* signaling molecules
-}}
-==FOS==
-{{medline-entry
-|title=Muscle atrophy-related myotube-derived exosomal microRNA in neuronal dysfunction: Targeting both coding and long noncoding RNAs.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32233025
-|keywords=* HIF-1α-AS2
-* aging
-* lncRNAs
-* miR-29b-3p
-* muscle atrophy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7253071
-}}
-==FOSL2==
-{{medline-entry
-|title=LncRNA GUARDIN suppresses cellular senescence through a LRP130-PGC1α-FOXO4-p21-dependent signaling axis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32149459
-|keywords=*
-GUARDIN
-* LRP130-PGC1α
-* cellular senescence
-* lncRNAs
-* p21
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7132339
-}}
-==FOXA1==
-{{medline-entry
-|title=Analyses of an epigenetic switch involved in the activation of pioneer factor [[FOXA1]] leading to the prognostic value of estrogen receptor and [[FOXA1]] co-expression in breast cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31562808
-|mesh-terms=* Breast Neoplasms
-* Down-Regulation
-* Epigenesis, Genetic
-* Female
-* Gene Expression Regulation, Neoplastic
-* Hepatocyte Nuclear Factor 3-alpha
-* Humans
-* Middle Aged
-* Prognosis
-* RNA, Messenger
-* Receptor, ErbB-2
-* Receptors, Estrogen
-* Receptors, Progesterone
-* Transcriptome
-* Up-Regulation
-|keywords=* FOXA1
-* age-related diseases
-* aging
-* breast cancer
-* hormone receptor
-* methylation
-* prognosis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6782010
-}}
-==FOXM1==
-{{medline-entry
-|title=Sirtuin 6 deficiency induces endothelial cell senescence via downregulation of forkhead box M1 expression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33171439
-|keywords=* FOXM1
-* SIRT6
-* cell cycle
-* endothelial cell
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7695388
-}}
-==FOXN1==
-{{medline-entry
-|title=Thymic rejuvenation via [[FOXN1]]-reprogrammed embryonic fibroblasts (FREFs) to counteract age-related inflammation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32790650
-|keywords=* Aging
-* Immunology
-* Immunotherapy
-* T cell development
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7526556
-}}
-==FOXO1==
-{{medline-entry
-|title=l-Theanine attenuates liver aging by inhibiting advanced glycation end products in d-galactose-induced rats and reversing an imbalance of oxidative stress and inflammation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31899338
-|keywords=* AGEs
-* Inflammatory response
-* Liver aging
-* Oxidative stress
-* l-Theanine
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2019.110823
-}}
-==FOXO3==
-{{medline-entry
-|title=The DNA methylation of [[FOXO3]] and TP53 as a blood biomarker of late-onset asthma.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33298101
-|keywords=* Aging
-* DNA methylation
-* FOXO3
-* Late-onset asthma
-* TP53
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7726856
-}}
-{{medline-entry
-|title=[[FOXO3]] targets are reprogrammed as Huntington's disease neural cells and striatal neurons face senescence with p16  increase.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33156570
-|keywords=* neurodegenerative disease
-* neuronal differentiation
-* neuronal senescence
-* response mechanisms
-* temporal dynamics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7681055
-}}
-{{medline-entry
-|title=Astaxanthin as a Putative Geroprotector: Molecular Basis and Focus on Brain Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32635607
-|keywords=* FOXO3
-* NRF2
-* SIRT1
-* astaxanthin
-* geroprotector
-* longevity
-* neuroprotection
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7401246
-}}
-{{medline-entry
-|title=Inflamma-miR-21 Negatively Regulates Myogenesis during Ageing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32340146
-|keywords=* IL6
-* IL6R
-* aging
-* cachexia
-* miR-21
-* microRNA
-* muscle
-* regeneration
-* sarcopenia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7222422
-}}
-{{medline-entry
-|title=Variable DNA methylation of aging-related genes is associated with male COPD.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31684967
-|mesh-terms=* Adolescent
-* Adult
-* Age Factors
-* Aged
-* Aged, 80 and over
-* Aging
-* Case-Control Studies
-* CpG Islands
-* DNA Methylation
-* Databases, Genetic
-* Female
-* Forced Expiratory Volume
-* Forkhead Transcription Factors
-* Genetic Predisposition to Disease
-* Humans
-* Lung
-* Male
-* Middle Aged
-* Pulmonary Disease, Chronic Obstructive
-* Risk Assessment
-* Risk Factors
-* Severity of Illness Index
-* Sex Factors
-* Transcriptome
-* Vital Capacity
-* Young Adult
-|keywords=* Aging
-* Aging-related genes
-* COPD
-* DNA methylation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6829949
-}}
-{{medline-entry
-|title=A conserved role of the insulin-like signaling pathway in diet-dependent uric acid pathologies in Drosophila melanogaster.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31415568
-|mesh-terms=* Animals
-* Animals, Genetically Modified
-* Cohort Studies
-* Disease Models, Animal
-* Drosophila melanogaster
-* Feeding Behavior
-* Female
-* Gene Knockdown Techniques
-* Gout
-* Humans
-* Insulin
-* Kidney Calculi
-* Longevity
-* Male
-* Metabolic Networks and Pathways
-* Middle Aged
-* NADPH Oxidases
-* Polymorphism, Single Nucleotide
-* Purines
-* Signal Transduction
-* Urate Oxidase
-* Uric Acid
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6695094
-}}
-==FOXO4==
-{{medline-entry
-|title=[[FOXO4]]-DRI alleviates age-related testosterone secretion insufficiency by targeting senescent Leydig cells in aged mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31959736
-|keywords=* FOXO4-DRI
-* Leydig cell
-* male late-onset hypogonadism
-* senescence
-* senolytics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053614
-}}
-==FOXP1==
-{{medline-entry
-|title=GATA6 regulates aging of human mesenchymal stem/stromal cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33252174
-|keywords=* aging
-* cell signaling
-* mesenchymal stem cells
-* reprogramming
-* transcription factors
-|full-text-url=https://sci-hub.do/10.1002/stem.3297
-}}
-==FSHR==
-{{medline-entry
-|title=[[FSHR]] ablation induces depression-like behaviors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32203083
-|keywords=* FSH
-* ROS
-* aging
-* antioxidants
-* depression
-* metabolism
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7468367
-}}
-{{medline-entry
-|title=Direct actions of gonadotropins beyond the reproductive system and their role in human aging and neoplasia [Bezpośrednie działanie gonadotropin poza układem rozrodczym i ich rola w starzeniu się i nowotworzeniu u człowieka].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31681968
-|mesh-terms=* Aging
-* Female
-* Gonadotropin-Releasing Hormone
-* Gonadotropins
-* Humans
-* Hypothalamo-Hypophyseal System
-* Luteinizing Hormone
-* Male
-* Receptors, FSH
-* Receptors, LH
-|keywords=* aging
-* folitropin
-* lutropin
-* neoplasia
-|full-text-url=https://sci-hub.do/10.5603/EP.a2019.0034
-}}
-==FTO==
-{{medline-entry
-|title=Decreased expression of m A demethylase [[FTO]] in ovarian aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33221958
-|keywords=* Epigenetics
-* FTO
-* Ovarian aging
-* Ovarian reserve
-* m6A
-|full-text-url=https://sci-hub.do/10.1007/s00404-020-05895-7
-}}
-==FYN==
-{{medline-entry
-|title=An inhibitor role of Nrf2 in the regulation of myocardial senescence and dysfunction after myocardial infarction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32781064
-|mesh-terms=* Animals
-* Cardiomyopathies
-* Cellular Senescence
-* Echocardiography
-* Gene Silencing
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Myocardial Infarction
-* Myocardium
-* Myocytes, Cardiac
-* NF-E2-Related Factor 2
-* RNA, Small Interfering
-* Ventricular Remodeling
-|keywords=* Cellular senescence
-* Myocardial infarction
-* Nrf2
-* Oxidative stress
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2020.118199
-}}
-==G6PD==
-{{medline-entry
-|title=[[G6PD]] overexpression protects from oxidative stress and age-related hearing loss.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33222382
-|keywords=* ARHL
-* NADPH
-* TrxR
-* aging
-* glutathione
-|full-text-url=https://sci-hub.do/10.1111/acel.13275
-}}
-{{medline-entry
-|title=The Sickle Effect: The Silent Titan Affecting Glycated Hemoglobin Reliability.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32923278
-|keywords=* diabetes
-* genetics
-* glycosylated hemoglobin
-* hba1c
-* hbas
-* race
-* rbc lifespan
-* sickle cell trait
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7486097
-}}
-{{medline-entry
-|title=DNA damage and synaptic and behavioural disorders in glucose-6-phosphate dehydrogenase-deficient mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31581069
-|mesh-terms=* Animals
-* Brain
-* DNA Breaks, Double-Stranded
-* DNA Breaks, Single-Stranded
-* DNA Damage
-* Disease Models, Animal
-* Enzyme Activation
-* Female
-* Glucosephosphate Dehydrogenase
-* Glucosephosphate Dehydrogenase Deficiency
-* Male
-* Mental Disorders
-* Mice
-* Oxidation-Reduction
-* Purkinje Cells
-|keywords=* 8-Oxo-2′-deoxyguanine (8-oxodG)
-* Aging
-* Behavioural disorders
-* Comet
-* DNA damage
-* Electrophysiology
-* Gamma-H2AX (γH2AX)
-* Glucose-6-phosphate dehydrogenase (G6PD)
-* Lifespan
-* Neurodegeneration
-* Reactive oxygen species (ROS)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6812046
-}}
-==GAA==
-{{medline-entry
-|title=Mitochondrial damage and senescence phenotype of cells derived from a novel frataxin G127V point mutation mouse model of Friedreich's ataxia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32586831
-|keywords=* Frataxin
-* Friedreich's ataxia
-* Mitochondria
-* Oxidative stress
-* Point mutation
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7406325
-}}
-{{medline-entry
-|title=Age-Related Changes in Serum Guanidinoacetic Acid in Women.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31647299
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aging
-* Biomarkers
-* Energy Metabolism
-* Exercise
-* Female
-* Glycine
-* Humans
-* Independent Living
-* Middle Aged
-* Young Adult
-|full-text-url=https://sci-hub.do/10.33549/physiolres.934189
-}}
-==GABARAP==
-{{medline-entry
-|title=Age-dependent loss of adipose Rubicon promotes metabolic disorders via excess autophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32811819
-|mesh-terms=* Adipocytes
-* Adipogenesis
-* Adipose Tissue
-* Adiposity
-* Aging
-* Animals
-* Apoptosis Regulatory Proteins
-* Autophagy
-* Fatty Liver
-* Gene Knockout Techniques
-* Glucose
-* HEK293 Cells
-* Humans
-* Intracellular Signaling Peptides and Proteins
-* Lipid Metabolism
-* Metabolic Diseases
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Microtubule-Associated Proteins
-* Nuclear Receptor Coactivator 1
-* Nuclear Receptor Coactivator 2
-* PPAR gamma
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7434891
-}}
-==GAL==
-{{medline-entry
-|title=Overexpression of Pitx1 attenuates the senescence of chondrocytes from osteoarthritis degeneration cartilage-A self-controlled model for studying the etiology and treatment of osteoarthritis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31783149
-|keywords=* Osteoarthritis
-* Pitx1
-* Senescence
-* Sirt1
-|full-text-url=https://sci-hub.do/10.1016/j.bone.2019.115177
-}}
-{{medline-entry
-|title=β-Caryophyllene Reduces DNA Oxidation and the Overexpression of Glial Fibrillary Acidic Protein in the Prefrontal Cortex and Hippocampus of d-Galactose-Induced Aged BALB/c Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31663807
-|mesh-terms=* Aging
-* Animals
-* Antioxidants
-* DNA Damage
-* Disease Models, Animal
-* Galactose
-* Glial Fibrillary Acidic Protein
-* Hippocampus
-* Male
-* Mice
-* Mice, Inbred BALB C
-* Neuroprotection
-* Oxidative Stress
-* Polycyclic Sesquiterpenes
-* Prefrontal Cortex
-|keywords=* CB2 receptor agonist
-* biological aging
-* cognitive flexibility
-* phytocannabinoid
-* β-caryophyllene
-|full-text-url=https://sci-hub.do/10.1089/jmf.2019.0111
-}}
-==GAP43==
-{{medline-entry
-|title=HDAC inhibition leads to age-dependent opposite regenerative effect upon PTEN deletion in rubrospinal axons after SCI.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32171589
-|mesh-terms=* Aging
-* Animals
-* Axons
-* GAP-43 Protein
-* Gene Deletion
-* Gene Expression
-* Histone Deacetylase Inhibitors
-* Histone Deacetylases
-* Hydroxamic Acids
-* Mice, Transgenic
-* Motor Activity
-* Nerve Regeneration
-* PTEN Phosphohydrolase
-* Recovery of Function
-* Spinal Cord
-* Spinal Cord Injuries
-|keywords=* Aging
-* Epigenetics
-* Histone deacetylase
-* Pten
-* Regeneration
-* Spinal cord injury
-|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.02.006
-}}
-==GATA4==
-{{medline-entry
-|title=Epigenetics and Vascular Senescence-Potential New Therapeutic Targets?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33101015
-|keywords=* calcification
-* cell senescence
-* epigenetics
-* inflammation
-* oxidation stress
-* vascular aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7556287
-}}
-{{medline-entry
-|title=Prolonged treatment with Y-27632 promotes the senescence of primary human dermal fibroblasts by increasing the expression of IGFBP-5 and transforming them into a CAF-like phenotype.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32843583
-|keywords=* IGFBP-5
-* Rho kinase inhibitor
-* Y-27632
-* dermal fibroblast
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7485707
-}}
-==GBA==
-{{medline-entry
-|title=Reduced sphingolipid hydrolase activities, substrate accumulation and ganglioside decline in Parkinson's disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31703585
-|mesh-terms=* Aged
-* Aging
-* Female
-* Glucosylceramidase
-* Humans
-* Hydrolases
-* Lysosomes
-* Male
-* Mutation
-* Parkinson Disease
-* Risk Factors
-* Substantia Nigra
-* alpha-Synuclein
-|keywords=* Ageing
-* Ganglioside
-* Glucocerebrosidase
-* Glycosphingolipid
-* Lysosome
-* Neurodegeneration
-* Parkinson’s disease
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6842240
-}}
-==GC==
-{{medline-entry
-|title=Body Size and Cuticular Hydrocarbons as Larval Age Indicators in the Forensic Blow Fly, Chrysomya albiceps (Diptera: Calliphoridae).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33274739
-|keywords=*
-          Chrysomya albiceps
-* body size
-* cuticular hydrocarbon
-* forensic
-* larval longevity
-|full-text-url=https://sci-hub.do/10.1093/jme/tjaa256
-}}
-{{medline-entry
-|title=Composition of peony petal fatty acids and flavonoids and their effect on Caenorhabditis elegans lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33092723
-|keywords=* Caenorhabditis elegans
-* Fatty acid
-* Flavonoid identification and composition
-* Lifespan extension
-* Tree peony petal
-|full-text-url=https://sci-hub.do/10.1016/j.plaphy.2020.06.029
-}}
-{{medline-entry
-|title=Photo aging and fragmentation of polypropylene food packaging materials in artificial seawater.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33039831
-|keywords=* Aging
-* Antioxidant
-* Food packaging materials
-* Microplastics
-* Polypropylene
-* seawater
-|full-text-url=https://sci-hub.do/10.1016/j.watres.2020.116456
-}}
-{{medline-entry
-|title=Secretory galectin-3 induced by glucocorticoid stress triggers stemness exhaustion of hepatic progenitor cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32989051
-|keywords=* AMP-activated kinase (AMPK)
-* Cell senescence
-* cell cycle
-* cellular senescence
-* galectin
-* galectin-3
-* glycoprotein
-* liver injury
-* proliferation
-* protein interaction
-* protein-protein interaction
-* quiescence
-* stem cells
-* stemness exhaustion
-|full-text-url=https://sci-hub.do/10.1074/jbc.RA120.012974
-}}
-{{medline-entry
-|title=Optimization of Ethanol Detection by Automatic Headspace Method for Cellulose Insulation Aging of Oil-immersed Transformers.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32679756
-|keywords=* aging
-* cellulose insulation
-* gas chromatography
-* headspace sampling
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7407484
-}}
-{{medline-entry
-|title=Sensory, olfactometric and chemical characterization of the aroma potential of Garnacha and Tempranillo winemaking grapes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32569964
-|mesh-terms=* Fruit
-* Gas Chromatography-Mass Spectrometry
-* Hexanols
-* Norisoprenoids
-* Odorants
-* Olfactometry
-* Principal Component Analysis
-* Sulfhydryl Compounds
-* Vitis
-* Volatile Organic Compounds
-|keywords=* Aging
-* Aroma precursors
-* Glycosides
-* Lipid-derived aroma
-* Norisoprenoids
-* Sensory properties
-* Terpenols
-* Volatile phenols
-|full-text-url=https://sci-hub.do/10.1016/j.foodchem.2020.127207
-}}
-{{medline-entry
-|title=Accelerated Cognitive Ageing in epilepsy: exploring the effective connectivity between resting-state networks and its relation to cognitive decline.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32529058
-|keywords=* Accelerated cognitive ageing
-* Ageing
-* Aging
-* Biomarkers
-* Clinical research
-* Cognition
-* Cognitive decline
-* Cognitive neuroscience
-* Effective connectivity
-* Epilepsy
-* Fmri
-* Granger causality
-* Image processing
-* Medical imaging
-* Mental health
-* Nervous system
-* Neuroscience
-* Psychiatry
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7283153
-}}
-{{medline-entry
-|title=Characterization of Jinhua ham aroma profiles in specific to aging time by gas chromatography-ion mobility spectrometry ([[GC]]-IMS).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32417671
-|keywords=* Aging
-* Electronic-nose
-* Gas chromatography-ion mobility spectrometry
-* Jinhua ham
-* Volatiles
-|full-text-url=https://sci-hub.do/10.1016/j.meatsci.2020.108178
-}}
-{{medline-entry
-|title=Quantitative Profiling of Lipid Species in Caenorhabditis elegans with Gas Chromatography-Mass Spectrometry.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32410029
-|keywords=* Aging
-* C. elegans
-* Fat
-* Fatty acids
-* Gas chromatography–mass spectrometry
-* Lipids
-* Phospholipids
-* Solid-phase chromatography
-* Triglycerides
-|full-text-url=https://sci-hub.do/10.1007/978-1-0716-0592-9_10
-}}
-{{medline-entry
-|title=Physicochemical characterization of a polysaccharide from Agrocybe aegirita and its anti-ageing activity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32172871
-|mesh-terms=* Aging
-* Agrocybe
-* Antioxidants
-* Carbohydrate Sequence
-* Cell Line
-* Chemical Phenomena
-* G1 Phase Cell Cycle Checkpoints
-* Humans
-* Membrane Potential, Mitochondrial
-* Mitochondria
-* Polysaccharides
-|keywords=* Agrocybe aegirita polysaccharide
-* Anti-ageing
-* Cell cycle
-* Mitochondrial membrane potential
-* Structure
-|full-text-url=https://sci-hub.do/10.1016/j.carbpol.2020.116056
-}}
-{{medline-entry
-|title=Structural characteristics, antioxidant properties and antiaging activities of galactan produced by Mentha haplocalyx Briq.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32070549
-|mesh-terms=* Aging
-* Animals
-* Antioxidants
-* Biphenyl Compounds
-* Carbohydrate Conformation
-* Galactans
-* Male
-* Mentha
-* Mice
-* Mice, Inbred Strains
-* Particle Size
-* Picrates
-* Surface Properties
-|keywords=* Anti-aging activity
-* Antioxidant activity
-* Mentha haplocalyx Briq
-* Polysaccharides
-|full-text-url=https://sci-hub.do/10.1016/j.carbpol.2020.115936
-}}
-{{medline-entry
-|title=Contribution of Volatile Odorous Terpenoid Compounds to Aged Cognac Spirits Aroma in a Context of Multicomponent Odor Mixtures.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32052967
-|keywords=* Cognac
-* aging aroma
-* lees
-* monoterpenes
-* perceptual synergic effects
-|full-text-url=https://sci-hub.do/10.1021/acs.jafc.9b06656
-}}
-{{medline-entry
-|title=Plasma Formate Is Greater in Fetal and Neonatal Rats Compared with Their Mothers.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31912134
-|mesh-terms=* Aging
-* Animals
-* Animals, Newborn
-* Female
-* Fetus
-* Formates
-* Liver
-* Maternal-Fetal Exchange
-* Mothers
-* Placenta
-* Pregnancy
-* Rats
-* Rats, Sprague-Dawley
-|keywords=* fetus
-* glycine
-* methionine
-* mitochondria
-* one-carbon metabolism
-* pregnancy
-* serine
-* tetrahydrofolate
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7198295
-}}
-{{medline-entry
-|title=Development of a new strategy for studying the aroma potential of winemaking grapes through the accelerated hydrolysis of phenolic and aromatic fractions (PAFs).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31882095
-|keywords=* Aging
-* Glycosidic precursors
-* Grape aroma
-* Grape quality
-* Hydrolysis
-* Polyphenols
-* Wine
-|full-text-url=https://sci-hub.do/10.1016/j.foodres.2019.108728
-}}
-{{medline-entry
-|title=Compromised steady-state germinal center activity with age in nonhuman primates.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31840398
-|mesh-terms=* Aging
-* Animals
-* Antigens, CD
-* B-Lymphocytes
-* CD4-Positive T-Lymphocytes
-* CD8-Positive T-Lymphocytes
-* Forkhead Transcription Factors
-* Germinal Center
-* Granulocytes
-* Immunity, Humoral
-* Inflammation
-* Lymph Nodes
-* Macaca mulatta
-* Monocytes
-|keywords=* B cells
-* Tfh cells
-* aging
-* follicles
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996951
-}}
-{{medline-entry
-|title=Endogenous Glucocorticoid Signaling in the Regulation of Bone and Marrow Adiposity: Lessons from Metabolism and Cross Talk in Other Tissues.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31749087
-|mesh-terms=* Adipose Tissue
-* Adiposity
-* Animals
-* Bone Marrow
-* Energy Metabolism
-* Glucocorticoids
-* Homeostasis
-* Humans
-* Liver
-* Muscle, Skeletal
-* Receptor Cross-Talk
-* Receptors, Glucocorticoid
-* Signal Transduction
-* Stress, Physiological
-|keywords=* Adipocyte
-* Aging
-* Bone marrow
-* Corticosterone
-* Cortisol
-* Cortisone
-* Glucocorticoid
-* Osteoblast
-|full-text-url=https://sci-hub.do/10.1007/s11914-019-00554-6
-}}
-{{medline-entry
-|title=4,5-Diphenyl-2-methyl picolinate induces cellular senescence by accumulating DNA damage and activating associated signaling pathways in gastric cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31639393
-|mesh-terms=* Animals
-* Antineoplastic Agents
-* Apoptosis
-* Cell Cycle
-* Cell Proliferation
-* Cellular Senescence
-* DNA Damage
-* Humans
-* Mice
-* Mice, Inbred BALB C
-* Mice, Nude
-* Picolinic Acids
-* Signal Transduction
-* Stomach Neoplasms
-* Tumor Cells, Cultured
-* Xenograft Model Antitumor Assays
-|keywords=* Cellular senescence
-* DNA damage
-* Gastric cancer
-* N-heterocyclic compound
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2019.116973
-}}
-{{medline-entry
-|title=Relationship Between the Dose Administered, Target Tissue Dose, and Toxicity Level After Acute Oral Exposure to Bifenthrin and Tefluthrin in Young Adult Rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31573616
-|mesh-terms=* Administration, Oral
-* Aging
-* Animals
-* Body Temperature
-* Cerebellum
-* Cyclopropanes
-* Dose-Response Relationship, Drug
-* Hydrocarbons, Fluorinated
-* Liver
-* Male
-* Pyrethrins
-* Rats
-* Rats, Wistar
-* Tissue Distribution
-* Toxicokinetics
-|keywords=* acute effects
-* bifenthrin
-* body temperature
-* disposition
-* rat
-* tefluthrin
-|full-text-url=https://sci-hub.do/10.1093/toxsci/kfz204
-}}
-{{medline-entry
-|title=Sugar Beet Pectin Supplementation Did Not Alter Profiles of Fecal Microbiota and Exhaled Breath in Healthy Young Adults and Healthy Elderly.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31547291
-|mesh-terms=* Aged
-* Beta vulgaris
-* Breath Tests
-* Dietary Supplements
-* Double-Blind Method
-* Exhalation
-* Fatty Acids, Volatile
-* Feces
-* Female
-* Gastrointestinal Microbiome
-* Healthy Volunteers
-* Humans
-* Male
-* Pectins
-* Volatile Organic Compounds
-* Young Adult
-|keywords=* aging
-* dietary fiber
-* elderly
-* exhaled air
-* microbiota
-* pectin
-* young adults
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6770243
-}}
-{{medline-entry
-|title=Identification and analysis of new α- and β-hydroxy ketones related to the formation of 3-methyl-2,4-nonanedione in musts and red wines.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31520920
-|mesh-terms=* Alkanes
-* Diacetyl
-* Ethanol
-* Fruit and Vegetable Juices
-* Gas Chromatography-Mass Spectrometry
-* Humans
-* Hydrogen-Ion Concentration
-* Ketones
-* Limit of Detection
-* Solid Phase Microextraction
-* Stereoisomerism
-* Time Factors
-* Wine
-|keywords=* 3-methyl-2,4-nonanedione
-* Aroma precursor
-* Hydroxy ketones
-* Oxidation
-* Premature aging
-* Wine
-|full-text-url=https://sci-hub.do/10.1016/j.foodchem.2019.125486
-}}
-{{medline-entry
-|title=Neonatal T Follicular Helper Cells Are Lodged in a Pre-T Follicular Helper Stage Favoring Innate Over Adaptive Germinal Center Responses.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31456798
-|mesh-terms=* Adaptive Immunity
-* Adjuvants, Immunologic
-* Aging
-* Animals
-* Animals, Newborn
-* Germinal Center
-* Immunity, Innate
-* Interleukin-13
-* Lymphopoiesis
-* Mice, Inbred C57BL
-* T-Lymphocytes, Helper-Inducer
-* Th2 Cells
-* Transcriptome
-|keywords=* T follicular helper cells
-* adjuvant
-* neonates
-* transcriptional profile analysis
-* vaccines
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6700230
-}}
-{{medline-entry
-|title=Identification of Dialkylpyrazines Off-Flavors in Oak Wood.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31423769
-|mesh-terms=* Flavoring Agents
-* Gas Chromatography-Mass Spectrometry
-* Odorants
-* Olfactometry
-* Pyrazines
-* Quercus
-* Wood
-|keywords=* aroma
-* barrel aging
-* dialkylpyrazine
-* oak wood
-* off-flavor
-* wine
-|full-text-url=https://sci-hub.do/10.1021/acs.jafc.9b03185
-}}
-{{medline-entry
-|title=Metabolomics Coupled with Transcriptomics Approach Deciphering Age Relevance in Sepsis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31440390
-|keywords=* aging
-* biomarker
-* metabolomics
-* sepsis
-* transcriptomics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6675524
-}}
-==GCA==
-{{medline-entry
-|title=Familial aggregation of longevity in giant cell arteritis and polymyalgia rheumatica.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32683496
-|keywords=* Giant cell arteritis
-* Longevity
-* Mortality
-* Polymyalgia rheumatica
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7591435
-}}
-{{medline-entry
-|title=Interaction between Alcohol Consumption and Apolipoprotein E (ApoE) Genotype with Cognition in Middle-Aged Men.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32662384
-|keywords=* Aging
-* Alcohol drinking
-* Apolipoprotein E4 (ApoE)
-* Cognitive abilities
-* Male
-* Middle aged
-* Risk factors
-|full-text-url=https://sci-hub.do/10.1017/S1355617720000570
-}}
-==GCK==
-{{medline-entry
-|title=The Impact of Biomarker Screening and Cascade Genetic Testing on the Cost-Effectiveness of MODY Genetic Testing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31558549
-|mesh-terms=* Biomarkers
-* Child
-* Cost-Benefit Analysis
-* Diabetes Mellitus, Type 2
-* Female
-* Genetic Testing
-* Health Care Costs
-* Humans
-* Life Expectancy
-* Male
-* Mass Screening
-* Pedigree
-* Precision Medicine
-* Quality-Adjusted Life Years
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6868460
-}}
-==GCLC==
-{{medline-entry
-|title=Aerobic exercise training partially reverses the impairment of Nrf2 activation in older humans.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32866619
-|keywords=* Aging
-* Exercise
-* GCLC
-* NQO1
-* Nrf2 signaling
-* Redox homeostasis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7704731
-}}
-==GCLM==
-{{medline-entry
-|title=Silencing Bach1 alters aging-related changes in the expression of Nrf2-regulated genes in primary human bronchial epithelial cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31422075
-|mesh-terms=* Adult
-* Aged
-* Aging
-* Basic-Leucine Zipper Transcription Factors
-* Bronchi
-* Epithelial Cells
-* Gene Expression
-* Gene Silencing
-* Glutamate-Cysteine Ligase
-* Heme Oxygenase-1
-* Humans
-* Isothiocyanates
-* Middle Aged
-* NAD(P)H Dehydrogenase (Quinone)
-* NF-E2-Related Factor 2
-* RNA, Messenger
-* RNA, Small Interfering
-* Signal Transduction
-* Young Adult
-|keywords=* Aging
-* Bach1
-* Glutamate cysteine ligase
-* Heme oxygenase
-* Nrf2
-* Sulforaphane
-|full-text-url=https://sci-hub.do/10.1016/j.abb.2019.108074
-}}
-==GDF11==
-{{medline-entry
-|title=Growth differentiation factor-11 supplementation improves survival and promotes recovery after ischemic stroke in aged mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32365331
-|keywords=* GDF11
-* White matter integrity
-* aging
-* gliosis
-* stroke
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244081
-}}
-{{medline-entry
-|title=Anti-Aging Effects of [[GDF11]] on Skin.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32283613
-|keywords=* disease
-* growth factors
-* regeneration
-* skin aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7177281
-}}
-{{medline-entry
-|title=Targeted Approach to Distinguish and Determine Absolute Levels of GDF8 and [[GDF11]] in Mouse Serum.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32104967
-|keywords=* GDF11
-* aging
-* immunoprecipitation
-* myostatin/GDF8
-* serum
-* targeted-quantitative proteomics
-|full-text-url=https://sci-hub.do/10.1002/pmic.201900104
-}}
-{{medline-entry
-|title=Growth differentiation factor 11 impairs titanium implant healing in the femur and leads to mandibular bone loss.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31983062
-|keywords=* aging
-* alveolar bone loss
-* dental implants
-* osseointegration
-* transforming growth factors
-|full-text-url=https://sci-hub.do/10.1002/JPER.19-0247
-}}
-{{medline-entry
-|title=Systemic [[GDF11]] stimulates the secretion of adiponectin and induces a calorie restriction-like phenotype in aged mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31637864
-|keywords=* GDF11
-* adiponectin
-* aging
-* calorie restriction
-* heterochronic parabiosis
-* rejuvenation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6974718
-}}
-{{medline-entry
-|title=Circulating factors in young blood as potential therapeutic agents for age-related neurodegenerative and neurovascular diseases.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31400495
-|mesh-terms=* Age Factors
-* Aging
-* Animals
-* Blood
-* Bone Morphogenetic Proteins
-* Chemokine CCL11
-* Enzyme Therapy
-* Enzymes
-* Growth Differentiation Factors
-* Mice
-* Neurodegenerative Diseases
-* Parabiosis
-* Vascular Diseases
-|keywords=* C-C motif chemokine 11
-* Circulating factor
-* Growth differentiation factor 11
-* Neurodegenerative diseases
-* Neurovascular diseases
-* Young blood
-|full-text-url=https://sci-hub.do/10.1016/j.brainresbull.2019.08.004
-}}
-{{medline-entry
-|title=Effects of Exercise Training on Growth and Differentiation Factor 11 Expression in Aged Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31417428
-|keywords=* aging
-* exercise
-* growth and differentiation factor 11
-* sarcopenia
-* skeletal muscle
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6684741
-}}
-==GDF15==
-{{medline-entry
-|title=Disease-specific plasma levels of mitokines FGF21, [[GDF15]], and Humanin in type II diabetes and Alzheimer's disease in comparison with healthy aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33131010
-|keywords=* AD
-* Aging
-* FGF21
-* GDF15
-* Humanin
-* T2D
-|full-text-url=https://sci-hub.do/10.1007/s11357-020-00287-w
-}}
-{{medline-entry
-|title=Growth differentiation factor 15 protects against the aging-mediated systemic inflammatory response in humans and mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32691494
-|keywords=* T cell
-* aging
-* inflammation
-* mitochondria
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431835
-}}
-{{medline-entry
-|title=Analysis of Epigenetic Age Predictors in Pain-Related Conditions.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32582603
-|keywords=* DNA methylation
-* aging biomarker
-* chronic pain
-* epigenetic aging
-* epigenetic clock
-* fibromyalgia
-* headache
-* pain sensitivity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7296181
-}}
-{{medline-entry
-|title=[[GDF15]] Plasma Level Is Inversely Associated With Level of Physical Activity and Correlates With Markers of Inflammation and Muscle Weakness.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32477368
-|keywords=* GDF15
-* healthy aging
-* inflammation
-* physical activity
-* sedentarity
-* skeletal muscle
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7235447
-}}
-{{medline-entry
-|title=[[GDF15]] is an epithelial-derived biomarker of idiopathic pulmonary fibrosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31432710
-|mesh-terms=* Aged
-* Alveolar Epithelial Cells
-* Animals
-* Bleomycin
-* Bronchoalveolar Lavage Fluid
-* Case-Control Studies
-* Disease Models, Animal
-* Female
-* Gene Expression Profiling
-* Growth Differentiation Factor 15
-* Humans
-* Idiopathic Pulmonary Fibrosis
-* Lung
-* Male
-* Mice
-* Middle Aged
-* Respiratory Function Tests
-* Severity of Illness Index
-* Survival Analysis
-* Telomere
-* Transcriptome
-|keywords=* MIC-1
-* NAG-1
-* SASP
-* aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6842909
-}}
-{{medline-entry
-|title=Senescence-associated tissue microenvironment promotes colon cancer formation through the secretory factor [[GDF15]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31389184
-|mesh-terms=* Aging
-* Cells, Cultured
-* Cellular Senescence
-* Colonic Neoplasms
-* Fibroblasts
-* Growth Differentiation Factor 15
-* HEK293 Cells
-* Humans
-* Phenotype
-* RNA, Messenger
-* Tumor Microenvironment
-|keywords=* GDF15
-* colon organoids
-* colorectal cancer
-* microenvironment
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826139
-}}
-==GDF5==
-{{medline-entry
-|title=An embryonic CaVβ1 isoform promotes muscle mass maintenance via [[GDF5]] signaling in adult mouse.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31694926
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Animals
-* Atrophy
-* Calcium Channels, L-Type
-* Denervation
-* Embryo, Mammalian
-* Exons
-* Female
-* Gene Expression Regulation, Developmental
-* Growth Differentiation Factor 5
-* Humans
-* Male
-* Mice
-* Muscles
-* Neuromuscular Junction
-* Organ Size
-* Physical Conditioning, Animal
-* Protein Isoforms
-* RNA Splicing
-* Signal Transduction
-* Young Adult
-|full-text-url=https://sci-hub.do/10.1126/scitranslmed.aaw1131
-}}
-==GDNF==
-{{medline-entry
-|title=GFR-α1 Expression in Substantia Nigra Increases Bilaterally Following Unilateral Striatal [[GDNF]] in Aged Rats and Attenuates Nigral Tyrosine Hydroxylase Loss Following 6-OHDA Nigrostriatal Lesion.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31538765
-|mesh-terms=* Aging
-* Animals
-* Dopamine
-* Glial Cell Line-Derived Neurotrophic Factor
-* Glial Cell Line-Derived Neurotrophic Factor Receptors
-* Neurons
-* Oxidopamine
-* Phosphorylation
-* Rats
-* Substantia Nigra
-* Tyrosine 3-Monooxygenase
-|keywords=* 6-hydroxydopamine
-* Parkinson’s disease
-* Substantia nigra
-* aging
-* nigrostriatal
-* tyrosine hydroxylase
-|full-text-url=https://sci-hub.do/10.1021/acschemneuro.9b00291
-}}
-==GEM==
-{{medline-entry
-|title=The Impact of Geriatric Emergency Management Nurses on the Care of Frail Older Patients in the Emergency Department: a Systematic Review.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32904804
-|keywords=* emergency department
-* geriatric emergency management nurses
-* geriatrics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7458600
-}}
-==GFAP==
-{{medline-entry
-|title=Immunohistological Detection of Active Satellite Cellsin Rat Dorsal Root Ganglia after Parenteral Administration of Lipopolysaccharide and during Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32990851
-|keywords=* aging
-* dorsal root ganglion
-* satellite cells
-* systemic inflammation
-|full-text-url=https://sci-hub.do/10.1007/s10517-020-04950-2
-}}
-{{medline-entry
-|title=Transgenic Mice Expressing Human α-Synuclein in Noradrenergic Neurons Develop Locus Ceruleus Pathology and Nonmotor Features of Parkinson's Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32868457
-|keywords=* Parkinson's disease
-* aging
-* locus ceruleus
-* nonmotor
-* norepinephrine
-* α-synuclein
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7511194
-}}
-{{medline-entry
-|title=ApoE Genotype-Dependent Response to Antioxidant and Exercise Interventions on Brain Function.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32630431
-|keywords=* Alzheimer’s disease
-* ApoE
-* aging
-* antioxidants
-* cognition
-* exercise
-* motor
-* oxidative stress
-* vitamin C
-* vitamin E
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7346214
-}}
-{{medline-entry
-|title=Age-Dependent Heterogeneity of Murine Olfactory Bulb Astrocytes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32581775
-|keywords=* Sholl analysis
-* aging
-* astrocyte
-* cell morphology
-* heterogeneity
-* olfactory bulb
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7296154
-}}
-{{medline-entry
-|title=Neuroinflammation in Aged Brain: Impact of the Oral Administration of Ellagic Acid Microdispersion.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32455600
-|keywords=* CD45
-* EA microdispersion (EAm)
-* GFAP
-* aging
-* behavioral skills
-* ellagic acid (EA)
-* mice
-* noradrenaline
-* oral administration
-* principal component analysis (PCA)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7279224
-}}
-{{medline-entry
-|title=Long-term treatment with spermidine increases health span of middle-aged Sprague-Dawley male rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32285289
-|keywords=* Autophagy
-* Behavior
-* Longevity
-* Middle-aged rats
-* Neuroinflammation
-* Spermidine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7287009
-}}
-{{medline-entry
-|title=Meta-analysis of human prefrontal cortex reveals activation of [[GFAP]] and decline of synaptic transmission in the aging brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32138778
-|keywords=* Aging
-* Meta-analysis
-* Prefrontal cortex
-* Sex-specific
-* Transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059712
-}}
-{{medline-entry
-|title=Astroglial biotin deprivation under endoplasmic reticulum stress uncouples BCAA-mTORC1 role in lipid synthesis to prolong autophagy inhibition in the aging brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32030764
-|keywords=* BCAA
-* ER stress
-* aging
-* autophagy
-* lipogenesis
-* mTORC1
-|full-text-url=https://sci-hub.do/10.1111/jnc.14979
-}}
-{{medline-entry
-|title=Long-lived mice with reduced growth hormone signaling have a constitutive upregulation of hepatic chaperone-mediated autophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32013718
-|keywords=* Aging
-* chaperone-mediated autophagy
-* endocrine control of autophagy
-* endocrine signaling
-* growth hormone
-|full-text-url=https://sci-hub.do/10.1080/15548627.2020.1725378
-}}
-{{medline-entry
-|title=Lipopolysaccharide exposure during late embryogenesis triggers and drives Alzheimer-like behavioral and neuropathological changes in CD-1 mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31997558
-|keywords=* Alzheimer's disease
-* aging
-* lipopolysaccharide
-* memory
-* mice
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066339
-}}
-{{medline-entry
-|title=Increased levels of Aβ42 decrease the lifespan of ob/ob mice with dysregulation of microglia and astrocytes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31907998
-|mesh-terms=* Alzheimer Disease
-* Amyloid beta-Peptides
-* Animals
-* Astrocytes
-* Gene Knock-In Techniques
-* Longevity
-* Mice
-* Mice, Knockout
-* Mice, Obese
-* Microglia
-* Peptide Fragments
-|keywords=* Alzheimer's disease
-* astrocytes
-* diabetes
-* lifespan
-* microglia
-* obesity
-|full-text-url=https://sci-hub.do/10.1096/fj.201901028RR
-}}
-{{medline-entry
-|title=Selective brain neuronal and glial losses without changes in [[GFAP]] immunoreactivity: Young versus mature adult Wistar rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31404554
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Glial Fibrillary Acidic Protein
-* Male
-* Neuroglia
-* Neurons
-* Rats
-* Rats, Wistar
-|keywords=* Ageing
-* Astrocytes
-* GFAP
-* Glia
-* Neurons
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2019.111128
-}}
-==GGCT==
-{{medline-entry
-|title=Blockade of γ-Glutamylcyclotransferase Enhances Docetaxel Growth Inhibition of Prostate Cancer Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31519583
-|mesh-terms=* Antineoplastic Agents
-* Apoptosis
-* Cell Line, Tumor
-* Cell Proliferation
-* Cellular Senescence
-* Docetaxel
-* Enzyme Inhibitors
-* Gene Expression
-* Humans
-* Immunohistochemistry
-* Male
-* Prostatic Neoplasms
-* RNA, Small Interfering
-* gamma-Glutamylcyclotransferase
-|keywords=* docetaxel
-* pro-GA
-* prostate cancer cells
-* senescence
-* γ-glutamylcyclotransferase
-|full-text-url=https://sci-hub.do/10.21873/anticanres.13666
-}}
-==GHR==
-{{medline-entry
-|title=Tissue-Specific [[GHR]] Knockout Mice: An Updated Review.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33162937
-|keywords=* aging
-* growth hormone
-* longevity
-* metabolism
-* mice
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7581730
-}}
-==GHRH==
-{{medline-entry
-|title=Physiological and metabolic features of mice with CRISPR/Cas9-mediated loss-of-function in growth hormone-releasing hormone.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32422607
-|keywords=* CRISPR
-* GHRH
-* aging
-* lifespan
-* metabolism
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7288930
-}}
-{{medline-entry
-|title=Transcriptomic and metabolomic profiling of long-lived growth hormone releasing hormone knock-out mice: evidence for altered mitochondrial function and amino acid metabolism.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32091406
-|keywords=* aging
-* growth hormone
-* metabolite
-* mouse
-* transcriptomics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066919
-}}
-==GIP==
-{{medline-entry
-|title=Absence of [[GIP]] secretion alleviates age-related obesity and insulin resistance.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31977316
-|mesh-terms=* Adiponectin
-* Adipose Tissue
-* Age Factors
-* Animals
-* Diet
-* Diet, High-Fat
-* Enteroendocrine Cells
-* Gastric Inhibitory Polypeptide
-* Gene Expression
-* Glucose Tolerance Test
-* Insulin
-* Insulin Resistance
-* Leptin
-* Male
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Mice, Transgenic
-* Obesity
-|keywords=* GIP
-* aging
-* incretin
-* obesity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7040458
-}}
-==GIT2==
-{{medline-entry
-|title=Multidimensional informatic deconvolution defines gender-specific roles of hypothalamic [[GIT2]] in aging trajectories.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31574270
-|mesh-terms=* Aging
-* Animals
-* Cluster Analysis
-* Computational Biology
-* Female
-* GTPase-Activating Proteins
-* Hypothalamus
-* Longevity
-* Male
-* Mice
-* Mice, Inbred C57BL
-* RNA
-* Sex Characteristics
-* Signal Transduction
-* Transcriptome
-|keywords=* Aging
-* Female
-* GIT2
-* Hypothalamus
-* Longevity
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2019.111150
-}}
-==GJC2==
-{{medline-entry
-|title=Zebrafish brain RNA sequencing reveals that cell adhesion molecules are critical in brain aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32629311
-|keywords=* Brain aging
-* Cell adhesion molecules
-* RNA sequencing
-* Zebrafish
-|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2020.04.017
-}}
-==GK==
-{{medline-entry
-|title=Progression of diabetic kidney disease in T2DN rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31566426
-|mesh-terms=* Aging
-* Albuminuria
-* Animals
-* Blood Glucose
-* Diabetes Mellitus, Type 2
-* Diabetic Nephropathies
-* Disease Progression
-* Hypertrophy
-* Kidney Glomerulus
-* Male
-* Membrane Proteins
-* Organ Size
-* Polyuria
-* Rats
-* Rats, Wistar
-* Renin-Angiotensin System
-* Water-Electrolyte Imbalance
-|keywords=* diabetic glomerular disease
-* diabetic nephropathy
-* podocyte pathology
-* renin-angiotensin-aldosterone system
-* scanning ion microscopy
-* type 2 diabetic nephropathy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6960784
-}}
-==GNAQ==
-{{medline-entry
-|title=[[GNAQ]]  expression initiated in multipotent neural crest cells drives aggressive melanoma of the central nervous system.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31680437
-|mesh-terms=* Aging
-* Animals
-* Central Nervous System Neoplasms
-* Disease Models, Animal
-* Disease Progression
-* Embryonic Development
-* Female
-* GTP-Binding Protein alpha Subunits, Gq-G11
-* Male
-* Melanocytes
-* Melanoma
-* Meningeal Neoplasms
-* Mice, Transgenic
-* Multipotent Stem Cells
-* Mutation
-* Neoplasm Invasiveness
-* Neural Crest
-* Nevus
-* Skin Neoplasms
-* Uveal Neoplasms
-|keywords=* GNAQ
-* Plp1
-* blue nevus
-* leptomeningeal melanocytoma
-* uveal melanoma
-|full-text-url=https://sci-hub.do/10.1111/pcmr.12843
-}}
-==GNE==
-{{medline-entry
-|title=Aberrant mitochondrial morphology and function associated with impaired mitophagy and DNM1L-MAPK/ERK signaling are found in aged mutant Parkinsonian LRRK2  mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33300446
-|keywords=* Aging
-* Dnm1l/DRP1
-* SQSTM1/p62
-* knockin mice
-* macroautophagy
-* mitochondria dysfunction
-* mitochondrial fission
-* mitophagy
-* parkinson disease
-* ubiquitination
-|full-text-url=https://sci-hub.do/10.1080/15548627.2020.1850008
-}}
-==GPC1==
-{{medline-entry
-|title=Decreased expression of [[GPC1]] in human skin keratinocytes and epidermis during ageing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31430521
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Cell Proliferation
-* Cells, Cultured
-* Epidermis
-* Female
-* Fibroblast Growth Factor 2
-* Gene Expression Regulation
-* Glypicans
-* Humans
-* Keratinocytes
-* Middle Aged
-* RNA, Messenger
-* Signal Transduction
-* Skin
-* Young Adult
-|keywords=* Ageing
-* Epidermis
-* Glypican 1
-* Human skin
-* Keratinocytes
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2019.110693
-}}
-==GPI==
-{{medline-entry
-|title=Blood factors transfer beneficial effects of exercise on neurogenesis and cognition to the aged brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32646997
-|mesh-terms=* Aging
-* Animals
-* Blood Circulation
-* Brain
-* Cognition
-* Cognitive Dysfunction
-* Glycosylphosphatidylinositols
-* Liver
-* Mice
-* Neurogenesis
-* Phospholipase D
-* Physical Conditioning, Animal
-* Regeneration
-* Signal Transduction
-|full-text-url=https://sci-hub.do/10.1126/science.aaw2622
-}}
-==GPR6==
-{{medline-entry
-|title=Accelerated Epigenetic Aging and Methylation Disruptions Occur in Human Immunodeficiency Virus Infection Prior to Antiretroviral Therapy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32959881
-|keywords=* HIV
-* aging
-* epigenetics
-* methylation
-|full-text-url=https://sci-hub.do/10.1093/infdis/jiaa599
-}}
-==GPT==
-{{medline-entry
-|title=Brain Structural-Behavioral Correlates Underlying Grooved Pegboard Test Performance Across Lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32631206
-|keywords=* aging
-* gray matter
-* visuomotor function
-* white matter
-|full-text-url=https://sci-hub.do/10.1080/00222895.2020.1787320
-}}
-==GPX1==
-{{medline-entry
-|title=Glutathione peroxidase-1 overexpression reduces oxidative stress, and improves pathology and proteome remodeling in the kidneys of old mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32400101
-|keywords=* glutathione peroxidase-1
-* kidney aging
-* mitochondria
-* proteomics
-* reactive oxygen species
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7294784
-}}
-==GPX3==
-{{medline-entry
-|title=Long noncoding RNA glutathione peroxidase 3-antisense inhibits lens epithelial cell apoptosis by upregulating glutathione peroxidase 3 expression in age-related cataract.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31814699
-|mesh-terms=* Aging
-* Anterior Capsule of the Lens
-* Apoptosis
-* Cataract
-* Cell Line
-* Cell Nucleus
-* Epithelial Cells
-* Glutathione Peroxidase
-* Humans
-* Hydrogen Peroxide
-* Lens, Crystalline
-* RNA, Long Noncoding
-* Up-Regulation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6857780
-}}
-==GPX4==
-{{medline-entry
-|title=l-carnitine supplementation during in vitro culture regulates oxidative stress in embryos from bovine aged oocytes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31837632
-|mesh-terms=* Animals
-* Carnitine
-* Cattle
-* Culture Media
-* Embryo Culture Techniques
-* Female
-* Fertilization in Vitro
-* In Vitro Oocyte Maturation Techniques
-* Oocytes
-* Oxidative Stress
-|keywords=* Bovine
-* Embryo development
-* Oocyte aging
-* l-carnitine
-|full-text-url=https://sci-hub.do/10.1016/j.theriogenology.2019.11.036
-}}
-{{medline-entry
-|title=Dietary Selenium Supplementation Ameliorates Female Reproductive Efficiency in Aging Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31835711
-|keywords=* GPX4
-* Gpx1
-* Gpx3
-* Selenof
-* apoptosis
-* embryo
-* follicle development
-* ovarian aging
-* selenium
-* selenoprotein
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6969897
-}}
-==GREM1==
-{{medline-entry
-|title=[[GREM1]] inhibits osteogenic differentiation, senescence and BMP transcription of adipose-derived stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32151168
-|keywords=* BMP
-* GREM1
-* adipose-derived stem cells (ADSCs)
-* osteogenic differentiation
-* senescence
-|full-text-url=https://sci-hub.do/10.1080/03008207.2020.1736054
-}}
-==GREM2==
-{{medline-entry
-|title=Increase of gremlin 2 with age in human adipose-derived stromal/stem cells and its inhibitory effect on adipogenesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31709279
-|keywords=* Adipogenic differentiation
-* Adipose-derived stromal/stem stem cells
-* Aging
-* DAPI, 4′,6-diamidino-2-phenylindole
-* FGF, fibroblast growth factor
-* GREM2
-* GREM2 knockdown
-* HE, hematoxylin eosin
-* Individual differences
-* PBS, phosphate buffered Solution
-* PFA, paraformaldehyde
-* TGF-β, transforming growth factor beta
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6831850
-}}
-==GRID1==
-{{medline-entry
-|title=Gene discovery for high-density lipoprotein cholesterol level change over time in prospective family studies.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109663
-|keywords=* GWAS
-* HDL-C metabolism
-* Healthy aging
-* Longevity
-* Longitudinal HDL-C change
-|full-text-url=https://sci-hub.do/10.1016/j.atherosclerosis.2020.02.005
-}}
-==GRIK2==
-{{medline-entry
-|title=Senescence of Normal Human Fibroblasts Relates to the Expression of Ionotropic Glutamate Receptor GluR6/Grik2.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33099472
-|keywords=* GluR6
-* Grik2
-* Senescence
-* cancer
-* glutamate receptor
-* normal fibroblasts
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7675648
-}}
-==GRK2==
-{{medline-entry
-|title=G protein-coupled receptor kinase 2 modifies the ability of Caenorhabditis elegans to survive oxidative stress.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33064264
-|keywords=* Aging
-* Caenorhabditis elegans (C. elegans)
-* G protein coupled receptor kinase (GRK)
-* Oxidative stress
-* Resistance
-* Stress response
-|full-text-url=https://sci-hub.do/10.1007/s12192-020-01168-z
-}}
-{{medline-entry
-|title=G protein coupled receptor kinases modulate Caenorhabditis elegans reactions to heat stresses.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32768194
-|keywords=* Aging
-* Biological control
-* Caenorhabditis elegans (C. elegans)
-* G protein coupled receptor (GPCR)
-* G protein coupled receptor kinase (GRK)
-* Heat stress
-* Resistance
-* Stress response
-|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2020.07.121
-}}
-{{medline-entry
-|title=Loss of dynamic regulation of G protein-coupled receptor kinase 2 by nitric oxide leads to cardiovascular dysfunction with aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32216616
-|mesh-terms=* Aging
-* Animals
-* Female
-* G Protein-Coupled Inwardly-Rectifying Potassium Channels
-* Heart
-* Heart Diseases
-* Homeostasis
-* Male
-* Mice
-* Mutation
-* Myocardium
-* Nitric Oxide
-|keywords=* S-nitrosylation
-* cardiac hypertrophy
-* heart disease
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7346533
-}}
-==GRM3==
-{{medline-entry
-|title=Profiling gene expression in the human dentate gyrus granule cell layer reveals insights into schizophrenia and its genetic risk.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32203495
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Bipolar Disorder
-* Dentate Gyrus
-* Depressive Disorder, Major
-* Female
-* Gene Expression Profiling
-* Genetic Predisposition to Disease
-* Genome-Wide Association Study
-* Humans
-* Male
-* Middle Aged
-* Neurons
-* Quantitative Trait Loci
-* Schizophrenia
-* Transcriptome
-* Young Adult
-|full-text-url=https://sci-hub.do/10.1038/s41593-020-0604-z
-}}
-==GRN==
-{{medline-entry
-|title=Stressful development: Integrating endoderm development, stress, and longevity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33307045
-|keywords=* Caenorhabditis elegans
-* Embryonic development
-* Epigenetics inheritance
-* Innate immunity
-* Longevity
-* Pleiotropy
-* Stress
-|full-text-url=https://sci-hub.do/10.1016/j.ydbio.2020.12.002
-}}
-{{medline-entry
-|title=A Scoping Review of the Evidence About the Nurses Improving Care for Healthsystem Elders (NICHE) Program.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31681955
-|keywords=* Aging
-* Geriatric nursing
-* Health care professionals
-* Intervention
-* Quality improvement
-|full-text-url=https://sci-hub.do/10.1093/geront/gnz150
-}}
-==GSC==
-{{medline-entry
-|title=[i]mastermind[/i] regulates niche ageing independently of the [i]Notch[/i] pathway in the [i]Drosophila[/i] ovary.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31744422
-|mesh-terms=* Aging
-* Animals
-* Cellular Senescence
-* Drosophila Proteins
-* Drosophila melanogaster
-* Female
-* Germ Cells
-* Nuclear Proteins
-* Ovary
-* Receptors, Notch
-* Signal Transduction
-* Stem Cell Niche
-* Transcriptome
-|keywords=* DE-cadherin
-* Drosophila oogenesis
-* Hedgehog
-* mastermind
-* niche ageing
-* reactive oxygen species
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6893403
-}}
-==GSTM1==
-{{medline-entry
-|title=The effects of everyday-life exposure to polycyclic aromatic hydrocarbons on biological age indicators.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33272294
-|keywords=* Biological aging
-* DNA adduct
-* Mitochondrial DNA copy number
-* Polycyclic aromatic hydrocarbon
-* Structural equation modelling
-* Telomere length
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7713168
-}}
-==GSTM2==
-{{medline-entry
-|title=Small Extracellular Vesicles Have GST Activity and Ameliorate Senescence-Related Tissue Damage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32574561
-|keywords=* 4-HNE
-* EV
-* GSH
-* GST
-* ROS
-* SASP
-* aging
-* extracellular vesicles
-* glutathione metabolism
-* glutathione-S-transferase
-* lipid peroxidation
-* rejuvenation
-* senescence
-* senescence-associated secretory phenotype
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7342013
-}}
-==GUK1==
-{{medline-entry
-|title=Characterization of the impact of GMP/GDP synthesis inhibition on replicative lifespan extension in yeast.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32232569
-|keywords=* Aging
-* GDP
-* GMP
-* Mycophenolic acid
-* Proteasome
-* Replicative lifespan
-* Yeast
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7367712
-}}
-==GZMK==
-{{medline-entry
-|title=Comprehensive Profiling of an Aging Immune System Reveals Clonal [[GZMK]]  CD8  T Cells as Conserved Hallmark of Inflammaging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33271118
-|keywords=* Aging
-* CD8 T cells
-* CITE-seq
-* granzyme K
-* immune system
-* inflammaging
-* single-cell ATAC-sequencing
-* single-cell BCR-sequencing
-* single-cell RNA-sequencing
-* single-cell TCR-sequencing
-|full-text-url=https://sci-hub.do/10.1016/j.immuni.2020.11.005
-}}
-==H2AX==
-{{medline-entry
-|title=Evaluation of Gamma[[H2AX]] in Buccal Cells as a Molecular Biomarker of DNA Damage in Alzheimer's Disease in the AIBL Study of Ageing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32781776
-|keywords=* Alzheimer’s disease
-* DNA damage
-* mild cognitive impairment
-* senescence
-* γH2AX
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7459751
-}}
-{{medline-entry
-|title=Cisplatin-induced peripheral neuropathy is associated to neuronal senescence-like response.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32597980
-|keywords=* cisplatin
-* neuropathy
-* neurotoxicity
-* p21
-* senescence
-|full-text-url=https://sci-hub.do/10.1093/neuonc/noaa151
-}}
-{{medline-entry
-|title=Guanine Deaminase Stimulates Ultraviolet-induced Keratinocyte Senescence in Seborrhoeic Keratosis via Guanine Metabolites.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32215662
-|keywords=*  DNA damage
-*  UV-induced keratinocyte senescence
-*  guanine deaminase
-*  reactive oxygen species
-*  uric acid
-* seborrhoeic keratosis
-|full-text-url=https://sci-hub.do/10.2340/00015555-3473
-}}
-{{medline-entry
-|title=Do BRCA1 and BRCA2 gene mutation carriers have a reduced ovarian reserve? Protocol for a prospective observational study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31772111
-|mesh-terms=* Adolescent
-* Adult
-* Aging
-* BRCA1 Protein
-* BRCA2 Protein
-* Female
-* Germ-Line Mutation
-* Heterozygote
-* Humans
-* Immunohistochemistry
-* Middle Aged
-* Observational Studies as Topic
-* Ovarian Follicle
-* Ovarian Reserve
-* Prospective Studies
-* Research Design
-* Young Adult
-|keywords=* BRCA
-* DNA repair
-* fertility
-* follicle
-* germline mutation
-* oocyte
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6887091
-}}
-{{medline-entry
-|title=Slower rates of accumulation of DNA damage in leukocytes correlate with longer lifespans across several species of birds and mammals.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31730540
-|mesh-terms=* Animals
-* Birds
-* Bottle-Nosed Dolphin
-* Cross-Sectional Studies
-* DNA Damage
-* Goats
-* Leukocytes
-* Longevity
-* Reindeer
-* Turtles
-* Vertebrates
-|keywords=* DNA damage
-* lifespan
-* short telomeres
-* species
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6874430
-}}
-{{medline-entry
-|title=Phosphoproteomic analysis reveals plant DNA damage signalling pathways with a functional role for histone [[H2AX]] phosphorylation in plant growth under genotoxic stress.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31410901
-|mesh-terms=* ATP-Binding Cassette Transporters
-* Aging
-* Arabidopsis
-* Arabidopsis Proteins
-* Cells, Cultured
-* DNA Damage
-* DNA Repair
-* Gene Expression Regulation, Plant
-* Gene Ontology
-* Germination
-* Histones
-* Mass Spectrometry
-* Phosphorylation
-* Proteome
-* Seeds
-* Serine
-* Signal Transduction
-* Stress, Physiological
-* X-Rays
-|keywords=* ATAXIA TELANGIECTASIA MUTATED (ATM)
-* DNA damage response
-* DNA repair
-* phosphorylation
-* seed
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6900162
-}}
-==HBM==
-{{medline-entry
-|title=The effects of dietary fatty acids on bone, hematopoietic marrow and marrow adipose tissue in a murine model of senile osteoporosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31553309
-|mesh-terms=* Adipose Tissue
-* Adiposity
-* Animals
-* Bone Density
-* Bone Marrow
-* Dietary Fats
-* Dietary Supplements
-* Disease Models, Animal
-* Fatty Acids, Omega-3
-* Female
-* Femur
-* Mice
-* Osteoporosis
-* X-Ray Microtomography
-|keywords=* SAMP8 mouse
-* aging
-* fish oil
-* marrow adipose tissue
-* osteoporosis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6781972
-}}
-==HBP1==
-{{medline-entry
-|title=Suppression of p38/[[HBP1]] pathway alleviates hyperosmotic stress-induced senescent progression of chondrocyte senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32549582
-|mesh-terms=* Cellular Senescence
-* Chondrocytes
-* Disease Progression
-* High Mobility Group Proteins
-* Humans
-* Osteoarthritis
-* Repressor Proteins
-* Up-Regulation
-* p38 Mitogen-Activated Protein Kinases
-|keywords=* HBP1
-* chondrocyte
-* osmolality stress
-* p38
-* senescence
-|full-text-url=https://sci-hub.do/10.23812/20-63-A-6
-}}
-==HCN1==
-{{medline-entry
-|title=Protein expression changes of [[HCN1]] and HCN2 in hippocampal subregions of gerbils during the normal aging process.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32128096
-|keywords=* Aging
-* Dentate gyrus
-* Granule cells
-* HCN channel
-* Hippocampus proper
-* Pyramidal cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7038419
-}}
-==HDAC1==
-{{medline-entry
-|title=[[HDAC1]] modulates OGG1-initiated oxidative DNA damage repair in the aging brain and Alzheimer's disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32424276
-|mesh-terms=* Acetylation
-* Aging
-* Alzheimer Disease
-* Animals
-* Astrocytes
-* Base Sequence
-* Benzophenones
-* Brain
-* Cognition
-* Cognition Disorders
-* DNA Damage
-* DNA Glycosylases
-* Down-Regulation
-* Gene Ontology
-* Guanine
-* Histone Deacetylase 1
-* Memory
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Neurons
-* Oxidative Stress
-* Promoter Regions, Genetic
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7235043
-}}
-==HDAC10==
-{{medline-entry
-|title=Middle-aged female rats lack changes in histone H3 acetylation in the anterior hypothalamus observed in young females on the day of a luteinizing hormone surge.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31434815
-|mesh-terms=* Acetylation
-* Age Factors
-* Animals
-* Estradiol
-* Female
-* Histones
-* Hypothalamus, Anterior
-* Luteinizing Hormone
-* Rats
-* Rats, Sprague-Dawley
-|keywords=* Histone acetylation
-* LH
-* aging
-* histone deacetylases
-* hypothalamus
-|full-text-url=https://sci-hub.do/10.5582/bst.2019.01162
-}}
-==HDAC2==
-{{medline-entry
-|title=EEF1A1 deacetylation enables transcriptional activation of remyelination.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32647127
-|mesh-terms=* Acetylation
-* Aging
-* Animals
-* Cell Dedifferentiation
-* Cell Nucleus
-* Histone Deacetylase 1
-* Histone Deacetylase 2
-* Lysine Acetyltransferase 5
-* Mice
-* Models, Biological
-* Oligodendroglia
-* Peptide Elongation Factor 1
-* Peripheral Nervous System
-* Recovery of Function
-* Remyelination
-* SOXE Transcription Factors
-* STAT3 Transcription Factor
-* Schwann Cells
-* Theophylline
-* Trans-Activators
-* Transcriptional Activation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7347577
-}}
-==HDAC3==
-{{medline-entry
-|title=Histone deacetylase-3: Friend and foe of the brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32486848
-|keywords=* Histone deacetylases
-* aging
-* histone deacetylase-3
-* learning and memory
-* neurodegenerative diseases
-* neurodevelopment
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7400723
-}}
-{{medline-entry
-|title=Loss of [[HDAC3]] contributes to meiotic defects in aged oocytes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31498540
-|mesh-terms=* Animals
-* Cells, Cultured
-* Cellular Senescence
-* Female
-* Histone Deacetylases
-* Meiosis
-* Mice
-* Mice, Inbred ICR
-* Oocytes
-|keywords=* HDACs
-* aneuploidy
-* maternal aging
-* oocyte quality
-* reproduction
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826132
-}}
-==HDAC4==
-{{medline-entry
-|title=The posttranslational modification of [[HDAC4]] in cell biology: Mechanisms and potential targets.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31588631
-|keywords=* HDAC4
-* cell senescence
-* cellular apoptosis and autophagy
-* glucose metabolism
-* inflammation and pathology
-* proliferation and differentiation
-|full-text-url=https://sci-hub.do/10.1002/jcb.29365
-}}
-==HDAC6==
-{{medline-entry
-|title=Inhibition of [[HDAC6]] Attenuates Diabetes-Induced Retinal Redox Imbalance and Microangiopathy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32660051
-|keywords=* HDAC6
-* diabetic retinopathy
-* oxidative stress
-* retinal endothelial cell senescence
-* retinal endothelial cells
-* tubastatin A
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7402090
-}}
-==HDC==
-{{medline-entry
-|title=Induced pluripotency and spontaneous reversal of cellular aging in supercentenarian donor cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115145
-|mesh-terms=* Adult
-* Aged, 80 and over
-* Cell Differentiation
-* Cell Line
-* Cellular Reprogramming
-* Cellular Senescence
-* Child
-* Clone Cells
-* Gene Expression Regulation
-* Humans
-* Induced Pluripotent Stem Cells
-* Mesenchymal Stem Cells
-* Telomere Homeostasis
-* Tissue Donors
-* Transcriptome
-|keywords=* Aging
-* Longevity
-* Reprogramming
-* Supercentenarian
-* Telomere
-* iPSC
-|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2020.02.092
-}}
-==HES1==
-{{medline-entry
-|title=A Single-Cell Transcriptomic Atlas of Human Skin Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33238152
-|keywords=* HES1
-* KLF6
-* aging
-* fibroblast
-* keratinocyte
-* quercetin
-* senescence
-* single-cell RNA sequencing
-* skin
-|full-text-url=https://sci-hub.do/10.1016/j.devcel.2020.11.002
-}}
-==HFE==
-{{medline-entry
-|title=Polyphenol Characterization and Skin-Preserving Properties of Hydroalcoholic Flower Extract from [i]Himantoglossum robertianum[/i] (Orchidaceae).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31739534
-|keywords=* Himantoglossum robertianum
-* antioxidants
-* collagenase
-* elastase
-* flavonoids
-* keratinocytes
-* skin aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6918203
-}}
-==HGD==
-{{medline-entry
-|title=High-glucose diets induce mitochondrial dysfunction in Caenorhabditis elegans.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31846489
-|mesh-terms=* Animals
-* Caenorhabditis elegans
-* Diet
-* Gene Expression Regulation
-* Glucose
-* Longevity
-* Mitochondria
-* Mitophagy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6917275
-}}
-==HGF==
-{{medline-entry
-|title=Age-related changes in the immunomodulatory effects of human dental pulp derived mesenchymal stem cells on the CD4  T cell subsets.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33223447
-|keywords=* Aging
-* CD4 T cell
-* Dental pulp
-* Immunomodulation
-* Mesenchymal stem cell
-|full-text-url=https://sci-hub.do/10.1016/j.cyto.2020.155367
-}}
-{{medline-entry
-|title=Hepatocyte growth factor ([[HGF]]) and stem cell factor (SCF) maintained the stemness of human bone marrow mesenchymal stem cells (hBMSCs) during long-term expansion by preserving mitochondrial function via the PI3K/AKT, ERK1/2, and STAT3 signaling pathways.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32736659
-|keywords=* Hepatocyte growth factor
-* Mitochondrial function
-* Osteogenic differentiation
-* Senescence
-* Stem cell factor
-* Stem cells from human exfoliated deciduous teeth
-* Stemness
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7393921
-}}
-{{medline-entry
-|title=Phenytoin sodium-ameliorated gingival fibroblast aging is associated with autophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32281104
-|keywords=* aging
-* autophagy
-* gingival fibroblast
-* phenytoin sodium
-|full-text-url=https://sci-hub.do/10.1111/jre.12750
-}}
-{{medline-entry
-|title=Impaired integrin α  /β  -mediated hepatocyte growth factor release by stellate cells of the aged liver.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32157808
-|keywords=* aging
-* hepatic stellate cells
-* integrins
-* laminins
-* mechanobiology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189994
-}}
-==HGS==
-{{medline-entry
-|title=Handgrip strength asymmetry is associated with future falls in older Americans.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33247424
-|keywords=* Aging
-* Functional laterality
-* Geriatric assessment
-* Geriatrics
-* Muscle strength dynamometer
-|full-text-url=https://sci-hub.do/10.1007/s40520-020-01757-z
-}}
-{{medline-entry
-|title=Examining Additional Aspects of Muscle Function with a Digital Handgrip Dynamometer and Accelerometer in Older Adults: A Pilot Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33142897
-|keywords=* aging
-* geriatric assessment
-* muscle strength
-* muscle weakness
-* physical functional performance
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7709634
-}}
-{{medline-entry
-|title=The Relationship between Muscular Strength and Depression in Older Adults with Chronic Disease Comorbidity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32962093
-|keywords=* aging
-* depression
-* disease comorbidities
-* muscular strength
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7558624
-}}
-{{medline-entry
-|title=Handgrip Strength in the Korean Population: Normative Data and Cutoff Values.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32743310
-|keywords=* Aging
-* Hand strength
-* Muscle strength
-* Nutrition surveys
-* Sarcopenia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7370763
-}}
-{{medline-entry
-|title=Handgrip Strength Asymmetry and Weakness Are Associated with Lower Cognitive Function: A Panel Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32473060
-|keywords=* aging
-* functional laterality
-* geriatric assessment
-* geriatrics
-* muscle strength dynamometer
-|full-text-url=https://sci-hub.do/10.1111/jgs.16556
-}}
-{{medline-entry
-|title=Handgrip Strength Asymmetry and Weakness are Differentially Associated with Functional Limitations in Older Americans.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32384713
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Female
-* Geriatric Assessment
-* Hand Strength
-* Humans
-* Male
-* Middle Aged
-* Muscle Strength
-* Muscle Strength Dynamometer
-* Muscle Weakness
-* Odds Ratio
-* United States
-|keywords=* aging
-* geriatrics
-* muscle strength
-* muscle strength dynamometer
-* nutrition surveys
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7246814
-}}
-{{medline-entry
-|title=Absolute and Body Mass Index Normalized Handgrip Strength Percentiles by Gender, Ethnicity, and Hand Dominance in Americans.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31930203
-|keywords=* aging
-* epidemiology
-* hand strength
-* human development
-* muscle weakness
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6954001
-}}
-{{medline-entry
-|title=Hand grip strength variability during serial testing as an entropic biomarker of aging: a Poincaré plot analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31931730
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Biomarkers
-* Cross-Sectional Studies
-* Entropy
-* Female
-* Hand Strength
-* Heart Rate
-* Humans
-* Male
-|keywords=* Aging
-* Entropy
-* Hand grip strength
-* Nonlinear dynamics
-* Poincaré plot
-* Time series
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6958685
-}}
-{{medline-entry
-|title=Physical Activity and Fitness in White- and Blue-Collar Retired Men.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31849269
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Body Mass Index
-* Exercise
-* Geriatric Assessment
-* Humans
-* Longitudinal Studies
-* Male
-* Men's Health
-* Occupations
-* Physical Fitness
-* Poland
-* Retirement
-* Social Class
-* Surveys and Questionnaires
-* Task Performance and Analysis
-|keywords=* Retirement
-* occupation
-* old men
-* physical activity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6920597
-}}
-{{medline-entry
-|title=Association between Hand Grip Strength and Self-Rated Health in Middle- and Old-Aged Korean Citizens.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31842533
-|keywords=* Hand Grip Strength
-* Korean Longitudinal Study of Aging
-* Self-Rated Health
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6987025
-}}
-{{medline-entry
-|title=Weakness May Have a Causal Association With Early Mortality in Older Americans: A Matched Cohort Analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31786197
-|keywords=* Aging
-* Epidemiology
-* Geriatrics
-* hand strength
-* muscle strength
-* sarcopenia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7186143
-}}
-{{medline-entry
-|title=Associations Between Dietary Patterns and Handgrip Strength: The Korea National Health and Nutrition Examination Survey 2014-2016.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31743070
-|keywords=* Dietary patterns
-* Korea National Health and Nutrition Examination Survey
-* aging
-* diet
-* handgrip strength
-|full-text-url=https://sci-hub.do/10.1080/07315724.2019.1691955
-}}
-{{medline-entry
-|title=Effect of relative handgrip strength on cardiovascular disease among Korean adults aged 45 years and older: Results from the Korean Longitudinal Study of Aging (2006-2016).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31574451
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Cardiovascular Diseases
-* Female
-* Hand Strength
-* Humans
-* Longitudinal Studies
-* Male
-* Middle Aged
-* Muscle Strength
-* Muscle, Skeletal
-* Republic of Korea
-* Risk Factors
-|keywords=* Cardiovascular disease
-* KLoSA
-* Relative handgrip strength
-|full-text-url=https://sci-hub.do/10.1016/j.archger.2019.103937
-}}
-{{medline-entry
-|title=Weakness and cognitive impairment are independently and jointly associated with functional decline in aging Americans.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31520335
-|mesh-terms=* Activities of Daily Living
-* Aged
-* Aging
-* Cognitive Dysfunction
-* Geriatric Assessment
-* Hand Strength
-* Humans
-* Middle Aged
-|keywords=* Dementia
-* Epidemiology
-* Geriatrics
-* Muscle strength
-* Nervous system
-|full-text-url=https://sci-hub.do/10.1007/s40520-019-01351-y
-}}
-{{medline-entry
-|title=Association of phase angle with sarcopenia and its components in physically active older women.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31463928
-|mesh-terms=* Aged
-* Cross-Sectional Studies
-* Electric Impedance
-* Female
-* Hand Strength
-* Humans
-* Muscle Strength
-* Sarcopenia
-* Walking Speed
-|keywords=* Aging
-* Bioimpedance
-* Muscle function
-* Muscle mass
-|full-text-url=https://sci-hub.do/10.1007/s40520-019-01325-0
-}}
-==HLA-DRB1==
-{{medline-entry
-|title=The pathophysiology of polymyalgia rheumatica, small pieces of a big puzzle.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32942037
-|keywords=* Aging
-* B cell
-* HLA-DR
-* Interleukin-6
-* Polymyalgia rheumatica
-* T cell
-|full-text-url=https://sci-hub.do/10.1016/j.autrev.2020.102670
-}}
-==HMGA1==
-{{medline-entry
-|title=Characterization of [i][[HMGA1]]P6[/i] transgenic mouse embryonic fibroblasts.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32787507
-|keywords=* CeRNA
-* HMGA1
-* HMGA1P6
-* pseudogenes
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7513866
-}}
-==HMGA2==
-{{medline-entry
-|title=4D Genome Rewiring during Oncogene-Induced and Replicative Senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32220303
-|mesh-terms=* Cells, Cultured
-* Cellular Senescence
-* Chromatin Assembly and Disassembly
-* DNA (Cytosine-5-)-Methyltransferase 1
-* DNA Methylation
-* Fibroblasts
-* Genome, Human
-* Heterochromatin
-* Humans
-* In Situ Hybridization, Fluorescence
-* Oncogenes
-|keywords=* 3D genome architecture
-* DNMT1
-* Hi-C
-* chromatin compartments
-* gene regulation
-* oncogene-induced senescence
-* replicative senescence
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7208559
-}}
-{{medline-entry
-|title=The protective effects of [[HMGA2]] in the senescence process of bone marrow-derived mesenchymal stromal cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32068957
-|keywords=* bone marrow derived mesenchymal stromal cells (MSCs)
-* high-mobility group AT-hook 2 (HMGA2)
-* regulator of G protein signaling 2 (Rgs2)
-* senescence
-|full-text-url=https://sci-hub.do/10.1002/term.3023
-}}
-==HMGB1==
-{{medline-entry
-|title=Senescent human melanocytes drive skin ageing via paracrine telomere dysfunction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31633821
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Atrophy
-* Cells, Cultured
-* Cellular Senescence
-* Cyclin-Dependent Kinase Inhibitor p16
-* Epidermis
-* Female
-* Humans
-* Male
-* Melanocytes
-* Middle Aged
-* Paracrine Communication
-* Reactive Oxygen Species
-* Receptors, CXCR4
-* Skin
-* Telomere
-* Young Adult
-|keywords=*
-SASP
-* melanocytes
-* senescence
-* skin ageing
-* telomeres
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6885734
-}}
-==HMGCR==
-{{medline-entry
-|title=Cholesterol Homeostasis: An In Silico Investigation into How Aging Disrupts Its Key Hepatic Regulatory Mechanisms.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33007859
-|keywords=* aging
-* cholesterol biosynthesis
-* mathematical model
-* reactive oxygen species
-* systems biology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7599957
-}}
-{{medline-entry
-|title=Artesunate inhibits the mevalonate pathway and promotes glioma cell senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31746143
-|keywords=* artesunate
-* distant seeding
-* glioma
-* mevalonate pathway
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6933330
-}}
-==HOXD8==
-{{medline-entry
-|title=Single-Cell Transcriptome Analysis Reveals Six Subpopulations Reflecting Distinct Cellular Fates in Senescent Mouse Embryonic Fibroblasts.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32849838
-|keywords=* Hoxd8
-* cellular senescence
-* mouse embryonic fibroblasts
-* senescence-associated secretory phenotype
-* single-cell RNA sequencing
-* transcriptomic heterogeneity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431633
-}}
-==HP==
-{{medline-entry
-|title=A narrative review of highly processed food addiction across the lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33127423
-|keywords=* Adolescence
-* Adulthood
-* Childhood
-* Food addiction
-* Infancy
-* Lifespan
-* Prenatal
-|full-text-url=https://sci-hub.do/10.1016/j.pnpbp.2020.110152
-}}
-{{medline-entry
-|title=Beta Human Papillomavirus 8E6 Attenuates LATS Phosphorylation after Failed Cytokinesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32238586
-|mesh-terms=* Apoptosis
-* Cell Cycle Proteins
-* Cell Line, Tumor
-* Cell Proliferation
-* Cell Survival
-* Cytochalasin B
-* Cytokinesis
-* DNA Repair
-* E1A-Associated p300 Protein
-* Gene Expression Regulation
-* HCT116 Cells
-* Host-Pathogen Interactions
-* Humans
-* Keratinocytes
-* Oncogene Proteins, Viral
-* Osteoblasts
-* Papillomaviridae
-* Phenotype
-* Phosphorylation
-* Primary Cell Culture
-* Protein-Serine-Threonine Kinases
-* Signal Transduction
-* Transcription Factors
-* Tumor Suppressor Protein p53
-|keywords=* Hippo signaling pathway
-* apoptosis
-* cancer
-* cytokinesis
-* human papillomavirus
-* senescence
-* skin cancer
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7307087
-}}
-==HPSE==
-{{medline-entry
-|title=Distribution of heparan sulfate correlated with the expression of heparanase-1 and matrix metalloproteinase-9 in an ovariectomized rats skin.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32159248
-|keywords=* aging
-* estrogen
-* extracellular matrix
-* heparan sulfate
-* heparanase-1
-* matrix metalloproteinase-9
-|full-text-url=https://sci-hub.do/10.1002/cbin.11339
-}}
-==HR==
-{{medline-entry
-|title=Patients with hip fracture and total hip arthroplasty surgery differ in anthropometric, but not cardiovascular screening abnormalities.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33267795
-|keywords=* Aging
-* Cardiovascular reactivity
-* Heart rate variability
-* Hip fracture
-* Total hip arthroplasty
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7713041
-}}
-{{medline-entry
-|title=Clinical Role of Lung Ultrasound for the Diagnosis and Prognosis of Coronavirus Disease Pneumonia in Elderly Patients: A Pivotal Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33271558
-|keywords=* Aging
-* Coronavirus disease
-* Elderly
-* Lung ultrasound
-* Severe acute respiratory syndrome-coronavirus-2
-|full-text-url=https://sci-hub.do/10.1159/000512209
-}}
-{{medline-entry
-|title=The Relationship of Accelerometer-Assessed Standing Time With and Without Ambulation and Mortality: The WHI OPACH Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33225345
-|keywords=* Accelerometer
-* Longevity
-* Physical activity
-|full-text-url=https://sci-hub.do/10.1093/gerona/glaa227
-}}
-{{medline-entry
-|title=Age-related myofiber atrophy in old mice is reversed by ten weeks voluntary high-resistance wheel running.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33181317
-|keywords=* Aging
-* Exercise
-* Mouse model
-* Muscle morphology
-* Skeletal muscle
-* Training
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.111150
-}}
-{{medline-entry
-|title=Predicted Skeletal Muscle Mass and 4-Year Cardiovascular Disease Incidence in Middle-Aged and Elderly Participants of IKARIA Prospective Epidemiological Study: The Mediating Effect of Sex and Cardiometabolic Factors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33121164
-|keywords=* aging
-* body composition
-* gender
-* heart disease
-* lean mass
-* obesity
-* primary prevention
-* women
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7693172
-}}
-{{medline-entry
-|title=Obesity is associated with early hip fracture risk in postmenopausal women: a 25-year follow-up.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33095419
-|keywords=* Aging
-* Body mass index
-* Bone mineral density
-* Follow-up study
-* General population
-* Hip fracture
-* Menopause
-* Obesity
-|full-text-url=https://sci-hub.do/10.1007/s00198-020-05665-w
-}}
-{{medline-entry
-|title=ATM inhibition synergizes with fenofibrate in high grade serous ovarian cancer cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33024871
-|keywords=* Biochemistry
-* Bioinformatics
-* Cancer research
-* Cell biology
-* Cellular metabolism
-* Cellular senescence
-* Drug combinations
-* Homologous recombination
-* Metabolite
-* Molecular biology
-* PPARa
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7527645
-}}
-{{medline-entry
-|title=Effectiveness of adjuvant FOLFOX vs 5FU/LV in adults over age 65 with stage II and III colon cancer using a novel hybrid approach.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33015888
-|keywords=* aging
-* cancer
-* chemotherapy
-* comparative effectiveness research
-* pharmacoepidemiology
-|full-text-url=https://sci-hub.do/10.1002/pds.5148
-}}
-{{medline-entry
-|title=Age, Frailty, and Comorbidity as Prognostic Factors for Short-Term Outcomes in Patients With Coronavirus Disease 2019 in Geriatric Care.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32978065
-|mesh-terms=* Age Factors
-* Aged
-* Aged, 80 and over
-* Betacoronavirus
-* COVID-19
-* Comorbidity
-* Coronavirus Infections
-* Female
-* Frail Elderly
-* Geriatrics
-* Humans
-* Male
-* Models, Statistical
-* Outcome Assessment, Health Care
-* Pandemics
-* Pneumonia, Viral
-* Prognosis
-* SARS-CoV-2
-* Survival Analysis
-* Sweden
-|keywords=* COVID-19
-* aging
-* comorbidity
-* frailty
-* geriatrics
-* survival
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7427570
-}}
-{{medline-entry
-|title=Clinical and demographic parameters predict the progression from mild cognitive impairment to dementia in elderly patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32918697
-|keywords=* Aging
-* Cox regression
-* Dementia
-* Follow-up
-* Mild cognitive impairment
-|full-text-url=https://sci-hub.do/10.1007/s40520-020-01697-8
-}}
-{{medline-entry
-|title=Plasma Dehydroepiandrosterone Sulfate and Cardiovascular Disease Risk in Older Men and Women.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32785663
-|keywords=* DHEA-S
-* aging
-* heart failure
-* mortality
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7526732
-}}
-{{medline-entry
-|title=High intensity interval training combined with L-citrulline supplementation: Effects on physical performance in healthy older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32721549
-|keywords=* Aging
-* Body composition
-* Exercise
-* Mobility
-* Nutrition
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.111036
-}}
-{{medline-entry
-|title=Associations of blood pressure with risk of injurious falls in old age vary by functional status: A cohort study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32738383
-|keywords=* Aging
-* Blood pressure
-* Falls
-* Injury
-* Swedish National study on Aging and Care in Kungsholmen (SNAC-K)
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.111038
-}}
-{{medline-entry
-|title=Epigenetic age acceleration and clinical outcomes in gliomas.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32692766
-|mesh-terms=* Adult
-* Aging
-* DNA Methylation
-* Epigenesis, Genetic
-* Female
-* Glioma
-* Humans
-* Male
-* Middle Aged
-* Prognosis
-* Survival Analysis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7373289
-}}
-{{medline-entry
-|title=Do Stairs Inhibit Seniors Who Live on Upper Floors From Going Out?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32666833
-|keywords=* active aging
-* activity monitor
-* homebound
-* mobility
-* walk-up buildings
-|full-text-url=https://sci-hub.do/10.1177/1937586720936588
-}}
-{{medline-entry
-|title=Age-specific acute changes in carotid-femoral pulse wave velocity with head-up tilt.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32634245
-|keywords=* arterial function
-* arterial stiffness
-* blood pressure
-* early vascular aging
-* pressure dependence
-|full-text-url=https://sci-hub.do/10.1093/ajh/hpaa101
-}}
-{{medline-entry
-|title=Pre-frailty status increases the risk of rehospitalization in patients after elective cardiac surgery without complication.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32531126
-|mesh-terms=* Aged
-* Cardiac Surgical Procedures
-* Elective Surgical Procedures
-* Female
-* Frailty
-* Humans
-* Male
-* Patient Readmission
-* Postoperative Complications
-* Retrospective Studies
-* Risk
-|keywords=* adverse events
-* aging
-* cardiac surgery
-* frailty
-* rehospitalization
-|full-text-url=https://sci-hub.do/10.1111/jocs.14550
-}}
-{{medline-entry
-|title=Comparative Performance of Creatinine-Based GFR Estimation Equations in Exceptional Longevity: The Rugao Longevity and Ageing Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32546991
-|mesh-terms=* Aged, 80 and over
-* Creatinine
-* Female
-* Glomerular Filtration Rate
-* Humans
-* Kidney Function Tests
-* Longevity
-* Male
-* Mortality
-* Predictive Value of Tests
-* Renal Insufficiency
-* Reproducibility of Results
-* Risk Factors
-|keywords=* equation
-* exceptional longevity
-* glomerular filtration rate
-* kidney function
-* mortality
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7266309
-}}
-{{medline-entry
-|title=Sex-and race-specific associations of protein intake with change in muscle mass and physical function in older adults: the Health, Aging, and Body Composition (Health ABC) Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32520344
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Biomass
-* Body Composition
-* Body Weight
-* Dietary Proteins
-* Female
-* Humans
-* Independent Living
-* Male
-* Muscle Development
-* Muscle Strength
-* Muscles
-* Prospective Studies
-* Sex Factors
-|keywords=* appendicular lean body mass
-* community-dwelling
-* gait speed
-* mobility limitation
-* old age
-* optimal intake
-* physical performance
-* spline functions
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7326591
-}}
-{{medline-entry
-|title=Deterioration of bone microstructure by aging and menopause in Japanese healthy women: analysis by [[HR]]-pQCT.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32519249
-|mesh-terms=* Absorptiometry, Photon
-* Adult
-* Aged
-* Aging
-* Asian Continental Ancestry Group
-* Bone Density
-* Bone and Bones
-* Cancellous Bone
-* Cortical Bone
-* Female
-* Finite Element Analysis
-* Humans
-* Japan
-* Linear Models
-* Menopause
-* Middle Aged
-* Porosity
-* Tomography, X-Ray Computed
-|keywords=* Bone microstructure
-* Estimated bone strength
-* High resolution peripheral quantitative CT (HR-pQCT)
-* Japanese women
-* Non-metric trabecular parameter
-|full-text-url=https://sci-hub.do/10.1007/s00774-020-01115-z
-}}
-{{medline-entry
-|title=Association between Low Protein Intake and Mortality in Patients with Type 2 Diabetes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32492838
-|keywords=* aging
-* diabetes
-* mortality
-* nutritional support
-* protein intake
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7352318
-}}
-{{medline-entry
-|title=CAUSES, mortality rates and risk factors of death in community-dwelling Europeans aged 50 years and over: Results from the Survey of Health, Ageing and Retirement in Europe 2013-2015.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32325305
-|mesh-terms=* Activities of Daily Living
-* Aged
-* Aging
-* Cohort Studies
-* Europe
-* Humans
-* Independent Living
-* Male
-* Middle Aged
-* Mortality
-* Proportional Hazards Models
-* Prospective Studies
-* Retirement
-* Risk Factors
-* Surveys and Questionnaires
-|keywords=* Aging
-* Comorbidity
-* Depressive symptoms
-* Diseases
-* Mortality risk
-|full-text-url=https://sci-hub.do/10.1016/j.archger.2020.104035
-}}
-{{medline-entry
-|title=Estimation of Wave Condition Number From Pressure Waveform Alone and Its Changes With Advancing Age in Healthy Women and Men.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32328003
-|keywords=* arterial wave reflection
-* cardiovascular biomarker
-* optimum cardiovascular function
-* vascular aging
-* wave condition number
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7161432
-}}
-{{medline-entry
-|title=Extended in vitro culture of primary human mesenchymal stem cells downregulates Brca1-related genes and impairs DNA double-strand break recognition.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32333827
-|keywords=*
-BRCA1
-* DNA repair
-* cellular aging
-* homologous recombination
-* mesenchymal stem cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7327915
-}}
-{{medline-entry
-|title=Effect of artificial dawn light on cardiovascular function, alertness, and balance in middle-aged and older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32307533
-|keywords=* aging
-* alertness
-* balance
-* blood pressure
-* heart rate
-* heart rate variability
-* light
-* sleep inertia
-|full-text-url=https://sci-hub.do/10.1093/sleep/zsaa082
-}}
-{{medline-entry
-|title=Heart Rate Performance Curve Is Dependent on Age, Sex, and Performance.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32300582
-|keywords=* aging
-* heart rate deflection
-* intensity prescription
-* maximal heart rate
-* sex differences
-* ß1-receptor sensitivity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7144539
-}}
-{{medline-entry
-|title=Physical activity trajectories, mortality, hospitalization, and disability in the Toledo Study of Healthy Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32163233
-|keywords=* Adverse outcomes
-* Healthy aging
-* Mortality
-* Older adults
-* Physical activity
-* Trajectories
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432572
-}}
-{{medline-entry
-|title=U-Shaped Association of Plasma Testosterone, and no Association of Plasma Estradiol, with Incidence of Fractures in Men.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32155267
-|keywords=* estradiol
-* fracture
-* male aging
-* osteoporosis
-* sex hormone-binding globulin
-* testosterone
-|full-text-url=https://sci-hub.do/10.1210/clinem/dgaa115
-}}
-{{medline-entry
-|title=Pregnancy-Related Bone Mineral and Microarchitecture Changes in Women Aged 30 to 45 Years.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32119748
-|keywords=* AGING
-* ANALYSIS/QUANTITATION OF BONE
-* BONE QCT/μCT
-* EPIDEMIOLOGY
-* GENERAL POPULATION STUDIES
-|full-text-url=https://sci-hub.do/10.1002/jbmr.3998
-}}
-{{medline-entry
-|title=Analysis of the world record time for combined father and son marathon.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31917623
-|keywords=* V̇o2max
-* aerobic exercise
-* aging
-* endurance
-* oxygen consumption
-* running
-|full-text-url=https://sci-hub.do/10.1152/japplphysiol.00819.2019
-}}
-{{medline-entry
-|title=Age-related reductions in heart rate variability do not worsen during exposure to humid compared to dry heat: A secondary analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31934605
-|keywords=* Aging
-* autonomic nervous system
-* heat stress
-* parasympathetic nervous system
-* relative humidity
-* sympathetic nervous system
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6949029
-}}
-{{medline-entry
-|title=Efficacy and Safety of Dapagliflozin in the Elderly: Analysis From the DECLARE-TIMI 58 Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31843945
-|mesh-terms=* Adult
-* Age Factors
-* Aged
-* Aged, 80 and over
-* Aging
-* Benzhydryl Compounds
-* Cardiovascular System
-* Diabetes Mellitus, Type 2
-* Diabetic Ketoacidosis
-* Female
-* Glucosides
-* Humans
-* Hypoglycemia
-* Hypoglycemic Agents
-* Incidence
-* Kidney
-* Male
-* Middle Aged
-* Sodium-Glucose Transporter 2 Inhibitors
-* Survival Analysis
-* Treatment Outcome
-* Urinary Tract Infections
-|full-text-url=https://sci-hub.do/10.2337/dc19-1476
-}}
-{{medline-entry
-|title=Validity of Prediction Equations of Maximal Heart Rate in Physically Active Female Adolescents and the Role of Maturation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31766291
-|mesh-terms=* Adolescent
-* Aging
-* Body Mass Index
-* Exercise
-* Exercise Test
-* Female
-* Heart Rate
-* Humans
-|keywords=* cardiac rate
-* exercise prescription
-* exercise testing
-* prediction equations
-* training zones
-* volleyball
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6915545
-}}
-{{medline-entry
-|title=Base excision repair but not DNA double-strand break repair is impaired in aged human adipose-derived stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31782607
-|mesh-terms=* Adipose Tissue
-* Adult
-* Aging
-* DNA Breaks, Double-Stranded
-* DNA End-Joining Repair
-* DNA Repair
-* Humans
-* Middle Aged
-* Recombinational DNA Repair
-* Stem Cells
-* Up-Regulation
-* X-ray Repair Cross Complementing Protein 1
-* Young Adult
-|keywords=* XRCC1
-* adipose-derived stem cells
-* base excision repair
-* genome integrity
-* human aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996963
-}}
-{{medline-entry
-|title=Urban-Rural Differences in Hip Fracture Mortality: A Nationwide NOREPOS Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31768493
-|keywords=* AGING
-* EPIDEMIOLOGY
-* GENERAL POPULATION STUDIES
-* OSTEOPOROSIS
-* STATISTICAL METHODS
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6874178
-}}
-{{medline-entry
-|title=Malnutrition as a Strong Predictor of the Onset of Sarcopenia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31783482
-|mesh-terms=* Aged
-* Aging
-* Cohort Studies
-* Female
-* Humans
-* Independent Living
-* Male
-* Malnutrition
-* Proportional Hazards Models
-* Prospective Studies
-* Risk Factors
-* Sarcopenia
-|keywords=* EWGSOP2
-* GLIM
-* SarcoPhAge
-* malnutrition
-* sarcopenia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6950107
-}}
-{{medline-entry
-|title=Acclimation to a thermoneutral environment abolishes age-associated alterations in heart rate and heart rate variability in conscious, unrestrained mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31776883
-|keywords=* Aging
-* Cardiac autonomic modulation
-* Heart rate
-* Heart rate variability
-* Thermoneutrality
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031176
-}}
-{{medline-entry
-|title=Long-term dementia risk prediction by the LIBRA score: A 30-year follow-up of the CAIDE study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31736136
-|mesh-terms=* Aged
-* Apolipoproteins E
-* Cognitive Dysfunction
-* Dementia
-* Female
-* Follow-Up Studies
-* Genetic Predisposition to Disease
-* Humans
-* Life Style
-* Male
-* Protective Factors
-* Risk Assessment
-* Risk Factors
-|keywords=* cognitive aging
-* cohort study
-* dementia
-* epidemiology
-* lifestyle
-* prevention
-* risk factors
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7003764
-}}
-{{medline-entry
-|title=Kidney function and its association to imminent, short- and long-term fracture risk-a longitudinal study in older women.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31754754
-|keywords=* Aging
-* Bone mineral density
-* Chronic kidney disease
-* Estimated glomerular filtration rate
-* Fracture
-* Women
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6946753
-}}
-{{medline-entry
-|title=Oxidatively Damaged DNA/RNA and 8-Isoprostane Levels Are Associated With the Development of Type 2 Diabetes at Older Age: Results From a Large Cohort Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31653645
-|mesh-terms=* Age of Onset
-* Aged
-* Aging
-* Biomarkers
-* Cohort Studies
-* DNA
-* DNA Damage
-* Diabetes Mellitus, Type 2
-* Dinoprost
-* Female
-* Follow-Up Studies
-* Germany
-* Humans
-* Incidence
-* Lipid Peroxidation
-* Male
-* Middle Aged
-* Oxidation-Reduction
-* Oxidative Stress
-* RNA
-|full-text-url=https://sci-hub.do/10.2337/dc19-1379
-}}
-{{medline-entry
-|title=Associations of vigorous physical activity with all-cause, cardiovascular and cancer mortality among 64 913 adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31548909
-|keywords=* cardio-protection
-* exercise
-* longevity
-* non-communicable diseases
-* physical activity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6733336
-}}
-{{medline-entry
-|title=Reduced cerebrovascular and cardioventilatory responses to intermittent hypoxia in elderly.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31557538
-|mesh-terms=* Adult
-* Aged
-* Aging
-* Blood Pressure
-* Brain
-* Cerebrovascular Circulation
-* Female
-* Heart Rate
-* Humans
-* Hypoxia
-* Male
-* Pulmonary Ventilation
-* Ultrasonography, Doppler, Transcranial
-* Young Adult
-|keywords=* Aging
-* Arterial oxygen saturation
-* Cerebral blood flow
-* Cerebral tissue oxygenation
-* Heart rate
-* Hypoxemia
-* Ventilation
-|full-text-url=https://sci-hub.do/10.1016/j.resp.2019.103306
-}}
-{{medline-entry
-|title=Vestibulo-sympathetic reflex in patients with bilateral vestibular loss.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31513442
-|mesh-terms=* Aging
-* Bilateral Vestibulopathy
-* Female
-* Humans
-* Male
-* Middle Aged
-* Reflex, Abnormal
-* Sympathetic Nervous System
-|keywords=* bilateral vestibular loss
-* compensation
-* multisensory integration
-* otolithic system
-* vestibulo-sympathetic reflex
-|full-text-url=https://sci-hub.do/10.1152/japplphysiol.00466.2019
-}}
-{{medline-entry
-|title=Heart rate and blood pressure in male Ts65Dn mice: a model to investigate cardiovascular responses in Down syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31496136
-|mesh-terms=* Animals
-* Autonomic Nervous System
-* Blood Pressure
-* Circadian Rhythm
-* Down Syndrome
-* Heart Rate
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Vascular Stiffness
-|keywords=* Aging
-* arterial stiffness
-* autonomic nervous system
-* circadian
-* pulse wave velocity
-* spectral analysis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6732568
-}}
-{{medline-entry
-|title=Body weight at 10 years of age and change in body composition between 8 and 10 years of age were related to survival in a longitudinal study of 39 Labrador retriever dogs.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31500653
-|mesh-terms=* Adipose Tissue
-* Animals
-* Body Composition
-* Body Weight
-* Dogs
-* Longevity
-* Longitudinal Studies
-* Survival Analysis
-|keywords=* Cohort
-* Cox
-* DEXA
-* Dogs
-* Fat mass
-* Healthspan
-* Lean mass
-* Lean to fat ratio
-* Longevity
-* Sarcopenia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6734441
-}}
-{{medline-entry
-|title=Dietary diversity offsets the adverse mortality risk among older indigenous Taiwanese.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31464406
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Asian Continental Ancestry Group
-* Diet
-* Female
-* Health Surveys
-* Humans
-* Indigenous Peoples
-* Longevity
-* Male
-* Mortality
-* Nutrition Surveys
-* Nutritional Status
-* Risk Factors
-* Taiwan
-|full-text-url=https://sci-hub.do/10.6133/apjcn.201909_28(3).0019
-}}
-{{medline-entry
-|title=Independent and joint effects of vascular and cardiometabolic risk factor pairs for risk of all-cause dementia: a prospective population-based study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31455442
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Apolipoprotein E4
-* Cognitive Dysfunction
-* Dementia
-* Exercise
-* Female
-* Heart Failure
-* Heterozygote
-* Humans
-* Hypertension
-* Male
-* Pennsylvania
-* Proportional Hazards Models
-* Prospective Studies
-* Risk Factors
-* Stroke
-|keywords=* Alzheimer‘s disease (AD)
-* apolipoprotein E (APOE)
-* cerebral vascular disease (CVD)
-* dementia
-* epidemiology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6948010
-}}
-{{medline-entry
-|title=Work Ability and Job Survival: Four-Year Follow-Up.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31466415
-|mesh-terms=* Adult
-* Brazil
-* Employment
-* Female
-* Follow-Up Studies
-* Hospitals
-* Humans
-* Male
-* Proportional Hazards Models
-* Work Capacity Evaluation
-|keywords=* aging
-* healthcare worker
-* life course
-* longitudinal studies
-* prolonged work career
-* work ability
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6747402
-}}
-{{medline-entry
-|title=Predictivity of bioimpedance phase angle for incident disability in older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31436391
-|keywords=* Aging
-* Body composition
-* Cellular health
-* Muscle mass
-* Nutrition
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7015240
-}}
-==HRAS==
-{{medline-entry
-|title=How do combinations of unhealthy behaviors relate to attitudinal factors and subjective health among the adult population in the Netherlands?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32245376
-|mesh-terms=* Adult
-* Alcohol Drinking
-* Attitude to Health
-* Cluster Analysis
-* Diagnostic Self Evaluation
-* Diet, Healthy
-* Exercise
-* Female
-* Health Risk Behaviors
-* Humans
-* Life Expectancy
-* Life Style
-* Logistic Models
-* Male
-* Middle Aged
-* Netherlands
-* Prevalence
-* Sedentary Behavior
-* Smoking
-* Surveys and Questionnaires
-* Young Adult
-|keywords=* Clustering risk attitude
-* Health behaviours
-* Subjective health
-* Time orientation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7126128
-}}
-{{medline-entry
-|title=Elucidating Proteoform Dynamics Underlying the Senescence Associated Secretory Phenotype.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31940439
-|keywords=* proteoform
-* quantitative proteomics
-* secretome
-* senescence
-* top-down proteomics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7032038
-}}
-==HS2ST1==
-{{medline-entry
-|title=Whole Genome Analysis of the Red-Crowned Crane Provides Insight into Avian Longevity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31940721
-|mesh-terms=* Animals
-* Avian Proteins
-* Birds
-* Endangered Species
-* Immunity
-* Longevity
-* Polymorphism, Genetic
-* Species Specificity
-* Transcriptome
-* Whole Genome Sequencing
-|keywords=* genome
-* longevity
-* red-crowned crane
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6999708
-}}
-==HSF1==
-{{medline-entry
-|title=A Mitochondrial Stress-Specific Form of [[HSF1]] Protects against Age-Related Proteostasis Collapse.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32735771
-|keywords=* HSF1
-* PP2A
-* aging
-* mitochondria
-* molecular chaperones
-* protein aggregation
-* proteostasis
-* stress responses
-|full-text-url=https://sci-hub.do/10.1016/j.devcel.2020.06.038
-}}
-{{medline-entry
-|title=Heat shock factor 1-mediated transcription activation of Omi/HtrA2 induces myocardial mitochondrial apoptosis in the aging heart.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31627188
-|mesh-terms=* Aging
-* Animals
-* Apoptosis
-* Heat Shock Transcription Factors
-* High-Temperature Requirement A Serine Peptidase 2
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Mitochondria, Heart
-* Myocytes, Cardiac
-* NIH 3T3 Cells
-* Transcriptional Activation
-* Up-Regulation
-|keywords=* Omi/HtrA2
-* age-related pathology
-* cardiovascular
-* mitochondria
-* transcriptional regulation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834417
-}}
-{{medline-entry
-|title=Multifactorial Attenuation of the Murine Heat Shock Response With Age.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31612204
-|keywords=* Aging
-* HSF1
-* Stress
-|full-text-url=https://sci-hub.do/10.1093/gerona/glz204
-}}
-==HSPA1A==
-{{medline-entry
-|title=Vitamin D3 treatment regulates apoptosis, antioxidant defense system, and DNA integrity in the epididymal sperm of an aged rat model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31566824
-|mesh-terms=* Aging
-* Animals
-* Antioxidants
-* Apoptosis
-* Cholecalciferol
-* Epididymis
-* Male
-* Rats
-* Rats, Wistar
-* Spermatozoa
-|keywords=* aging
-* apoptosis
-* oxidative stress
-* sperm
-|full-text-url=https://sci-hub.do/10.1002/mrd.23280
-}}
-==HSPA1L==
-{{medline-entry
-|title=Melatonin suppresses senescence-derived mitochondrial dysfunction in mesenchymal stem cells via the [[HSPA1L]]-mitophagy pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31965731
-|keywords=* HSPA1L
-* melatonin
-* mesenchymal stem cells
-* mitochondria
-* mitophagy
-* replicative senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059143
-}}
-==HTT==
-{{medline-entry
-|title=Biological Aging and the Cellular Pathogenesis of Huntington's Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32417788
-|keywords=* Biological aging
-* DNA damage
-* Huntington’s disease
-* cellular aging
-* microsatellite instability
-* neurodegeneration
-* oxidative stress
-* proteostasis
-* telomere
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7369111
-}}
-==ICE1==
-{{medline-entry
-|title=ATBS1-INTERACTING FACTOR 2 negatively regulates dark- and brassinosteroid-induced leaf senescence through interactions with INDUCER OF CBF EXPRESSION 1.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31783407
-|keywords=* ATBS1-INTERACTING FACTOR 2 (AIF2)
-* Arabidopsis
-* C-REPEAT BINDING FACTOR (CBF)
-* INDUCER OF CBF EXPRESSION 1 (ICE1)
-* PHYTOCHROME-INTERACTING FACTORS (PIFs)
-* basic helix–loop–helix (bHLH)
-* brassinosteroid (BR)
-* leaf senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031079
-}}
-==IDE==
-{{medline-entry
-|title=Dendrobium nobile Lindl. Alkaloids Ameliorate Cognitive Dysfunction in Senescence Accelerated SAMP8 Mice by Decreasing Amyloid-β Aggregation and Enhancing Autophagy Activity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32538851
-|keywords=* Aging
-* Dendrobium nobile Lindl. alkaloid (DNLA)
-* amyloid-β
-* autophagy
-* metformin
-* senescence accelerated mouse prone 8 (SAMP8)
-|full-text-url=https://sci-hub.do/10.3233/JAD-200308
-}}
-==IDH2==
-{{medline-entry
-|title=Reactive oxygen species-mediated senescence is accelerated by inhibiting Cdk2 in Idh2-deficient conditions.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31503005
-|mesh-terms=* Animals
-* Cellular Senescence
-* Cyclin-Dependent Kinase 2
-* Cyclin-Dependent Kinase Inhibitor p21
-* Embryo, Mammalian
-* Fibroblasts
-* Isocitrate Dehydrogenase
-* Mice
-* Mice, Knockout
-* NIH 3T3 Cells
-* Reactive Oxygen Species
-|keywords=* cell cycle
-* cyclin-dependent kinase 2 (Cdk2)
-* isocitrate dehydrogenase 2 (IDH2)
-* reactive oxygen species (ROS)
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6756887
-}}
-==IDS==
-{{medline-entry
-|title=Effect of immediate dentine sealing on the aging and fracture strength of lithium disilicate inlays and overlays.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32957211
-|keywords=* Aging
-* Ceramic
-* Fracture strength
-* Immediate dentin sealing
-* Inlay
-* Overlay
-|full-text-url=https://sci-hub.do/10.1016/j.jmbbm.2020.103906
-}}
-==IFI27==
-{{medline-entry
-|title=Ultraviolet B irradiation-induced keratinocyte senescence and impaired development of 3D epidermal reconstruct.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33151171
-|keywords=* epidermis
-* keratinocytes
-* reactive oxygen species
-* senescence
-* skin aging
-* ultraviolet radiation
-|full-text-url=https://sci-hub.do/10.2478/acph-2021-0011
-}}
-==IGF1==
-{{medline-entry
-|title=Genetic differences and longevity-related phenotypes influence lifespan and lifespan variation in a sex-specific manner in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33105070
-|keywords=* IGF1
-* antagonistic gene
-* female sexual maturation
-* lifespan variation
-* maximum lifespan
-* sex difference in lifespan
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7681063
-}}
-{{medline-entry
-|title=17α-estradiol modulates [[IGF1]] and hepatic gene expression in a sex-specific manner.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32857104
-|keywords=* 17α-estradiol
-* aging
-* growth hormone
-* insulin
-* insulin-like growth factor-1
-* liver
-|full-text-url=https://sci-hub.do/10.1093/gerona/glaa215
-}}
-{{medline-entry
-|title=Pan-mammalian analysis of molecular constraints underlying extended lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32043462
-|keywords=* RERconverge
-* computational biology
-* evolution
-* genetics
-* genomics
-* longevity
-* mammals
-* phylogenomics
-* systems biology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7012612
-}}
-{{medline-entry
-|title=17α-Estradiol promotes ovarian aging in growth hormone receptor knockout mice, but not wild-type littermates.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31698046
-|keywords=* Follicles
-* Ovarian aging
-* Ovarian reserve
-* Reproductive lifespan
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6911620
-}}
-==IGF1R==
-{{medline-entry
-|title=Comparison of mitochondrial transplantation by using a stamp-type multineedle injector and platelet-rich plasma therapy for hair aging in naturally aging mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32707439
-|keywords=* Aging mice
-* Hair growth
-* Mitochondrial transplantation
-* Pep-1
-* Platelet-rich plasma
-|full-text-url=https://sci-hub.do/10.1016/j.biopha.2020.110520
-}}
-==IGFBP1==
-{{medline-entry
-|title=Role of [[IGFBP1]] in the senescence of vascular endothelial cells and severity of aging‑related coronary atherosclerosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31545483
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Atherosclerosis
-* Cells, Cultured
-* Cellular Senescence
-* Coronary Artery Disease
-* Coronary Vessels
-* Down-Regulation
-* Endothelial Cells
-* Female
-* Humans
-* Insulin-Like Growth Factor Binding Protein 1
-* Jagged-1 Protein
-* Male
-* Middle Aged
-* Signal Transduction
-* Up-Regulation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6777673
-}}
-==IGFBP2==
-{{medline-entry
-|title=Intracellular Insulin-like growth factor binding protein 2 ([[IGFBP2]]) contributes to the senescence of keratinocytes in psoriasis by stabilizing cytoplasmic p21.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32302288
-|keywords=* insulin-like growth factor binding protein 2
-* keratinocytes
-* p21CIP1/WAF1
-* psoriasis
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7202509
-}}
-==IGFBP3==
-{{medline-entry
-|title=Cellular and Molecular Biomarkers Indicate Premature Aging in Pseudoxanthoma Elasticum Patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32489700
-|keywords=* CCL11
-* GDF11
-* IGF1
-* IGFBP
-* aging
-* pseudoxanthoma elasticum
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7220280
-}}
-{{medline-entry
-|title=Paracrine senescence of human endometrial mesenchymal stem cells: a role for the insulin-like growth factor binding protein 3.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31951594
-|keywords=* IGFBP3
-* endocytosis
-* endometrial stem cells
-* paracrine senescence
-* secretome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053595
-}}
-==IGFBP4==
-{{medline-entry
-|title=Quantitative iTRAQ-based proteomic analysis of differentially expressed proteins in aging in human and monkey.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31601169
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Animals
-* Cognition
-* Female
-* Gene Expression Regulation
-* Gene Regulatory Networks
-* Haplorhini
-* Humans
-* Insulin-Like Growth Factor Binding Protein 4
-* Male
-* Mice
-* Proteomics
-|keywords=* Cognitive dysfunction
-* IGFBP4
-* Plasma
-* Quantitative proteomics
-* iTRAQ
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6788010
-}}
-==IGFBP7==
-{{medline-entry
-|title=Reprogramming of human fibroblasts into osteoblasts by insulin-like growth factor-binding protein 7.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31904196
-|keywords=* IGFBP7
-* IL-6
-* human fibroblast
-* osteoblast
-* reprogramming
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031646
-}}
-==IHH==
-{{medline-entry
-|title=Indian Hedgehog regulates senescence in bone marrow-derived mesenchymal stem cell through modulation of ROS/mTOR/4EBP1, p70S6K1/2 pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32235006
-|keywords=* Indian hedgehog
-* aging
-* differentiation
-* mammalian target of rapamycin
-* mesenchymal stem cell
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185126
-}}
-==IL10==
-{{medline-entry
-|title=The beneficial effect of physical exercise on inflammatory makers in older individuals.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32504508
-|keywords=* IL-6 expression
-* Inflammatory markers
-* aerobic exercise
-* aging
-* plasma IL-6 levels
-* resistance training
-|full-text-url=https://sci-hub.do/10.2174/1871530320666200606225357
-}}
-{{medline-entry
-|title=Astrocyte senescence may drive alterations in GFAPα, CDKN2A p14 , and TAU3 transcript expression and contribute to cognitive decline.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31654269
-|mesh-terms=* Aged
-* Alternative Splicing
-* Astrocytes
-* Cells, Cultured
-* Cellular Senescence
-* Cognitive Dysfunction
-* Cytokines
-* Gene Expression
-* Glial Fibrillary Acidic Protein
-* Humans
-* Matrix Metalloproteinases
-* Transcription, Genetic
-* Tumor Suppressor Protein p14ARF
-* tau Proteins
-|keywords=* Alternative splicing
-* Gene expression
-* Neurodegenerative disease
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6885035
-}}
-{{medline-entry
-|title=Dietary Spray-Dried Porcine Plasma Prevents Cognitive Decline in Senescent Mice and Reduces Neuroinflammation and Oxidative Stress.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31562503
-|mesh-terms=* Animals
-* Cognition Disorders
-* Encephalitis
-* Male
-* Mice
-* Oxidative Stress
-* Plasma
-* Swine
-|keywords=* aging
-* cognitive decline
-* dietary supplementation
-* neuroinflammation
-* spray-dried animal plasma
-|full-text-url=https://sci-hub.do/10.1093/jn/nxz239
-}}
-==IL15==
-{{medline-entry
-|title=Moderate physical activity associated with a higher naïve/memory T-cell ratio in healthy old individuals: potential role of [[IL15]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32221610
-|keywords=* T cells
-* ageing
-* immune senescence
-* older people
-* physical activity
-|full-text-url=https://sci-hub.do/10.1093/ageing/afaa035
-}}
-==IL1A==
-{{medline-entry
-|title=IL1B triggers inflammatory cytokine production in bovine oviduct epithelial cells and induces neutrophil accumulation via CCL2.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33099841
-|keywords=* CCL2
-* cellular senescence
-* inflammaging
-* senescence-associated secretory phenotype
-|full-text-url=https://sci-hub.do/10.1111/aji.13365
-}}
-==IL2==
-{{medline-entry
-|title=Impact of Aging on the Phenotype of Invariant Natural Killer T Cells in Mouse Thymus.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33193368
-|keywords=* IL2
-* aging
-* invariant natural killer T cells
-* thymus
-* transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7662090
-}}
-==IL6==
-{{medline-entry
-|title=Basic immunology may lead to translational therapeutic rationale: SARS-CoV-2 and rheumatic diseases.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32645207
-|mesh-terms=* Adaptive Immunity
-* Aged
-* Antirheumatic Agents
-* COVID-19
-* Comorbidity
-* Coronavirus Infections
-* Disease Outbreaks
-* Female
-* Humans
-* Hydroxychloroquine
-* Immunity, Innate
-* Immunologic Factors
-* Immunosuppressive Agents
-* Italy
-* Male
-* Middle Aged
-* Pandemics
-* Pneumonia, Viral
-* Rheumatic Diseases
-* Risk Assessment
-* Severe Acute Respiratory Syndrome
-|keywords=* COVID-19
-* SARS-CoV-2
-* geriatrics
-* pathophysiology
-* pediatrics
-* rheumatology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7404583
-}}
-{{medline-entry
-|title=ATM-deficient neural precursors develop senescence phenotype with disturbances in autophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32621937
-|keywords=* ATM
-* Ataxia-telangiectasia
-* Autophagy
-* Mitophagy
-* Neural progenitors
-* Oxidative stress
-* Senescence
-* hiPSCs
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2020.111296
-}}
-{{medline-entry
-|title=The microRNA-34a-Induced Senescence-Associated Secretory Phenotype (SASP) Favors Vascular Smooth Muscle Cells Calcification.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32585876
-|keywords=* IL6
-* SASP
-* VSMCs
-* inflammaging
-* senescence
-* vascular calcification
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7352675
-}}
-{{medline-entry
-|title=Impact of Influenza on Pneumococcal Vaccine Effectiveness during [i]Streptococcus pneumoniae[/i] Infection in Aged Murine Lung.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32545261
-|keywords=* Streptococcus pneumoniae
-* aging
-* influenza
-* vaccine effectiveness
-* viral immune imprinting
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7349919
-}}
-{{medline-entry
-|title=Patterns of multi-domain cognitive aging in participants of the Long Life Family Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32514870
-|keywords=* Aging
-* Biomarker
-* Cognition
-* Neuropsychology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7525612
-}}
-{{medline-entry
-|title=Cholest-4,6-Dien-3-One Promote Epithelial-To-Mesenchymal Transition (EMT) in Biliary Tree Stem/Progenitor Cell Cultures In Vitro.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31731674
-|mesh-terms=* Biliary Tract
-* Cell Differentiation
-* Cell Proliferation
-* Cells, Cultured
-* Cellular Senescence
-* Cholestenones
-* Epithelial-Mesenchymal Transition
-* Histone Deacetylase 6
-* Humans
-* Interleukin-6
-* Signal Transduction
-* Stem Cells
-* Tissue Donors
-|keywords=* BMP pathway
-* SHH pathway
-* biliary tree stem/progenitor cells (BTSCs)
-* epithelial-to-mesenchymal transition (EMT)
-* primary sclerosing cholangitis (PSC)
-* senescence
-* telomerase
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6912632
-}}
-{{medline-entry
-|title=Single xenotransplant of rat brown adipose tissue prolonged the ovarian lifespan of aging mice by improving follicle survival.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31389140
-|mesh-terms=* Adipose Tissue, Brown
-* Animals
-* Cellular Senescence
-* Female
-* Longevity
-* Male
-* Mice
-* Ovarian Follicle
-* Ovary
-* Rats
-* Rats, Sprague-Dawley
-* Transplantation, Heterologous
-|keywords=* aging
-* brown adipose tissue (BAT)
-* lifespan
-* mice
-* ovary
-* rat
-* xenotransplant
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826128
-}}
-==ILDR1==
-{{medline-entry
-|title=Genome-wide association meta-analysis identifies five novel loci for age-related hearing impairment.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31645637
-|mesh-terms=* Aging
-* Animals
-* Auditory Pathways
-* Female
-* Gene Expression Regulation
-* Genetic Loci
-* Genetic Predisposition to Disease
-* Genome-Wide Association Study
-* Hearing Loss
-* Humans
-* Male
-* Mice
-* Middle Aged
-* Molecular Sequence Annotation
-* Phenotype
-* Reproducibility of Results
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6811684
-}}
-==IMPACT==
-{{medline-entry
-|title=Load-dependent modulation of alpha oscillations during working memory encoding and retention in young and older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33141460
-|keywords=* EEG
-* alpha oscillations
-* cognitive aging
-* working memory
-|full-text-url=https://sci-hub.do/10.1111/psyp.13719
-}}
-{{medline-entry
-|title=Using Video Telehealth to Deliver Patient-Centered Collaborative Care: The G-[[IMPACT]] Pilot.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32228299
-|keywords=* Telehealth
-* aging
-* care coordination
-* home care
-* interdisciplinary
-* medicine
-* older adult
-* video
-|full-text-url=https://sci-hub.do/10.1080/07317115.2020.1738000
-}}
-{{medline-entry
-|title=AGING, HEART RATE VARIABILITY AND METABOLIC [[IMPACT]] OF OBESITY.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31969754
-|mesh-terms=* Aging
-* Autonomic Nervous System
-* Autonomic Nervous System Diseases
-* Female
-* Heart Rate
-* Humans
-* Male
-* Metabolic Diseases
-* Metabolism
-* Middle Aged
-* Obesity
-|keywords=* Aging
-* Autonomic nervous system
-* Heart rate
-* Obesity, metabolically benign
-* Parasympathetic nervous system
-* Sympathetic nervous system
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6971797
-}}
-==INS==
-{{medline-entry
-|title=Melatonin protects [[INS]]-1 pancreatic β-cells from apoptosis and senescence induced by glucotoxicity and glucolipotoxicity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32673151
-|keywords=* Melatonin
-* Senescence
-* glucolipotoxicity
-* glucotoxicity
-* pancreatic β-cell
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7527021
-}}
-{{medline-entry
-|title=Nicotine triggers islet β cell senescence to facilitate the progression of type 2 diabetes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32473187
-|mesh-terms=* Animals
-* Blotting, Western
-* Calcium
-* Cellular Senescence
-* Diabetes Mellitus, Type 2
-* Disease Progression
-* Dose-Response Relationship, Drug
-* Enzyme-Linked Immunosorbent Assay
-* Glucose
-* Insulin-Secreting Cells
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Nicotine
-* Reactive Oxygen Species
-* Real-Time Polymerase Chain Reaction
-* beta-Galactosidase
-|keywords=* ROS
-* islet β cells
-* nicotine
-* senescence
-* type 2 diabetes
-|full-text-url=https://sci-hub.do/10.1016/j.tox.2020.152502
-}}
-==INSL3==
-{{medline-entry
-|title=Effect of Thyroxine Replacement on Leydig Cell and Sertoli Cell Function in Men with Hypothyroidism.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33083267
-|keywords=* Androgen deficiency in aging male
-* arizona sexual experience scale
-* hypothyroidism
-* inhibin B
-* insulin-like factor 3
-* semen analysis
-* sperm motility
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7539029
-}}
-==IP6K1==
-{{medline-entry
-|title=The Role of the IGF-1 Signaling Cascade in Muscle Protein Synthesis and Anabolic Resistance in Aging Skeletal Muscle.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31552262
-|keywords=* Akt
-* IP6K1
-* aging
-* anabolic resistance
-* mTOR
-* protein
-* resistance exercise
-* sarcopenia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6746962
-}}
-==IQGAP1==
-{{medline-entry
-|title=[[IQGAP1]]-dysfunction leads to induction of senescence in human vascular smooth muscle cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32592713
-|keywords=* Cellular bridges (CBs)
-* IQGAP1
-* Intercellular communication
-* Senescence
-* Tunneling nanotubes (TNTs)
-* Vascular smooth muscle cells (VSMCs)
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2020.111295
-}}
-{{medline-entry
-|title=Hyaluronan-binding protein 1 (HABP1) overexpression triggers induction of senescence in fibroblasts cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32068317
-|keywords=* F-HABP07
-* HABP1
-* IQGAP1
-* senescence
-|full-text-url=https://sci-hub.do/10.1002/cbin.11326
-}}
-==IRF8==
-{{medline-entry
-|title=[[IRF8]] induces senescence of lung cancer cells to exert its tumor suppressive function.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31594449
-|mesh-terms=* A549 Cells
-* Animals
-* Carcinogenesis
-* Carcinoma, Non-Small-Cell Lung
-* Cell Movement
-* Cell Proliferation
-* Cellular Senescence
-* Gene Expression Regulation, Neoplastic
-* Heterografts
-* Humans
-* Interferon Regulatory Factors
-* Mice
-* Prognosis
-* Signal Transduction
-* Tumor Suppressor Proteins
-|keywords=* IRF8
-* NSCLC
-* cell cycle arrest
-* cell senescence
-* tumor suppresser gene
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6927690
-}}
-==IRS1==
-{{medline-entry
-|title=MicroRNA-34a causes ceramide accumulation and effects insulin signaling pathway by targeting ceramide kinase (CERK) in aging skeletal muscle.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32056304
-|keywords=* CERK
-* aging muscle
-* insulin signaling pathway
-* miR-34a
-|full-text-url=https://sci-hub.do/10.1002/jcb.29312
-}}
-{{medline-entry
-|title=Longevity in response to lowered insulin signaling requires glycine N-methyltransferase-dependent spermidine production.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31721422
-|keywords=* IGF
-* aging
-* autophagy
-* insulin
-* lifespan
-* metabolism
-* polyamine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6974722
-}}
-{{medline-entry
-|title=Serine Phosphorylation of [[IRS1]] Correlates with Aβ-Unrelated Memory Deficits and Elevation in Aβ Level Prior to the Onset of Memory Decline in AD.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31426549
-|mesh-terms=* Aging
-* Alzheimer Disease
-* Amyloid beta-Peptides
-* Amyloid beta-Protein Precursor
-* Animals
-* Brain
-* Diabetes Mellitus, Type 2
-* Humans
-* Insulin
-* Insulin Receptor Substrate Proteins
-* Male
-* Memory
-* Memory Disorders
-* Mice, Inbred C57BL
-* Mice, Transgenic
-* Phosphorylation
-* Serine
-* Signal Transduction
-|keywords=* AMPK
-* Alzheimer’s disease
-* Aβ
-* IRS1
-* aging
-* diabetes
-* energy depletion
-* hippocampus
-* memory decline
-* serine phosphorylation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6723493
-}}
-==IRS2==
-{{medline-entry
-|title=Effects of Heshouwuyin on gene expression of the insulin/IGF signalling pathway in rat testis and spermatogenic cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33264567
-|keywords=* IGF1
-* IGFBP3
-* INSR
-* IRS1
-* IRS2
-* Male reproduction
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7717869
-}}
-==ITGA3==
-{{medline-entry
-|title=A transcriptomic analysis of serial-cultured, tonsil-derived mesenchymal stem cells reveals decreased integrin α3 protein as a potential biomarker of senescent cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32807231
-|keywords=* AKT
-* Culture-aged
-* ECM-receptor protein
-* Integrin α3
-* Senescence
-* Serial passaging
-* Tonsil-derived mesenchymal stem cells
-* Transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7430027
-}}
-==ITGA5==
-{{medline-entry
-|title=Kaempferol alleviates the reduction of developmental competence during aging of porcine oocytes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31486245
-|mesh-terms=* Animals
-* Blastocyst
-* Cellular Senescence
-* Embryo Culture Techniques
-* Embryo, Mammalian
-* Embryonic Development
-* Female
-* Integrins
-* Kaempferols
-* Mitochondria
-* Nanog Homeobox Protein
-* Octamer Transcription Factor-3
-* Oocytes
-* Oxidative Stress
-* RNA, Messenger
-* Reactive Oxygen Species
-* Swine
-|keywords=* embryonic development
-* kaempferol
-* oocyte aging
-* porcine
-|full-text-url=https://sci-hub.do/10.1111/asj.13280
-}}
-==ITGAM==
-{{medline-entry
-|title=Comparative Analysis of Gene Expression Patterns for Oral Epithelium-Related Functions with Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31732940
-|mesh-terms=* Aging
-* Animals
-* Disease Models, Animal
-* Epithelial Cells
-* Gingiva
-* Macaca mulatta
-* Oligonucleotide Array Sequence Analysis
-* Transcriptome
-|full-text-url=https://sci-hub.do/10.1007/978-3-030-28524-1_11
-}}
-==IVD==
-{{medline-entry
-|title=MicroRNAs in Intervertebral Disc Degeneration, Apoptosis, Inflammation, and Mechanobiology.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32443722
-|keywords=* ECM
-* MMP
-* annulus fibrosus
-* cartilaginous endplate
-* degenerative disc disease
-* miRNA
-* nucleus pulposus
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7279351
-}}
-{{medline-entry
-|title=A step-by-step protocol for isolation of murine nucleus pulposus cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31891122
-|keywords=* aging
-* gene expression
-* intervertebral disc degeneration
-* nucleus pulposus
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6920701
-}}
-{{medline-entry
-|title=Caspase-3 knockout inhibits intervertebral disc degeneration related to injury but accelerates degeneration related to aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31852919
-|mesh-terms=* Aging
-* Animals
-* Annulus Fibrosus
-* Apoptosis
-* Biomarkers
-* Carcinogenesis
-* Caspase 3
-* Cell Count
-* Extracellular Matrix
-* Intervertebral Disc
-* Intervertebral Disc Degeneration
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Nucleus Pulposus
-* Up-Regulation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6920379
-}}
-{{medline-entry
-|title=Finite element and deformation analyses predict pattern of bone failure in loaded zebrafish spines.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31690186
-|mesh-terms=* Aging
-* Animals
-* Back Pain
-* Disease Models, Animal
-* Finite Element Analysis
-* Humans
-* Intervertebral Disc
-* Movement
-* Weight-Bearing
-* Zebrafish
-|keywords=* deformation
-* finite element
-* geometric morphometrics
-* mechanics
-* spine
-* zebrafish
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6893493
-}}
-{{medline-entry
-|title=Improvement in determining the risk of damage to the human lumbar functional spinal unit considering age, height, weight and sex using a combination of FEM and RSM.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31473842
-|mesh-terms=* Adult
-* Age Factors
-* Aging
-* Analysis of Variance
-* Biomechanical Phenomena
-* Body Height
-* Body Mass Index
-* Body Weight
-* Cortical Bone
-* Female
-* Finite Element Analysis
-* Humans
-* Imaging, Three-Dimensional
-* Intervertebral Disc
-* Lumbar Vertebrae
-* Male
-* Models, Biological
-* Range of Motion, Articular
-* Risk Factors
-* Sex Characteristics
-|keywords=* Age
-* Biomechanics
-* Body mass index (BMI)
-* Finite element method (FEM)
-* Functional spinal unit (FSU)
-* Height
-* Response surface method (RSM)
-* Sex
-* Weight
-|full-text-url=https://sci-hub.do/10.1007/s10237-019-01215-4
-}}
-{{medline-entry
-|title=In vivo contrast-enhanced microCT for the monitoring of mouse thoracic, lumbar, and coccygeal intervertebral discs.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31463468
-|keywords=* Contrast‐enhanced microCT
-* aging
-* intervertebral disc
-* mouse model
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6686789
-}}
-==JAK1==
-{{medline-entry
-|title=Irradiation-induced senescence of bone marrow mesenchymal stem cells aggravates osteogenic differentiation dysfunction via paracrine signaling.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32233952
-|mesh-terms=* Bone Resorption
-* Cell Cycle Checkpoints
-* Cell Differentiation
-* Cell Proliferation
-* Cellular Senescence
-* DNA Damage
-* Gene Expression Regulation, Developmental
-* Histones
-* Humans
-* Janus Kinase 1
-* Mesenchymal Stem Cells
-* Mitochondria
-* Osteogenesis
-* Paracrine Communication
-* Radiation
-* Reactive Oxygen Species
-* STAT3 Transcription Factor
-* Signal Transduction
-|keywords=* SASP
-* bone marrow mesenchymal stem cells
-* cellular senescence
-* irradiation
-* osteogenic differentiation
-|full-text-url=https://sci-hub.do/10.1152/ajpcell.00520.2019
-}}
-{{medline-entry
-|title=The Upregulation of Toll-Like Receptor 3 via Autocrine IFN-β Signaling Drives the Senescence of Human Umbilical Cord Blood-Derived Mesenchymal Stem Cells Through [[JAK1]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31396213
-|mesh-terms=* Autocrine Communication
-* Cellular Senescence
-* Fetal Blood
-* Humans
-* Interleukin-6
-* Janus Kinase 1
-* Mesenchymal Stem Cells
-* Toll-Like Receptor 3
-* Up-Regulation
-|keywords=* Janus kinase 1 (JAK1)
-* Toll-like receptor 3 (TLR3)
-* interferon-β (IFN-β)
-* mesenchymal stromal cell (MSC)
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6665952
-}}
-==JAK2==
-{{medline-entry
-|title=Senescence in Monocytes Facilitates Dengue Virus Infection by Increasing Infectivity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32850477
-|keywords=* DC-SIGN
-* IL-10
-* dengue virus
-* monocytes
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7399640
-}}
-{{medline-entry
-|title=Quercetin Directly Targets [[JAK2]] and PKCδ and Prevents UV-Induced Photoaging in Human Skin.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31652815
-|mesh-terms=* Antioxidants
-* Cell Line
-* Cells, Cultured
-* Cyclooxygenase 2
-* Humans
-* Janus Kinase 2
-* MAP Kinase Signaling System
-* Matrix Metalloproteinase 1
-* NF-kappa B
-* Protein Kinase C-delta
-* Quercetin
-* STAT3 Transcription Factor
-* Skin
-* Skin Aging
-* Transcription Factor AP-1
-* Ultraviolet Rays
-|keywords=* JAK2
-* PKC-delta
-* quercetin
-* skin aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6862686
-}}
-{{medline-entry
-|title=[Red blood cell lifespan detected by endogenous carbon monoxide breath test in patients with polycythemia vera].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31594177
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Breath Tests
-* Carbon Monoxide
-* Case-Control Studies
-* Erythrocyte Count
-* Erythrocytes
-* Female
-* Humans
-* Janus Kinase 2
-* Longevity
-* Male
-* Middle Aged
-* Polycythemia Vera
-|keywords=* Carbon monoxide breath test
-* Polycythemia vera
-* Red blood cell lifespan
-|full-text-url=https://sci-hub.do/10.3760/cma.j.issn.0578-1426.2019.10.010
-}}
-{{medline-entry
-|title=Roles of [[JAK2]] in Aging, Inflammation, Hematopoiesis and Malignant Transformation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31398915
-|mesh-terms=* Aging
-* Animals
-* Hematopoiesis
-* Humans
-* Inflammation
-* Janus Kinase 2
-* Mice
-* Myeloproliferative Disorders
-* Neoplasms
-|keywords=* JAK2
-* Janus-kinase
-* aging
-* clonal hematopoiesis (CHIP), myeloproliferative neoplasia (MPN)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6721738
-}}
-==JUN==
-{{medline-entry
-|title=Age-Onset Phosphorylation of a Minor Actin Variant Promotes Intestinal Barrier Dysfunction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31794717
-|mesh-terms=* Actin Cytoskeleton
-* Actins
-* Aging
-* Animals
-* Binding Sites
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* Intercellular Junctions
-* Intestinal Mucosa
-* JNK Mitogen-Activated Protein Kinases
-* Phosphorylation
-* Protein Phosphatase 1
-* Transcription Factors
-* Troponin
-|keywords=* HSF-1
-* actin
-* aging
-* barrier
-* intestine
-* junctions
-* kinase
-* pathogenesis
-* phosphorylation
-* stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6897307
-}}
-==JUNB==
-{{medline-entry
-|title=Promotion of cellular senescence by THG-1/TSC22D4 knockout through activation of [[JUNB]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31806366
-|mesh-terms=* Cell Line, Tumor
-* Cell Proliferation
-* Cellular Senescence
-* Cyclin-Dependent Kinase Inhibitor p21
-* Gene Expression Regulation, Neoplastic
-* Gene Knockout Techniques
-* HEK293 Cells
-* Humans
-* Transcription Factors
-* Transcription, Genetic
-* Up-Regulation
-|keywords=* Cellular senescence
-* JUNB
-* P21(CDKN1A)
-* THG-1(TSC22D4)
-|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2019.11.145
-}}
-==KAT6B==
-{{medline-entry
-|title=Aging-associated decrease in the histone acetyltransferase [[KAT6B]] is linked to altered hematopoietic stem cell differentiation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32014431
-|mesh-terms=* Aging
-* Animals
-* Cell Differentiation
-* Epigenesis, Genetic
-* Erythroid Cells
-* Gene Expression Profiling
-* Gene Expression Regulation, Enzymologic
-* Gene Knockout Techniques
-* Histone Acetyltransferases
-* Male
-* Mice
-* Mice, Transgenic
-* Myeloid Progenitor Cells
-* Transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7179256
-}}
-==KCNK2==
-{{medline-entry
-|title=Brain age prediction using deep learning uncovers associated sequence variants.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31776335
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Brain
-* Databases, Factual
-* Deep Learning
-* Genome-Wide Association Study
-* Humans
-* Iceland
-* Magnetic Resonance Imaging
-* Middle Aged
-* Neural Networks, Computer
-* Neuropsychological Tests
-* Polymorphism, Single Nucleotide
-* United Kingdom
-* Young Adult
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6881321
-}}
-==KCNQ4==
-{{medline-entry
-|title=Guanylyl Cyclase A/cGMP Signaling Slows Hidden, Age- and Acoustic Trauma-Induced Hearing Loss.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32327991
-|keywords=* KCNQ4
-* PARP-1
-* aging
-* cGMP
-* guanylyl cyclase A
-* hidden hearing loss
-* inner ear
-* otoprotection
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7160671
-}}
-==KCTD12==
-{{medline-entry
-|title=The association between poverty and gene expression within peripheral blood mononuclear cells in a diverse Baltimore City cohort.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32970748
-|mesh-terms=* Adult
-* Demography
-* Female
-* Gene Expression Profiling
-* Humans
-* Longevity
-* Male
-* Metabolic Networks and Pathways
-* Middle Aged
-* Monocytes
-* Poverty
-* Transcriptome
-* Urban Population
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7514036
-}}
-==KDM2A==
-{{medline-entry
-|title=SIRT6 mono-ADP ribosylates [[KDM2A]] to locally increase H3K36me2 at DNA damage sites to inhibit transcription and promote repair.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32584788
-|keywords=* DNA repair
-* SIRT6
-* genome stability
-* longevity
-* transcription
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343504
-}}
-==KDM2B==
-{{medline-entry
-|title=Identification of Structural Elements of the Lysine Specific Demethylase 2B CxxC Domain Associated with Replicative Senescence Bypass in Primary Mouse Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32270414
-|keywords=* Lysine demethylase
-* Non-methylated CpG
-* Oncogene
-* Polycomb repressive complex
-* Replicative senescence
-* Zn-finger
-|full-text-url=https://sci-hub.do/10.1007/s10930-020-09895-z
-}}
-==KDM3A==
-{{medline-entry
-|title=[[KDM3A]] and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin Reorganization.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31704649
-|keywords=* Cell Biology
-* DNA damage
-* Molecular Mechanism of Gene Regulation
-* Stem Cells Research
-* bone aging
-* condensin
-* epigenetic regulation
-* histone demethylase
-* mesenchymal stromal cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6888768
-}}
-==KEAP1==
-{{medline-entry
-|title=NRF2 pathway activation by [[KEAP1]] inhibition attenuates the manifestation of aging phenotypes in salivary glands.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32590331
-|keywords=* Aging
-* KEAP1
-* Mouse
-* NRF2
-* Salivary glands
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7322188
-}}
-{{medline-entry
-|title=Adaptation of the master antioxidant response connects metabolism, lifespan and feather development pathways in birds.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32424161
-|mesh-terms=* Adaptation, Physiological
-* Animals
-* Antioxidants
-* Basal Metabolism
-* Biological Evolution
-* Birds
-* Cell Nucleus
-* Feathers
-* Fibroblasts
-* Genomics
-* Glutathione Transferase
-* HEK293 Cells
-* Humans
-* Kelch-Like ECH-Associated Protein 1
-* Longevity
-* NF-E2-Related Factor 2
-* Oxidative Stress
-* Phylogeny
-* Proteasome Endopeptidase Complex
-* Protein Binding
-* Protein Transport
-* Ubiquitination
-* Up-Regulation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7234996
-}}
-==KIN==
-{{medline-entry
-|title=The noncanonical small heat shock protein HSP-17 from [i]Caenorhabditis elegans[/i] is a selective protein aggregase.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32001616
-|mesh-terms=* Animals
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* Casein Kinase I
-* Heat-Shock Proteins, Small
-* Longevity
-* Malate Dehydrogenase
-* Peptides
-* Protein Aggregates
-* Protein Folding
-* RNA Interference
-* RNA, Small Interfering
-* Recombinant Proteins
-|keywords=* Caenorhabditis elegans (C. elegans)
-* chaperone
-* protein aggregates
-* protein aggregation
-* protein folding
-* proteostasis
-* selective protein aggregase
-* small heat shock protein (sHsp)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7062175
-}}
-==KIT==
-{{medline-entry
-|title=Prediction of ovarian aging using ovarian expression of BMP15, GDF9, and C-[[KIT]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32223330
-|keywords=* BMP15
-* C-KIT
-* GDF9
-* Ovarian aging
-* biomarkers
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7221484
-}}
-==KLF2==
-{{medline-entry
-|title=[[KLF2]] induces the senescence of pancreatic cancer cells by cooperating with FOXO4 to upregulate p21.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31866399
-|mesh-terms=* Animals
-* Carcinogenesis
-* Cell Cycle Proteins
-* Cell Line
-* Cells, Cultured
-* Cellular Senescence
-* Cyclin-Dependent Kinase Inhibitor p21
-* Forkhead Transcription Factors
-* Kruppel-Like Transcription Factors
-* Male
-* Mice
-* Mice, Nude
-* Pancreatic Neoplasms
-* Protein Binding
-* Up-Regulation
-|keywords=* FOXO4
-* KLF2
-* Pancreatic cancer
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.yexcr.2019.111784
-}}
-==KLF4==
-{{medline-entry
-|title=Extracellular Vesicles from Healthy Cells Improves Cell Function and Stemness in Premature Senescent Stem Cells by miR-302b and HIF-1α Activation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32630449
-|keywords=* aging
-* extracellular vesicles
-* oxygen
-* physiological oxygen concentration
-* physioxia
-* redox
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7357081
-}}
-{{medline-entry
-|title=Soluble klotho regulates the function of salivary glands by activating [[KLF4]] pathways.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31581134
-|mesh-terms=* Animals
-* Cells, Cultured
-* Down-Regulation
-* Gene Expression Regulation
-* Glucuronidase
-* HEK293 Cells
-* Humans
-* Kruppel-Like Transcription Factors
-* Membrane Proteins
-* Mice
-* Mice, Knockout
-* Nuclear Proteins
-* RNA Interference
-* RNA, Small Interfering
-* Salivary Glands
-|keywords=* KLF4
-* aging
-* salivary gland
-* soluble klotho
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6814581
-}}
-==KLF6==
-{{medline-entry
-|title=Krüppel-Like Factor 6 Is Required for Oxidative and Oncogene-Induced Cellular Senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31824948
-|keywords=* DNA damage
-* KLF6
-* cell proliferation
-* cellular senescence
-* ras oncogene
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6882731
-}}
-==KRAS==
-{{medline-entry
-|title=Chemical Pathology of Homocysteine VIII. Effects of Tocotrienol, Geranylgeraniol, and Squalene on Thioretinaco Ozonide, Mitochondrial Permeability, and Oxidative Phosphorylation in Arteriosclerosis, Cancer, Neurodegeneration and Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33067202
-|keywords=* adenosine triphosphate
-* aging
-* antioxidant
-* apoptosis
-* atherogenesis
-* cancer
-* carcinogenesis
-* cholesterol
-* free radical
-* geraniol
-* geranylgeraniol
-* homocysteine
-* menoquinone
-* mitochondrial dysfunction
-* mitochondrial membrane potential
-* mitochondrial permeability transition pore
-* mitophagy
-* neuro-degeneration
-* oxidative phosphorylation
-* oxidative stress
-* squalene
-* statin
-* stellate cells
-* testosterone
-* thioretinaco ozonide
-* thioretinamide
-* tocopherol
-* tocotrienol
-* ubiquinone
-}}
-{{medline-entry
-|title=Senescence-Induced Vascular Remodeling Creates Therapeutic Vulnerabilities in Pancreas Cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32234521
-|mesh-terms=* Aging
-* Animals
-* CD8-Positive T-Lymphocytes
-* Carcinoma, Pancreatic Ductal
-* Cell Line, Tumor
-* Cell Proliferation
-* Cyclin-Dependent Kinase 4
-* Cyclin-Dependent Kinase 6
-* Gene Expression Regulation, Neoplastic
-* Genes, ras
-* Humans
-* Immunotherapy
-* MAP Kinase Signaling System
-* Mice
-* Pancreatic Neoplasms
-* Retinoblastoma Protein
-* Signal Transduction
-* Tumor Microenvironment
-* Vascular Remodeling
-|keywords=* T cells
-* chemotherapy resistance
-* endothelial cell activation
-* immunotherapy
-* pancreatic cancer
-* senescence
-* senescence-associated secretory phenotype
-* targeted therapy
-* tumor microenvironment
-* vascular biology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7278897
-}}
-==L1CAM==
-{{medline-entry
-|title=Glioma malignancy is linked to interdependent and inverse AMOG and L1 adhesion molecule expression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31510944
-|mesh-terms=* Adenosine Triphosphatases
-* Apoptosis
-* Biomarkers
-* Brain Neoplasms
-* Cation Transport Proteins
-* Cell Adhesion
-* Cell Adhesion Molecules, Neuronal
-* Cell Line, Tumor
-* Cellular Senescence
-* Gene Expression Profiling
-* Gene Expression Regulation, Neoplastic
-* Glioblastoma
-* Humans
-* Immunohistochemistry
-* Neural Cell Adhesion Molecule L1
-* RNA, Small Interfering
-* Signal Transduction
-|keywords=* AMOG
-* Apoptosis
-* Glioma
-* Human
-* L1CAM
-* Senescence
-* Therapy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6739972
-}}
-==LAG3==
-{{medline-entry
-|title=T Cell Transcriptional Profiling and Immunophenotyping Uncover [[LAG3]] as a Potential Significant Target of Immune Modulation in Multiple Myeloma.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31445183
-|keywords=* Autologous stem cell transplant
-* Exhaustion
-* LAG3
-* Multiple myeloma
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6952061
-}}
-==LAMP1==
-{{medline-entry
-|title=Differential accumulation of storage bodies with aging defines discrete subsets of microglia in the healthy brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32579115
-|keywords=* CLN3
-* TREM2
-* aging
-* autofluorescence
-* immunology
-* inflammation
-* lysosomal storage disorder
-* microglia
-* mouse
-* neuroscience
-* rhesus macaque
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7367682
-}}
-==LBP==
-{{medline-entry
-|title=Lipopolysaccharide binding protein is associated with CVD risk in older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32895891
-|keywords=* Aging
-* Cardiovascular disease risk
-* Intestinal permeability
-* Lipopolysaccharide binding protein
-|full-text-url=https://sci-hub.do/10.1007/s40520-020-01684-z
-}}
-{{medline-entry
-|title=Aging-related liver degeneration is associated with increased bacterial endotoxin and lipopolysaccharide binding protein levels.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32090603
-|mesh-terms=* Acute-Phase Proteins
-* Aging
-* Animals
-* Apoptosis
-* Biomarkers
-* Carrier Proteins
-* Endotoxins
-* Female
-* Gene Expression Regulation
-* Glucose
-* Inflammation
-* Insulin Receptor Substrate Proteins
-* Liver
-* Liver Cirrhosis
-* Malate Dehydrogenase
-* Male
-* Membrane Glycoproteins
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* RNA, Messenger
-* Receptor, Insulin
-* Toll-Like Receptor 4
-|keywords=* Tlr-4 signaling
-* aging
-* bacterial endotoxin
-* lipopolysaccharide binding protein
-* liver degeneration
-|full-text-url=https://sci-hub.do/10.1152/ajpgi.00345.2018
-}}
-{{medline-entry
-|title=Biomarkers of leaky gut are related to inflammation and reduced physical function in older adults with cardiometabolic disease and mobility limitations.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31654268
-|mesh-terms=* Aged
-* Aging
-* Biomarkers
-* Exercise Therapy
-* Female
-* Follow-Up Studies
-* Humans
-* Inflammation
-* Male
-* Metabolic Syndrome
-* Middle Aged
-* Mobility Limitation
-* Motor Activity
-* Obesity
-* Retrospective Studies
-* Weight Loss
-|keywords=* Ageing
-* Lipopolysaccharide-binding protein
-* Microbial translocation
-* Physical function
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6925090
-}}
-{{medline-entry
-|title=Needle-shaped amyloid deposition in rat mammary gland: evidence of a novel amyloid fibril protein.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31615282
-|mesh-terms=* Aging
-* Amyloidogenic Proteins
-* Amyloidosis
-* Animals
-* Antigens, Surface
-* Female
-* Mammary Glands, Animal
-* Milk Proteins
-* Plaque, Amyloid
-* Rats
-* Rats, Sprague-Dawley
-|keywords=* Amyloidosis
-* lipopolysaccharide binding protein
-* mammary gland
-* pathology
-* rat
-|full-text-url=https://sci-hub.do/10.1080/13506129.2019.1675623
-}}
-{{medline-entry
-|title=Effects of Lycium barbarum Polysaccharides on Health and Aging of [i]C. elegans[/i] Depend on [i]daf-12/daf-16[/i].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31583041
-|mesh-terms=* Aging
-* Animals
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* Drugs, Chinese Herbal
-* Receptors, Cytoplasmic and Nuclear
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6754959
-}}
-==LBR==
-{{medline-entry
-|title=Lamin B receptor: role on chromatin structure, cellular senescence and possibly aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32726434
-|keywords=* Aging
-* cancer
-* cellular senescence
-* chromatine structure
-* nuclear envelop
-|full-text-url=https://sci-hub.do/10.1042/BCJ20200165
-}}
-{{medline-entry
-|title=The impact of age beyond ploidy: outcome data from 8175 euploid single embryo transfers.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32173784
-|keywords=* Aneuploidy
-* Pregestational genetic testing
-* Reproductive aging
-* Single embryo transfer
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7125286
-}}
-{{medline-entry
-|title=The role of lamin B receptor in the regulation of senescence-associated secretory phenotype (SASP).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32126237
-|keywords=* Gene expression
-* LBR
-* SAHF
-* SASP
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.yexcr.2020.111927
-}}
-{{medline-entry
-|title=Lamin B receptor plays a key role in cellular senescence induced by inhibition of the proteasome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31825172
-|keywords=* LBR
-* autophagy
-* proteasome
-* protein accumulation
-* senescence
-* unbalanced growth
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996348
-}}
-==LEP==
-{{medline-entry
-|title=Age- and Sex-Specific Changes in Lower-Limb Muscle Power Throughout the Lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31943003
-|keywords=* Aging
-* Body mass index
-* Dynapenia
-* Leg extension power
-* Sarcopenia
-* Skeletal muscle
-|full-text-url=https://sci-hub.do/10.1093/gerona/glaa013
-}}
-{{medline-entry
-|title=The Copenhagen Sarcopenia Study: lean mass, strength, power, and physical function in a Danish cohort aged 20-93 years.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31419087
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Body Composition
-* Cohort Studies
-* Cross-Sectional Studies
-* Denmark
-* Female
-* Hand Strength
-* Humans
-* Leg
-* Longevity
-* Middle Aged
-* Prospective Studies
-* Sarcopenia
-* Young Adult
-|keywords=* Body composition
-* DXA
-* Handgrip strength
-* Lean mass
-* Leg power
-* Sarcopenia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6903448
-}}
-==LGR6==
-{{medline-entry
-|title=Effect of defensins-containing eye cream on periocular rhytids and skin quality.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32614135
-|keywords=* aging
-* defensins
-* periocular
-* rhytids
-* skin
-|full-text-url=https://sci-hub.do/10.1111/jocd.13424
-}}
-==LHCGR==
-{{medline-entry
-|title=Comparative Study of the Steroidogenic Effects of Human Chorionic Gonadotropin and Thieno[2,3-D]pyrimidine-Based Allosteric Agonist of Luteinizing Hormone Receptor in Young Adult, Aging and Diabetic Male Rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33050653
-|keywords=* aging rats
-* diabetes mellitus
-* human chorionic gonadotropin
-* low-molecular-weight agonist
-* luteinizing hormone receptor
-* spermatogenesis
-* steroidogenesis
-* testes
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7590010
-}}
-==LMNA==
-{{medline-entry
-|title=Metformin alters peripheral blood mononuclear cells (PBMC) senescence biomarkers gene expression in type 2 diabetic patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33187870
-|keywords=* Inflammation and cellular senescence
-* Insulin resistance
-* LMNA/C transcript variants
-* Mononuclear cells
-* Type 2 diabetes mellitus
-|full-text-url=https://sci-hub.do/10.1016/j.jdiacomp.2020.107758
-}}
-{{medline-entry
-|title=Protein structural and mechanistic basis of progeroid laminopathies.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32799420
-|keywords=* 3D structure
-* aging disorders
-* contact sites
-* lamin
-* nuclear structure
-|full-text-url=https://sci-hub.do/10.1111/febs.15526
-}}
-{{medline-entry
-|title=Progerin Expression Induces Inflammation, Oxidative Stress and Senescence in Human Coronary Endothelial Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32408587
-|keywords=* Hutchinson–Gilford progeria syndrome
-* LMNA
-* aging
-* atherosclerosis
-* endothelial dysfunction
-* inflammation
-* lamin A
-* prenylation
-* progerin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7290406
-}}
-{{medline-entry
-|title=The JAK1/2 inhibitor ruxolitinib delays premature aging phenotypes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32196928
-|keywords=* JAK/STAT pathway
-* cellular senescence
-* progeria
-* ruxolitinib
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189991
-}}
-{{medline-entry
-|title=Pharmacotherapy to gene editing: potential therapeutic approaches for Hutchinson-Gilford progeria syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32048129
-|keywords=* Aging
-* Extracellular vesicles
-* Hutchinson–Gilford progeria syndrome
-* Progerin
-* Stem cells
-* Therapeutics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7205988
-}}
-{{medline-entry
-|title=Long term breeding of the Lmna G609G progeric mouse: Characterization of homozygous and heterozygous models.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31794853
-|keywords=* Aging
-* Animal model breeding
-* Bone strength
-* Hutchinson-Gilford Progeria Syndrome (HGPS)
-* Kyphosis
-* Quality of life
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2019.110784
-}}
-==LMNB1==
-{{medline-entry
-|title=SIRT1 - a new mammalian substrate of nuclear autophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33292048
-|keywords=* Aging
-* SIRT1
-* nuclear autophagy
-* senescence
-* sirtuin
-|full-text-url=https://sci-hub.do/10.1080/15548627.2020.1860541
-}}
-{{medline-entry
-|title=Cellular senescence as a response to multiwalled carbon nanotube (MWCNT) exposure in human mesothelial cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33279583
-|keywords=* alpha tubulin
-* cellular senescence
-* mesothelial cells
-* microarray analysis
-* multiwalled carbon nanotubes
-* γH2A.X
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2020.111412
-}}
-{{medline-entry
-|title=Inflammatory Drivers of Cardiovascular Disease: Molecular Characterization of Senescent Coronary Vascular Smooth Muscle Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32523550
-|keywords=* aging
-* cardiovascular
-* inflammation
-* senescence
-* smooth muscle cell
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7261939
-}}
-==LOX==
-{{medline-entry
-|title=12-[[LOX]] catalyzes the oxidation of 2-arachidonoyl-lysolipids in platelets generating eicosanoid-lysolipids that are attenuated by iPLA γ knockout.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32161117
-|keywords=* 2-arachidonoyl-lysophospholipids
-* aging
-* calcium
-* eicosanoid
-* iPLA2γ
-* lysophospholipid
-* myocardium
-* platelet
-* platelet-type 12-lipoxygenase (12-LOX)
-* polyunsaturated fatty acids (PUFAs)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7170522
-}}
-==LOXL1==
-{{medline-entry
-|title=A blackberry-dill extract combination synergistically increases skin elasticity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32583541
-|keywords=* blackberry-dill
-* elasticity
-* skin aging
-* skin physiology/structure
-* skin repair
-|full-text-url=https://sci-hub.do/10.1111/ics.12644
-}}
-==LOXL2==
-{{medline-entry
-|title=Lysyl Oxidase-Like 2 Protects against Progressive and Aging Related Knee Joint Osteoarthritis in Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31569601
-|mesh-terms=* Adenoviridae
-* Aging
-* Amino Acid Oxidoreductases
-* Animals
-* Arthritis, Experimental
-* Cartilage, Articular
-* Disease Models, Animal
-* Disease Progression
-* Gene Expression
-* Gene Transfer Techniques
-* Genetic Vectors
-* Interleukin-1beta
-* Mice
-* Mice, Transgenic
-* NF-kappa B
-* Osteoarthritis, Knee
-* Transduction, Genetic
-|keywords=* Lysyl oxidase like-2
-* adenovirus delivery
-* anabolic response
-* articular cartilage
-* knee joint
-* osteoarthritis
-* regeneration
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6801581
-}}
-==LPA==
-{{medline-entry
-|title=Ginseng gintonin, aging societies, and geriatric brain diseases.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32817818
-|keywords=* Brain aging
-* Gintonin
-* Neurodegenerative diseases
-* Panax ginseng
-* Rejuvenation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7426447
-}}
-{{medline-entry
-|title=Late-life related subtypes of depression - a data-driven approach on cognitive domains and physical frailty.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32442243
-|keywords=* cognitive aging
-* depression
-* frailty
-|full-text-url=https://sci-hub.do/10.1093/gerona/glaa110
-}}
-{{medline-entry
-|title=Does sedentary time increase in older adults in the days following participation in intense exercise?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32130714
-|mesh-terms=* Accelerometry
-* Aged
-* Exercise
-* Exercise Test
-* Humans
-* Sedentary Behavior
-* Sleep
-|keywords=* Aging
-* Compensation
-* High intensity
-* Movement behaviours
-|full-text-url=https://sci-hub.do/10.1007/s40520-020-01502-6
-}}
-{{medline-entry
-|title=Association of Long-term Exposure to Elevated Lipoprotein(a) Levels With Parental Life Span, Chronic Disease-Free Survival, and Mortality Risk: A Mendelian Randomization Analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32108890
-|mesh-terms=* Aged
-* Case-Control Studies
-* Cross-Sectional Studies
-* Female
-* Humans
-* Lipoprotein(a)
-* Longevity
-* Male
-* Mendelian Randomization Analysis
-* Middle Aged
-* Parents
-* Phenotype
-* Prospective Studies
-* Risk Factors
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7049087
-}}
-{{medline-entry
-|title=Elevated Autotaxin and [[LPA]] Levels During Chronic Viral Hepatitis and Hepatocellular Carcinoma Associate with Systemic Immune Activation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31769428
-|keywords=* Aging
-* Autotaxin
-* Hepatitis
-* Hepatocellular Carcinoma
-* Immune Activation
-* Immunity
-* Inflammation
-* Liver
-* Lysophosphatidic Acid
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6966516
-}}
-{{medline-entry
-|title=Lysophosphatidic acid receptor [[LPA]]  prevents oxidative stress and cellular senescence in Hutchinson-Gilford progeria syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31714004
-|keywords=* 1-Oleoyl-2-O-methyl-rac-glycerophosphothionate
-* Hutchinson-Gilford progeria syndrome
-* LPA3
-* cell senescence
-* lysophosphatidic acid
-* reactive oxygen species
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6974717
-}}
-{{medline-entry
-|title=Associations of Sedentary and Physically-Active Behaviors With Cognitive-Function Decline in Community-Dwelling Older Adults: Compositional Data Analysis From the NEIGE Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31656243
-|keywords=* accelerometry
-* aging
-* exercise
-* neurocognitive disorders
-* sedentary lifestyle
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7557173
-}}
-{{medline-entry
-|title=Validation and comparison of two automated methods for quantifying brain white matter hyperintensities of presumed vascular origin.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31612759
-|keywords=* White matter hyperintensity
-* brain aging
-* cerebral small vessel disease
-* lesion segmentation
-* methodology
-* validation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7607266
-}}
-{{medline-entry
-|title=The Sedentary Time and Physical Activity Levels on Physical Fitness in the Elderly: A Comparative Cross Sectional Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31581429
-|mesh-terms=* Accelerometry
-* Aged
-* Aged, 80 and over
-* Aging
-* Body Mass Index
-* Cross-Sectional Studies
-* Exercise
-* Female
-* Humans
-* Male
-* Physical Fitness
-* Sedentary Behavior
-|keywords=* accelerometry
-* ageing
-* health
-* physical fitness
-* sedentary behaviour
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6801920
-}}
-{{medline-entry
-|title=Light-Intensity Physical Activity in a Large Prospective Cohort of Older US Adults: A 21-Year Follow-Up of Mortality.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31600755
-|mesh-terms=* Aged
-* Cardiovascular Diseases
-* Cohort Studies
-* Exercise
-* Female
-* Follow-Up Studies
-* Humans
-* Leisure Activities
-* Male
-* Middle Aged
-* Mortality
-* Neoplasms
-* Proportional Hazards Models
-* Prospective Studies
-* Respiratory Tract Diseases
-* Risk Factors
-* Surveys and Questionnaires
-* United States
-|keywords=* Aging
-* Cancer prevention study
-* Leisure time physical activity
-* Light-intensity physical activity
-|full-text-url=https://sci-hub.do/10.1159/000502860
-}}
-==LPL==
-{{medline-entry
-|title=Survival analyses in Holstein cows considering direct disease diagnoses and specific SNP marker effects.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32684467
-|keywords=* SNP effect
-* Weibull hazards model
-* genetic parameter
-* health disorder
-* longevity
-|full-text-url=https://sci-hub.do/10.3168/jds.2020-18174
-}}
-{{medline-entry
-|title=Influence of common health disorders on the length of productive life and stayability in German Holstein cows.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31677834
-|mesh-terms=* Animals
-* Breeding
-* Cattle
-* Cattle Diseases
-* Dairying
-* Farmers
-* Female
-* Lactation
-* Longevity
-* Phenotype
-|keywords=* genetic parameter
-* health disorder
-* longevity
-* subjective culling reason
-|full-text-url=https://sci-hub.do/10.3168/jds.2019-16985
-}}
-==LPO==
-{{medline-entry
-|title=[Features of the changes in lipid peroxidation and activity of Na+/K+-ATPase in the brain of the aged rats in the conditions of two-vessel cerebral ischemia/reperfusion.]
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32160433
-|mesh-terms=* Aging
-* Animals
-* Brain Ischemia
-* Disease Models, Animal
-* Lipid Peroxidation
-* Rats
-* Reperfusion Injury
-* Sodium-Potassium-Exchanging ATPase
-|keywords=* Na+/K+-ATPase
-* aging
-* brain
-* lipid peroxidation
-* oxidative stress
-* stroke
-}}
-==LRP1==
-{{medline-entry
-|title=Drug Targeting of Plasminogen Activator Inhibitor-1 Inhibits Metabolic Dysfunction and Atherosclerosis in a Murine Model of Metabolic Syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32268785
-|mesh-terms=* Animals
-* Atherosclerosis
-* Cellular Senescence
-* Diet, Western
-* Disease Models, Animal
-* Indoleacetic Acids
-* Macrophages
-* Metabolic Syndrome
-* Mice
-* Mice, Knockout
-* Obesity
-* Plaque, Atherosclerotic
-* Plasminogen Activator Inhibitor 1
-* Receptors, LDL
-|keywords=* atherosclerosis
-* cellular senescence
-* fibrinolysis
-* metabolic syndrome
-* muscle, smooth
-* obesity
-* plasminogen activator inhibitor-1
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7255962
-}}
-==LRP4==
-{{medline-entry
-|title=Multiple MuSK signaling pathways and the aging neuromuscular junction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32353380
-|keywords=* Aging
-* BMP signaling
-* MuSK
-* Neuromuscular junction
-* Synaptic maintenance
-|full-text-url=https://sci-hub.do/10.1016/j.neulet.2020.135014
-}}
-==LRP6==
-{{medline-entry
-|title=Low-density lipoprotein receptor-related protein 6-mediated signaling pathways and associated cardiovascular diseases: diagnostic and therapeutic opportunities.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32076828
-|mesh-terms=* Aging
-* Animals
-* Cardiovascular Diseases
-* Humans
-* Low Density Lipoprotein Receptor-Related Protein-6
-* Muscle, Smooth, Vascular
-* Myocytes, Smooth Muscle
-* Obesity
-* Signal Transduction
-* Structure-Activity Relationship
-* Vascular Calcification
-* Wnt Signaling Pathway
-|full-text-url=https://sci-hub.do/10.1007/s00439-020-02124-8
-}}
-==LRRK2==
-{{medline-entry
-|title=Accelerated telomere shortening independent of [[LRRK2]] variants in Chinese patients with Parkinson's disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33122450
-|keywords=* LRRK2 variants
-* Parkinson’s disease
-* aging
-* telomere length
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7655166
-}}
-{{medline-entry
-|title=The effect of [[LRRK2]] loss-of-function variants in humans.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32461697
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Biological Specimen Banks
-* Cell Line
-* Embryonic Stem Cells
-* Female
-* Gain of Function Mutation
-* Heterozygote
-* Humans
-* Leucine-Rich Repeat Serine-Threonine Protein Kinase-2
-* Longevity
-* Loss of Function Mutation
-* Lymphocytes
-* Male
-* Middle Aged
-* Myocytes, Cardiac
-* Parkinson Disease
-* Phenotype
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7303015
-}}
-{{medline-entry
-|title=Parkinson's disease-related Leucine-rich repeat kinase 2 modulates nuclear morphology and genomic stability in striatal projection neurons during aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32075681
-|keywords=* And aging
-* Dendritic hypotrophy
-* Excitability
-* G2019S
-* GABAA
-* LRRK2
-* Nuclear DNA damage
-* Nuclear hypertrophy
-* Nuclear invagination
-* Parkinson’s disease
-* R1441C
-* Striatal spiny projection neuron
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031993
-}}
-{{medline-entry
-|title=Autophagy and [[LRRK2]] in the Aging Brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31920513
-|keywords=* LAMP2A
-* LC3
-* LRRK2
-* Parkinson’s disease
-* aging
-* autophagy
-* lysosomes
-* α-synuclein
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6928047
-}}
-==LSS==
-{{medline-entry
-|title=Surgical results in older patients with lumbar spinal stenosis according to gait speed in relation to the diagnosis for sarcopenia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32329390
-|keywords=* aging
-* elderly person
-* gait speed
-* lumbar spinal stenosis
-* lumbar spine
-* muscle strength
-* sarcopenia
-* skeletal muscle mass
-* surgical result
-|full-text-url=https://sci-hub.do/10.1177/2309499020918422
-}}
-{{medline-entry
-|title=Streamlining an existing hip fracture patient pathway in an acute tertiary adult Irish hospital to improve patient experience and outcomes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31867664
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Delivery of Health Care, Integrated
-* Geriatrics
-* Hip Fractures
-* Hospitals, Teaching
-* Humans
-* Ireland
-* Length of Stay
-* Nerve Block
-* Orthopedics
-* Pain Management
-* Total Quality Management
-* Treatment Outcome
-|keywords=* Lean Six Sigma
-* healthcare outcomes
-* hip fracture care
-* integrated care pathways
-* interdisciplinary working
-* process improvement
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6926383
-}}
-==LTA==
-{{medline-entry
-|title=Lipoteichoic acid from the cell wall of a heat killed Lactobacillus paracasei D3-5 ameliorates aging-related leaky gut, inflammation and improves physical and cognitive functions: from C. elegans to mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31814084
-|keywords=* Aging
-* Cell wall
-* Cognition
-* Goblet cell
-* Inflammation
-* Leaky gut
-* Lipoteichoic acid
-* Metabolism
-* Mucin
-* Physical function
-* Probiotics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031475
-}}
-{{medline-entry
-|title=The change of pain classes over time: a latent transition analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31680381
-|mesh-terms=* Aged
-* Aging
-* Humans
-* Life Style
-* Longitudinal Studies
-* Middle Aged
-* Pain
-* Quality of Life
-|full-text-url=https://sci-hub.do/10.1002/ejp.1502
-}}
-==LY6D==
-{{medline-entry
-|title=[[LY6D]]-induced macropinocytosis as a survival mechanism of senescent cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33168631
-|keywords=* LY6D
-* Ras protein
-* cellular senescence
-* endocytosis
-* lipid raft
-* macropinocytosis
-* vacuole
-|full-text-url=https://sci-hub.do/10.1074/jbc.RA120.013500
-}}
-==MAG==
-{{medline-entry
-|title=Exploration of life satisfaction of Korean people with sensory impairments across the lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32327387
-|keywords=* Across the lifespan
-* Leisure domain
-* Life satisfaction
-* Sensory impairment
-* Social domain
-|full-text-url=https://sci-hub.do/10.1016/j.dhjo.2020.100931
-}}
-==MALT1==
-{{medline-entry
-|title=MALT-1 mediates IL-17 neural signaling to regulate C. elegans behavior, immunity and longevity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32350248
-|mesh-terms=* Animals
-* Behavior, Animal
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* Gene Expression Regulation
-* Green Fluorescent Proteins
-* Immunity
-* Interleukin-17
-* Interneurons
-* Longevity
-* Models, Biological
-* Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein
-* Neurons
-* Oxygen
-* Signal Transduction
-* Subcellular Fractions
-* Transgenes
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7190641
-}}
-{{medline-entry
-|title=[[MALT1]]-Deficient Mice Develop Atopic-Like Dermatitis Upon Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31632405
-|mesh-terms=* Age Factors
-* Animals
-* CTLA-4 Antigen
-* Cytokines
-* Dermatitis, Atopic
-* Disease Models, Animal
-* Disease Susceptibility
-* Gene Expression
-* Genetic Predisposition to Disease
-* Immunoglobulin E
-* Lymphocyte Activation
-* Mice
-* Mice, Knockout
-* Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein
-* Skin
-* T-Lymphocyte Subsets
-|keywords=* MALT1
-* Th2
-* Tregs
-* aging
-* atopic dermatitis
-* lymphocytes
-* skin inflammation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6779721
-}}
-==MAP2==
-{{medline-entry
-|title=Protective effects of ischemic preconditioning against neuronal apoptosis and dendritic injury in the hippocampus are age-dependent.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32314365
-|keywords=* aging
-* diffusion tensor imaging
-* immunohistochemistry
-* ischemic preconditioning
-|full-text-url=https://sci-hub.do/10.1111/jnc.15029
-}}
-==MAP4K3==
-{{medline-entry
-|title=[[MAP4K3]]/GLK in autoimmune disease, cancer and aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31640697
-|mesh-terms=* Aging
-* Autoimmune Diseases
-* Humans
-* Neoplasms
-* Protein-Serine-Threonine Kinases
-|keywords=* Aging
-* Autoimmune disease
-* Autophagy
-* Cancer metastasis
-* HPK1
-* IL-17A
-* IQGAP1
-* MAP4K3 (GLK)
-* PKCθ
-* Verteporfin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6806545
-}}
-==MAPK1==
-{{medline-entry
-|title=Purified Vitexin Compound 1 Inhibits UVA-Induced Cellular Senescence in Human Dermal Fibroblasts by Binding Mitogen-Activated Protein Kinase 1.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32850814
-|keywords=* MAPK1
-* VB1
-* purified vitexin compound 1
-* senescence
-* skin photoaging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7413062
-}}
-==MAPKAPK2==
-{{medline-entry
-|title=Quantitative In Vivo Proteomics of Metformin Response in Liver Reveals AMPK-Dependent and -Independent Signaling Networks.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31801093
-|mesh-terms=* AMP-Activated Protein Kinases
-* Animals
-* Calcium
-* Cell Line
-* Endocytosis
-* HEK293 Cells
-* Homeostasis
-* Humans
-* Intracellular Signaling Peptides and Proteins
-* Liver
-* Metformin
-* Mice
-* Phosphorylation
-* Protein Kinase C
-* Protein-Serine-Threonine Kinases
-* Proteomics
-* Signal Transduction
-|keywords=* AMPK3
-* LKB1
-* PKD1
-* STIM1
-* aging
-* calcium
-* diabetes
-* kinases
-* liver
-* metformin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6980792
-}}
-==MAPT==
-{{medline-entry
-|title=Association of relative brain age with tobacco smoking, alcohol consumption, and genetic variants.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32001736
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Alcohol Drinking
-* Biological Specimen Banks
-* Brain
-* Cognition
-* Female
-* Humans
-* Magnetic Resonance Imaging
-* Male
-* Middle Aged
-* Neuroimaging
-* Polymorphism, Single Nucleotide
-* Smoking
-* United Kingdom
-* tau Proteins
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6992742
-}}
-{{medline-entry
-|title=A blood-based nutritional risk index explains cognitive enhancement and decline in the multidomain Alzheimer prevention trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31921969
-|keywords=* Aging
-* Biomarkers of diet quality
-* Cognitive decline
-* DHA
-* EPA
-* Elderly
-* Homocysteine
-* Metabolomics
-* Nutrient biomarkers
-* Omega-3 fatty acids
-* Vitamin D
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6944714
-}}
-{{medline-entry
-|title=Longitudinal associations of physical activity levels with morphological and functional changes related with aging: The [[MAPT]] study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31669813
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Alzheimer Disease
-* Body Composition
-* Brain
-* Cognition
-* Exercise
-* Female
-* Humans
-* Longitudinal Studies
-* Male
-|keywords=* Aging
-* Biomarkers
-* Phenotype
-* Physical activity
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2019.110758
-}}
-{{medline-entry
-|title=Ageing and amyloidosis underlie the molecular and pathological alterations of tau in a mouse model of familial Alzheimer's disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31673052
-|mesh-terms=* Aging
-* Alzheimer Disease
-* Amyloid beta-Peptides
-* Amyloidosis
-* Animals
-* Disease Models, Animal
-* Mice
-* Mice, Transgenic
-* tau Proteins
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6823454
-}}
-{{medline-entry
-|title=Revisiting the intersection of amyloid, pathologically modified tau and iron in Alzheimer's disease from a ferroptosis perspective.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31604111
-|keywords=* Alzheimer’s disease
-* Ferroptosis
-* Iron
-* Reactive oxygen species
-* Senescence
-* Tau
-|full-text-url=https://sci-hub.do/10.1016/j.pneurobio.2019.101716
-}}
-==MATN3==
-{{medline-entry
-|title=Mice Lacking the Matrilin Family of Extracellular Matrix Proteins Develop Mild Skeletal Abnormalities and Are Susceptible to Age-Associated Osteoarthritis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31963938
-|mesh-terms=* Aging
-* Animals
-* Cell Proliferation
-* Cells, Cultured
-* Chondrocytes
-* Disease Models, Animal
-* Female
-* Gene Knockout Techniques
-* Humans
-* Male
-* Matrilin Proteins
-* Mice
-* Mice, Knockout
-* Microscopy, Atomic Force
-* Muscle, Skeletal
-* Osteoarthritis
-|keywords=* articular cartilage
-* bone development
-* cartilage
-* matrilin
-* osteoarthritis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7013758
-}}
-==MB==
-{{medline-entry
-|title=Probing menstrual bloodstain aging with fluorescence spectroscopy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33279406
-|keywords=* Aging
-* Analytical methods
-* Blood
-* Fluorescence spectroscopy
-* Forensics
-|full-text-url=https://sci-hub.do/10.1016/j.saa.2020.119172
-}}
-{{medline-entry
-|title=Effect of physical exercise and medication on enhancing cognitive function in older adults with vascular risk.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32989840
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Cognition
-* Cross-Sectional Studies
-* Exercise
-* Exercise Therapy
-* Female
-* Humans
-* Male
-* Middle Aged
-* Risk Factors
-* Vascular Diseases
-|keywords=* active aging
-* cognitive preservation
-* exercise habit
-* lifestyle advice
-* vascular care
-|full-text-url=https://sci-hub.do/10.1111/ggi.14048
-}}
-{{medline-entry
-|title=A novel indenone derivative selectively induces senescence in MDA-[[MB]]-231 (breast adenocarcinoma) cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32956706
-|mesh-terms=* Antineoplastic Agents
-* Breast Neoplasms
-* Catalysis
-* Cell Line, Tumor
-* Cell Survival
-* Cellular Senescence
-* Cyclin-Dependent Kinase Inhibitor p21
-* Down-Regulation
-* Female
-* G1 Phase Cell Cycle Checkpoints
-* Humans
-* Palladium
-* Sulfonamides
-* Survivin
-* Tumor Suppressor Protein p53
-* Up-Regulation
-|keywords=* Cell cycle arrest
-* Novel indenone derivative
-* Senescence
-* Triple-negative breast cancer
-|full-text-url=https://sci-hub.do/10.1016/j.cbi.2020.109250
-}}
-{{medline-entry
-|title=Improved Autophagic Flux in Escapers from Doxorubicin-Induced Senescence/Polyploidy of Breast Cancer Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32846959
-|keywords=* DNA damage
-* Rubicon
-* SQSTM1/p62
-* TFEB
-* autophagic index
-* autophagy
-* cancer
-* polyploidy
-* senescence
-* senescence escape
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7504443
-}}
-{{medline-entry
-|title=Lifespan regulation in α/β posterior neurons of the fly mushroom bodies by Rab27.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32627932
-|keywords=* Drosophila
-* Rab27
-* S6K
-* TOR
-* lifespan extension
-* mushroom body
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431830
-}}
-{{medline-entry
-|title=Tailored Functionalized Magnetic Nanoparticles to Target Breast Cancer Cells Including Cancer Stem-Like Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32485849
-|keywords=* apoptosis
-* cancer stem-like cells
-* doxorubicin
-* magnetic iron oxide nanoparticles
-* mitotic catastrophe
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7352336
-}}
-{{medline-entry
-|title="Mitotic Slippage" and Extranuclear DNA in Cancer Chemoresistance: A Focus on Telomeres.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32316332
-|keywords=* ALT
-* SQSTM1/p62
-* amoeboid conversion
-* budding of mitotic progeny
-* cellular senescence
-* extranuclear DNA
-* genotoxic treatment
-* inverted meiosis
-* mtTP53 cancer
-* polyploidization
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7215480
-}}
-{{medline-entry
-|title=Diversity of the Senescence Phenotype of Cancer Cells Treated with Chemotherapeutic Agents.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31771226
-|mesh-terms=* Antineoplastic Agents
-* Cell Proliferation
-* Cellular Senescence
-* Cyclin-Dependent Kinase Inhibitor p21
-* Doxorubicin
-* Fluorouracil
-* Humans
-* Irinotecan
-* Methotrexate
-* Neoplasms
-* Oxaliplatin
-* Paclitaxel
-* Phenotype
-* Tumor Cells, Cultured
-|keywords=* DNA damage
-* SASP
-* cancer
-* chemotherapy
-* senescence
-* senescence markers
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6952928
-}}
-{{medline-entry
-|title=Downregulation of the inflammatory network in senescent fibroblasts and aging tissues of the long-lived and cancer-resistant subterranean wild rodent, Spalax.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31605433
-|keywords=*
-Spalax
-* DNA damage
-* DNA repair
-* cellular senescence
-* interleukin-1 alpha (IL1α)
-* nuclear factor κB (NF-κB)
-* senescence-associated secretory phenotype (SASP)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6974727
-}}
-{{medline-entry
-|title=Quantification of the health-status of the Dutch Labrador retriever population.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31494529
-|mesh-terms=* Animals
-* Dog Diseases
-* Dogs
-* Female
-* Health Status
-* Insurance
-* Laboratories
-* Longevity
-* Male
-* Netherlands
-* Proportional Hazards Models
-* Risk Factors
-|keywords=* Canine health
-* Data analysis
-* Health parameters
-* Labrador retriever
-* Lifespan
-* Oncology
-|full-text-url=https://sci-hub.do/10.1016/j.prevetmed.2019.104764
-}}
-{{medline-entry
-|title=Conjugated Physiological Resveratrol Metabolites Induce Senescence in Breast Cancer Cells: Role of p53/p21 and p16/Rb Pathways, and ABC Transporters.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31441212
-|mesh-terms=* ATP-Binding Cassette Transporters
-* Breast Neoplasms
-* Cell Cycle Checkpoints
-* Cellular Senescence
-* Cyclin-Dependent Kinase Inhibitor p16
-* Cyclin-Dependent Kinase Inhibitor p21
-* Female
-* Glucuronides
-* Humans
-* MCF-7 Cells
-* Resveratrol
-* Retinoblastoma Protein
-* Signal Transduction
-* Stilbenes
-* Tumor Suppressor Protein p53
-|keywords=* ABC transporters
-* breast cancer
-* deconjugation
-* resveratrol metabolites
-* senescence
-|full-text-url=https://sci-hub.do/10.1002/mnfr.201900629
-}}
-==MBP==
-{{medline-entry
-|title=Demyelination associated with chronic arsenic exposure in Wistar rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32171569
-|mesh-terms=* Aging
-* Amyloid beta-Protein Precursor
-* Animals
-* Arsenic Poisoning
-* Arsenites
-* Axons
-* Corpus Callosum
-* Demyelinating Diseases
-* Diffusion Tensor Imaging
-* Drinking Water
-* Immunohistochemistry
-* Male
-* Mitochondria
-* Myelin Basic Protein
-* Neurofilament Proteins
-* Prefrontal Cortex
-* Rats
-* Rats, Wistar
-* Sodium Compounds
-* White Matter
-|keywords=* Amyloid
-* Anisotropy
-* Arsenic
-* Axonal damage
-* DTI
-* Demyelination
-* Development
-* MRI
-* Microstructure
-* Mitochondria
-|full-text-url=https://sci-hub.do/10.1016/j.taap.2020.114955
-}}
-{{medline-entry
-|title=Natural killer cells as participants in pathogenesis of rat experimental autoimmune encephalomyelitis (EAE): lessons from research on rats with distinct age and strain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32140045
-|keywords=* EAE
-* NK cells
-* aging
-* dendritic cells
-* strain differences
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7050050
-}}
-==MCC==
-{{medline-entry
-|title=Multiple chronic conditions and risk of cognitive impairment and dementia among older Americans: findings from the Aging, Demographics, and Memory Study (ADAMS).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32633198
-|keywords=* Aging
-* and memory study
-* cognitive impairment with no dementia
-* dementia
-* demographics
-* multimorbidity
-* multiple chronic conditions
-|full-text-url=https://sci-hub.do/10.1080/13825585.2020.1790492
-}}
-{{medline-entry
-|title=Behaviour consistency is a sensitive tool for distinguishing the effects of aging on physical activity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32348871
-|keywords=* Aging
-* Behaviour consistency
-* Heart rate
-* Physical activity
-* Treadmill running
-|full-text-url=https://sci-hub.do/10.1016/j.bbr.2020.112619
-}}
-{{medline-entry
-|title=Burden on Caregivers of Adults with Multiple Chronic Conditions: Intersectionality of Age, Gender, Education level, Employment Status, and Impact on Social Life.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31475644
-|keywords=* aging
-* analyse d’intersectionnalité
-* caregiver burden
-* fardeau de l’aidant
-* gender
-* interférence sociale
-* intersectionality analysis
-* maladies chroniques multiples
-* multiple chronic conditions
-* sexe
-* social interference
-* vieillissement
-|full-text-url=https://sci-hub.do/10.1017/S071498081900045X
-}}
-==MCM9==
-{{medline-entry
-|title=MCM8- and [[MCM9]] Deficiencies Cause Lifelong Increased Hematopoietic DNA Damage Driving p53-Dependent Myeloid Tumors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31509747
-|mesh-terms=* Aging
-* Animals
-* Apoptosis
-* Bone Marrow
-* Cell Differentiation
-* Cell Proliferation
-* DNA Damage
-* Gene Expression Regulation, Leukemic
-* Hematologic Neoplasms
-* Mice
-* Mice, Knockout
-* Minichromosome Maintenance Proteins
-* Retinoblastoma Protein
-* Signal Transduction
-* Splenomegaly
-* Tumor Suppressor Protein p53
-|keywords=* DNA damage
-* DNA repair
-* MCM8
-* MCM9
-* cancer
-* hematopoiesis
-* homologous recombination
-* myelodysplastic syndrome
-|full-text-url=https://sci-hub.do/10.1016/j.celrep.2019.07.095
-}}
-==MCU==
-{{medline-entry
-|title=A rare case of Epstein-Barr virus-positive mucocutaneous ulcer that developed into an intestinal obstruction: a case report.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31931725
-|mesh-terms=* Aged, 80 and over
-* Colon, Transverse
-* Epstein-Barr Virus Infections
-* Herpesvirus 4, Human
-* Humans
-* Intestinal Mucosa
-* Intestinal Obstruction
-* Male
-* Ulcer
-|keywords=* Aging
-* Epstein–Barr virus-positive mucocutaneous ulcer (EBV-MCU)
-* Immunosuppression
-* Intestinal obstruction
-* Surgical resection
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6958744
-}}
-{{medline-entry
-|title=Inhibition of Mitochondrial Calcium Overload by SIRT3 Prevents Obesity- or Age-Related Whitening of Brown Adipose Tissue.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31712319
-|mesh-terms=* Adipocytes, Brown
-* Adipose Tissue, Brown
-* Aging
-* Animals
-* Calcium
-* Capsaicin
-* Gene Expression Regulation
-* Mice
-* Mice, Knockout
-* Mitochondria
-* Obesity
-* Sirtuin 3
-|full-text-url=https://sci-hub.do/10.2337/db19-0526
-}}
-==MDH1==
-{{medline-entry
-|title=Oxidative Damage to the TCA Cycle Enzyme [[MDH1]] Dysregulates Bioenergetic Enzymatic Activity in the Aged Murine Brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32175745
-|keywords=* DPM
-* MRM
-* TCA cycle
-* aging
-* brain
-|full-text-url=https://sci-hub.do/10.1021/acs.jproteome.9b00861
-}}
-==MDM2==
-{{medline-entry
-|title=SENEBLOC, a long non-coding RNA suppresses senescence via p53-dependent and independent mechanisms.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32030426
-|mesh-terms=* Aging
-* Animals
-* Carcinogenesis
-* Cyclin-Dependent Kinase Inhibitor p21
-* Gene Expression Regulation, Neoplastic
-* HCT116 Cells
-* Heterografts
-* Histone Deacetylases
-* Humans
-* Mice
-* Neoplasms
-* Protein Binding
-* RNA, Long Noncoding
-* Signal Transduction
-* Tumor Suppressor Protein p53
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102969
-}}
-{{medline-entry
-|title=Disruption of Robo2-Baiap2 integrated signaling drives cystic disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31534052
-|mesh-terms=* Animals
-* Cell Differentiation
-* Cell Proliferation
-* Cellular Senescence
-* Cilia
-* Disease Models, Animal
-* Epithelial Cells
-* Humans
-* Kidney
-* Kidney Diseases, Cystic
-* Mice
-* Mice, Knockout
-* Nerve Tissue Proteins
-* Protein Binding
-* Protein Domains
-* Receptors, Immunologic
-* Signal Transduction
-* Tumor Suppressor Protein p53
-|keywords=* Cellular senescence
-* Development
-* Genetic diseases
-* Nephrology
-* Signal transduction
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6795383
-}}
-{{medline-entry
-|title=Senescence-induced immunophenotype, gene expression and electrophysiology changes in human amniocytes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31478614
-|mesh-terms=* Amniocentesis
-* Amnion
-* Biomarkers
-* Cell Proliferation
-* Cells, Cultured
-* Cellular Senescence
-* Electrophysiological Phenomena
-* Female
-* Gene Expression Regulation
-* Humans
-* Immunophenotyping
-* Phenotype
-|keywords=* amniocyte
-* automated patch-clamp
-* flow cytometry
-* mesenchymal stem cell
-* qRT-PCR
-* replicative senescence
-* senescence-associated secretory phenotype
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6815807
-}}
-==MED25==
-{{medline-entry
-|title=The [i]HAC1[/i] histone acetyltransferase promotes leaf senescence and regulates the expression of [i]ERF022[/i].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31468026
-|keywords=* ERF022
-* H3K9ac
-* HAC1
-* Mediator complex
-* histone acetylation
-* leaf senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6710649
-}}
-==MEFV==
-{{medline-entry
-|title=The grandfather's fever.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31401792
-|mesh-terms=* Age of Onset
-* Aged, 80 and over
-* Familial Mediterranean Fever
-* Female
-* Humans
-* Male
-* Pedigree
-* Pyrin
-|keywords=* Autoinflammatory diseases
-* FMF
-* Genetics
-* Geriatrics
-* Periodic fever
-|full-text-url=https://sci-hub.do/10.1007/s10067-019-04741-9
-}}
-==MEOX2==
-{{medline-entry
-|title=Reduced expression of microRNA-130a promotes endothelial cell senescence and age-dependent impairment of neovascularization.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32457253
-|keywords=* aging
-* angiogenesis
-* microRNA
-* neovascularization
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7346016
-}}
-==MET==
-{{medline-entry
-|title=Self-rated health in relation to fruit and vegetable consumption and physical activity among older cancer survivors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32979089
-|keywords=* Cancer survivorship
-* Epidemiology
-* Fruit and vegetable
-* Gerontology
-* Physical activity
-|full-text-url=https://sci-hub.do/10.1007/s00520-020-05782-6
-}}
-{{medline-entry
-|title=Leisure-time physical activity volume, intensity, and duration from mid- to late-life in U.S. subpopulations by race and sex. The Atherosclerosis Risk In Communities (ARIC) Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32170049
-|keywords=* exercise
-* healthy aging
-* physical activity
-* retirement
-* successful aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7093185
-}}
-{{medline-entry
-|title=Repressive H3K9me2 protects lifespan against the transgenerational burden of COMPASS activity in [i]C. elegans[/i].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31815663
-|mesh-terms=* Animals
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* Heterochromatin
-* Histone-Lysine N-Methyltransferase
-* Histones
-* Inheritance Patterns
-* Jumonji Domain-Containing Histone Demethylases
-* Longevity
-* Lysine
-* Methylation
-* Mutation
-|keywords=* C. elegans
-* COMPASS
-* aging
-* chromatin
-* chromosomes
-* epigenetics
-* gene expression
-* genetics
-* genomics
-* heterochromatin
-* transgenerational inheritance
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7299346
-}}
-{{medline-entry
-|title=Influence of Anthropometrics on Step-Rate Thresholds for Moderate and Vigorous Physical Activity in Older Adults: Scientific Modeling Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31518246
-|keywords=* aging
-* cadence
-* physical activity intensity
-* public health
-* walking
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6715008
-}}
-==MFI==
-{{medline-entry
-|title=The Influence of the Accelerated Aging Conditions on the Properties of Polyolefin Geogrids Used for Landfill Slope Reinforcement.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32825284
-|keywords=* HDPE
-* accelerated aging tests
-* decrease mechanical properties
-* degradation
-* geosynthetics
-* landfill
-* polyolefin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7564637
-}}
-{{medline-entry
-|title=Changes in Physical Meat Traits, Protein Solubility, and the Microstructure of Different Beef Muscles during Post-Mortem Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32575353
-|keywords=* aging
-* beef muscle
-* microstructure
-* myofibril fragmentation
-* protein solubility
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7353465
-}}
-{{medline-entry
-|title=Effect of a low-voltage electrical stimulation on yak meat tenderness during postmortem aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32583539
-|mesh-terms=* Animals
-* Cattle
-* Cold Temperature
-* Electric Stimulation
-* Food Handling
-* Food Quality
-* Food Storage
-* Hydrogen-Ion Concentration
-* Male
-* Meat
-* Muscle, Skeletal
-* Polysaccharides
-* Postmortem Changes
-* Time Factors
-|keywords=* Yak
-* electrical stimulation
-* postmortem aging
-* tenderness
-|full-text-url=https://sci-hub.do/10.1111/asj.13410
-}}
-{{medline-entry
-|title=Comparative effects of dry-aging and wet-aging on physicochemical properties and digestibility of Hanwoo beef.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31480178
-|keywords=* Beef Loin
-* Digestibility
-* Dry Aging
-* Shear Force
-* Wet Aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7054618
-}}
-==MFN2==
-{{medline-entry
-|title=Thioredoxin protects mitochondrial structure, function and biogenesis in myocardial ischemia-reperfusion via redox-dependent activation of AKT-CREB- PGC1α pathway in aged mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33049718
-|keywords=* aging
-* heart
-* ischemia-reperfusion
-* mitochondria
-* thioredoxin
-|full-text-url=https://sci-hub.do/10.18632/aging.104071
-}}
-{{medline-entry
-|title=[[MFN2]] contributes to metabolic disorders and inflammation in the aging of rat chondrocytes and osteoarthritis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32416221
-|keywords=* Aging
-* Inflammation
-* MFN2
-* Metabolic disorders
-* Osteoarthritis
-|full-text-url=https://sci-hub.do/10.1016/j.joca.2019.11.011
-}}
-==MFSD2A==
-{{medline-entry
-|title=Decreased Blood Level of MFSD2a as a Potential Biomarker of Alzheimer's Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31861865
-|mesh-terms=* Aged
-* Alzheimer Disease
-* Biomarkers
-* Brain
-* Fatty Acids
-* Female
-* Humans
-* Male
-* Symporters
-|keywords=* Alzheimer’s disease
-* MFSD2a carrier
-* aging
-* neurologic disorders
-* omega-3 PUFA
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6981746
-}}
-==MGMT==
-{{medline-entry
-|title=Cytotoxic and Senolytic Effects of Methadone in Combination with Temozolomide in Glioblastoma Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32977591
-|keywords=* apoptosis
-* cancer therapy
-* drug resistance
-* glioblastoma
-* methadone
-* senescence
-* temozolomide
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7582495
-}}
-==MIA==
-{{medline-entry
-|title=Age, cohort, and period effects on metamemory beliefs.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31804113
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Cohort Studies
-* Cross-Sectional Studies
-* Female
-* Humans
-* Longitudinal Studies
-* Male
-* Metacognition
-* Middle Aged
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6901096
-}}
-{{medline-entry
-|title=Memory Age-based Stereotype Threat: Role of Locus of Control and Anxiety.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31752597
-|mesh-terms=* Aged
-* Aging
-* Anxiety
-* Female
-* Humans
-* Internal-External Control
-* Male
-* Memory, Episodic
-* Metacognition
-* Middle Aged
-* Stereotyping
-|full-text-url=https://sci-hub.do/10.1080/0361073X.2019.1693009
-}}
-==MIB1==
-{{medline-entry
-|title=Immunohistochemical detection of senescence markers in human sarcomas.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31899047
-|keywords=* SenTraGor
-* Senescence
-* p16
-* p21
-* sarcoma
-|full-text-url=https://sci-hub.do/10.1016/j.prp.2019.152800
-}}
-==MIP==
-{{medline-entry
-|title=Inspiratory muscle training improves cerebrovascular and postural control responses during orthostatic stress in older women.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32705393
-|keywords=* Aging
-* Cardiac output
-* Center-of-pressure
-* Middle cerebral artery blood flow velocity
-* Respiratory muscles
-|full-text-url=https://sci-hub.do/10.1007/s00421-020-04441-2
-}}
-{{medline-entry
-|title=A novel multi-marker discovery approach identifies new serum biomarkers for Parkinson's disease in older people: an EXosomes in PArkiNson Disease (EXPAND) ancillary study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32458283
-|keywords=* Aging
-* Amino acids
-* Cytokines
-* Metabolomics
-* Neurodegeneration
-* Personalized medicine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7525911
-}}
-{{medline-entry
-|title=Sexual dimorphism of physical activity on cognitive aging: Role of immune functioning.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32387511
-|keywords=* Brain aging
-* Chemokines
-* Cognitive aging
-* Exercise
-* Gender
-* Inflammation
-* Lifestyle
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7416443
-}}
-{{medline-entry
-|title=Comparison of balance changes after inspiratory muscle or Otago exercise training.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31978126
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Breathing Exercises
-* Exercise
-* Exercise Therapy
-* Female
-* Humans
-* Male
-* Maximal Respiratory Pressures
-* Muscle Strength
-* Physical Endurance
-* Postural Balance
-* Respiratory Muscles
-* Respiratory Therapy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6980667
-}}
-==MITF==
-{{medline-entry
-|title=Thymocid , a Standardized Black Cumin ([i]Nigella sativa[/i]) Seed Extract, Modulates Collagen Cross-Linking, Collagenase and Elastase Activities, and Melanogenesis in Murine B16F10 Melanoma Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32707654
-|keywords=* Nigella sativa
-* Thymocid®
-* black cumin
-* collagen
-* collagenase
-* cosmeceutical
-* elastase
-* glycation
-* melanogenesis
-* skin aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7400895
-}}
-{{medline-entry
-|title=HuRdling Senescence: HuR Breaks BRAF-Induced Senescence in Melanocytes and Supports Melanoma Growth.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32455577
-|keywords=* HuR
-* MITF
-* Microphthalmia-associated transcription factor
-* malignant melanoma
-* oncogene induced senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7281285
-}}
-==MLH1==
-{{medline-entry
-|title=The somatic mutation landscape of the human body.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31874648
-|mesh-terms=* Age Factors
-* Aging
-* Humans
-* Mutation
-* Neoplasms
-* Selection, Genetic
-* Sex Factors
-|keywords=* Aging
-* Cancer
-* Genomic instability
-* Human
-* Somatic evolution
-* Somatic mutation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6930685
-}}
-==MLKL==
-{{medline-entry
-|title=Remifentanil preconditioning protects against hypoxia-induced senescence and necroptosis in human cardiac myocytes [i]in vitro[/i].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32584786
-|keywords=* cardiomyocytes
-* hypoxia
-* necroptosis
-* remifentanil
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7425462
-}}
-==MLN==
-{{medline-entry
-|title=Age-Dependent Decrease in the Induction of Regulatory T Cells Is Associated With Decreased Expression of RALDH2 in Mesenteric Lymph Node Dendritic Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32849526
-|keywords=* RALDH2
-* aging
-* dendritic cells
-* epigenetic regulation
-* regulatory T cells
-* retinoic acid
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432217
-}}
-==MMD==
-{{medline-entry
-|title=Association between a Deficit Accumulation Frailty Index and Mobility Outcomes in Older Adults: Secondary Analysis of the Lifestyle Interventions and Independence for Elders (LIFE) Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33266358
-|keywords=* LIFE Study
-* deficit accumulation
-* disability
-* frailty
-* healthy aging
-* mobility
-* older adults
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7700674
-}}
-{{medline-entry
-|title=Impact of Anticholinergic Medication Burden on Mobility and Falls in the Lifestyle Interventions for Elders (LIFE) Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32947839
-|keywords=* anticholinergic burden
-* falls
-* mobility
-* physical activity
-* successful aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7564216
-}}
-{{medline-entry
-|title=Impact and Lessons From the Lifestyle Interventions and Independence for Elders (LIFE) Clinical Trials of Physical Activity to Prevent Mobility Disability.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32105353
-|keywords=* aging
-* mobility disability
-* multicenter trialphysical activity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7187344
-}}
-==MME==
-{{medline-entry
-|title=Geriatric Opioid Harm Reduction: Interprofessional Student Learning Outcomes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32284953
-|keywords=* aging
-* older adults
-* opioid harm reduction
-* overdose risk
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139179
-}}
-{{medline-entry
-|title=Effectiveness of local anesthetic injection in geriatric patients following operative management of proximal and diaphyseal femur fracture.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31564373
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Analgesics, Opioid
-* Anesthetics, Local
-* Delirium
-* Female
-* Femoral Fractures
-* Fracture Fixation, Internal
-* Geriatrics
-* Humans
-* Injections, Intra-Articular
-* Intraoperative Care
-* Male
-* Pain Management
-* Pain, Postoperative
-* Retrospective Studies
-|keywords=* Geriatrics
-* Hip fracture
-* Local anesthetic
-* Narcotics
-|full-text-url=https://sci-hub.do/10.1016/j.injury.2019.09.013
-}}
-==MMP1==
-{{medline-entry
-|title=Reacquisition of a spindle cell shape does not lead to the restoration of a youthful state in senescent human skin fibroblasts.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32533368
-|keywords=* Cell shape
-* Fibroblast
-* Lithography
-* SASP
-* Senescence
-|full-text-url=https://sci-hub.do/10.1007/s10522-020-09886-8
-}}
-{{medline-entry
-|title=A novel multifunctional skin care formulation with a unique blend of antipollution, brightening and antiaging active complexes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31584241
-|keywords=* anti-wrinkle
-* pigmentation
-* pollution
-* skin aging
-* skin barrier
-|full-text-url=https://sci-hub.do/10.1111/jocd.13176
-}}
-==MMP13==
-{{medline-entry
-|title=Aging aggravates intervertebral disc degeneration by regulating transcription factors toward chondrogenesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31909538
-|mesh-terms=* Aging
-* Animals
-* Antigens, Differentiation
-* Chondrocytes
-* Chondrogenesis
-* Core Binding Factor Alpha 1 Subunit
-* Fetal Proteins
-* Gene Expression Regulation
-* Intervertebral Disc Degeneration
-* Mice
-* Mice, Transgenic
-* Sp7 Transcription Factor
-* T-Box Domain Proteins
-|keywords=* Wnt/β-catenin/LRPs
-* biomechanics
-* genetic animal models
-* osterix
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7018543
-}}
-==MOS==
-{{medline-entry
-|title=Effect of mannan oligosaccharides on the microbiota and productivity parameters of Litopenaeus vannamei shrimp under intensive cultivation in Ecuador.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32066764
-|mesh-terms=* Actinobacteria
-* Aeromonas
-* Animal Feed
-* Animals
-* Aquaculture
-* Bacterial Adhesion
-* Ecuador
-* Flavobacteriaceae
-* Lactococcus
-* Longevity
-* Mannans
-* Microbiota
-* Oligosaccharides
-* Penaeidae
-* Proteobacteria
-* Seafood
-* Shewanella
-* Verrucomicrobia
-* Vibrio
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7026423
-}}
-{{medline-entry
-|title=Predictors of health-related quality of life among older adults living with HIV in Thailand: results from the baseline and follow-up surveys.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31870166
-|keywords=* Chiang Mai
-* HIV and aging
-* Older adults living with HIV
-* Thailand
-* health-related quality of life
-* quality of life
-|full-text-url=https://sci-hub.do/10.1080/09540121.2019.1707472
-}}
-{{medline-entry
-|title=Comparison of health-related quality of life between the Han and Yi ethnicity elderly in the Yi autonomous areas of Yunnan Province.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31766992
-|mesh-terms=* Activities of Daily Living
-* Aged
-* Aged, 80 and over
-* Aging
-* China
-* Cross-Sectional Studies
-* Ethnic Groups
-* Female
-* Humans
-* Male
-* Middle Aged
-* Quality of Life
-|keywords=* ADL
-* Elderly
-* Health-related quality of life
-* IADL
-* Yi ethnic minority
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6878633
-}}
-{{medline-entry
-|title=Mannan oligosaccharide increases the growth performance, immunity and resistance capability against Vibro Parahemolyticus in juvenile abalone Haliotis discus hannai Ino.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31561025
-|mesh-terms=* Animal Feed
-* Animals
-* Antioxidants
-* Diet
-* Dietary Supplements
-* Dose-Response Relationship, Drug
-* Gastropoda
-* Immunity, Innate
-* Longevity
-* Mannans
-* Oligosaccharides
-* Vibrio parahaemolyticus
-|keywords=* Abalone
-* Antioxidation
-* Bacterial challenge
-* Disease resistance
-* Growth
-* Immunity
-* Mannan oligosaccharide
-|full-text-url=https://sci-hub.do/10.1016/j.fsi.2019.09.058
-}}
-==MPHOSPH6==
-{{medline-entry
-|title=Genome-wide Association Analysis in Humans Links Nucleotide Metabolism to Leukocyte Telomere Length.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109421
-|mesh-terms=* Genome-Wide Association Study
-* Humans
-* Leukocytes
-* Nucleotides
-* Telomere
-|keywords=* Mendelian randomisation
-* age-related disease
-* biological aging
-* telomere length
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7058826
-}}
-==MPI==
-{{medline-entry
-|title=Age-related decline of lymphatic drainage from the eye: A noninvasive in vivo photoacoustic tomography study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32251650
-|keywords=* Age-related
-* Aging
-* Aqueous humor
-* Drainage
-* Eye
-* Glaucoma
-* Imaging
-* In vivo
-* Lymph node
-* Lymphatic
-* Mice
-* Photoacoustic tomography
-* Uveoscleral
-|full-text-url=https://sci-hub.do/10.1016/j.exer.2020.108029
-}}
-{{medline-entry
-|title=Interest of the multidimensional prognostic index ([[MPI]]) as an assessment tool in hospitalized patients in geriatrics.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31570330
-|mesh-terms=* Aged, 80 and over
-* Female
-* Geriatric Assessment
-* Hospital Mortality
-* Hospitalization
-* Humans
-* Length of Stay
-* Male
-* Patient Readmission
-* Prognosis
-|keywords=* elderly
-* geriatrics
-* hospitalization
-* multidimensional prognostic index
-|full-text-url=https://sci-hub.do/10.1684/pnv.2019.0823
-}}
-==MRE11==
-{{medline-entry
-|title=Chromosomal alterations among age-related haematopoietic clones in Japan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32581364
-|mesh-terms=* Aged, 80 and over
-* Aging
-* Alleles
-* Cell Lineage
-* Chromosome Aberrations
-* Chromosomes, Human
-* Clone Cells
-* Cohort Studies
-* Female
-* Genetic Loci
-* Genome, Human
-* Hematopoiesis
-* Hematopoietic Stem Cells
-* Humans
-* Japan
-* Leukemia, Lymphocytic, Chronic, B-Cell
-* Leukemia, T-Cell
-* Male
-* Mosaicism
-* Mutation
-* United Kingdom
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7489641
-}}
-==MSC==
-{{medline-entry
-|title=Rejuvenation of Senescent Endothelial Progenitor Cells by Extracellular Vesicles Derived From Mesenchymal Stromal Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33294742
-|keywords=* BM, bone marrow
-* CVD, cardiovascular disease
-* EC, endothelial cell
-* EPC, endothelial progenitor cell
-* EV, extracellular vesicle
-* FBS, fetal bovine serum
-* MEM, minimum essential medium
-* MI, myocardial infarction
-* MSC, mesenchymal stromal cell
-* NTA, nanotracking analysis
-* PBS, phosphate-buffered saline
-* TEV, tailored extracellular vesicle
-* VEGF, vascular endothelial growth factor
-* acellular
-* angiogenesis
-* extracellular vesicles
-* lin− BMC, lineage negative bone marrow cell
-* miR, microRNA
-* qPCR, quantitative transcription polymerase chain reaction
-* regeneration
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7691285
-}}
-{{medline-entry
-|title=Extracellular vesicles derived from bone marrow mesenchymal stem cells enhance myelin maintenance after cortical injury in aged rhesus monkeys.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33264634
-|keywords=* Aging
-* Cortical injury
-* Extracellular vesicles
-* Monkeys
-* Myelin
-* Non-human primates
-* Oligodendrocytes
-* Stroke
-* White matter
-|full-text-url=https://sci-hub.do/10.1016/j.expneurol.2020.113540
-}}
-{{medline-entry
-|title=TPP1 Enhances the Therapeutic Effects of Transplanted Aged Mesenchymal Stem Cells in Infarcted Hearts via the MRE11/AKT Pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33195247
-|keywords=* DNA repair
-* aging
-* myocardial infarction
-* stem cells therapy
-* telomere
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7658181
-}}
-{{medline-entry
-|title=Aging-Affected [[MSC]] Functions and Severity of Periodontal Tissue Destruction in a Ligature-Induced Mouse Periodontitis Model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33143068
-|keywords=* aging
-* bone resorption
-* immunomodulation
-* mesenchymal stem cell
-* periodontitis
-* tissue destruction
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7663404
-}}
-{{medline-entry
-|title=Human placenta-derived mesenchymal stem cells stimulate ovarian function via miR-145 and bone morphogenetic protein signaling in aged rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33153492
-|keywords=* Aging
-* Follicular development
-* Hormone biosynthesis
-* Primordial follicle activation
-* Stem cell therapy
-* miR-145
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7643421
-}}
-{{medline-entry
-|title=Mesenchymal Stromal Cells as Critical Contributors to Tissue Regeneration.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33102483
-|keywords=* adult stem cells
-* aging
-* mesenchymal stromal cells (MSC)
-* regenerative medicine
-* stem cell niche
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7546871
-}}
-{{medline-entry
-|title=The biology of human hair greying.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32965076
-|keywords=* ageing
-* endocrine
-* graying
-* melanin
-* senescence
-|full-text-url=https://sci-hub.do/10.1111/brv.12648
-}}
-{{medline-entry
-|title=[i]Tsc1[/i] Regulates the Proliferation Capacity of Bone-Marrow Derived Mesenchymal Stem Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32927859
-|keywords=* TSC1
-* mammalian target of rapamycin (mTOR)
-* mesenchymal stem cell
-* senescence
-* stem cell proliferation
-* tuberous sclerosis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7565438
-}}
-{{medline-entry
-|title=The role of mitochondrial dysfunction in mesenchymal stem cell senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32803322
-|keywords=* Mesenchymal stem cells
-* Mitochondrial dysfunction
-* Mitophagy
-* Reactive oxygen species
-* Senescence
-|full-text-url=https://sci-hub.do/10.1007/s00441-020-03272-z
-}}
-{{medline-entry
-|title=Metabolic syndrome increases senescence-associated micro-RNAs in extracellular vesicles derived from swine and human mesenchymal stem/stromal cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32787856
-|keywords=* EV
-* MSC
-* Metabolic syndrome
-* RNA-sequencing
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7425605
-}}
-{{medline-entry
-|title=Functional heterogeneity of mesenchymal stem cells from natural niches to culture conditions: implications for further clinical uses.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32699947
-|keywords=* Aging diseases
-* Conditioned medium
-* Diabetes
-* Exosomes
-* Extracellular vesicles
-* Lupus
-* Regenerative medicine
-* Secretome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7375036
-}}
-{{medline-entry
-|title=Functional crosstalk between mTORC1/p70S6K pathway and heterochromatin organization in stress-induced senescence of [[MSC]]s.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32660632
-|keywords=* Aging
-* Heterochromatin
-* MSC senescence
-* mTORC1/p70S6K
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7359252
-}}
-{{medline-entry
-|title=Increased cellular senescence in the murine and human stenotic kidney: Effect of mesenchymal stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32657444
-|keywords=* cellular senescence
-* exosomes
-* kidney
-* mesenchymal stem cells
-* renal artery obstruction
-|full-text-url=https://sci-hub.do/10.1002/jcp.29940
-}}
-{{medline-entry
-|title=Intrinsic Type 1 Interferon (IFN1) Profile of Uncultured Human Bone Marrow CD45 CD271  Multipotential Stromal Cells (BM-[[MSC]]s): The Impact of Donor Age, Culture Expansion and IFNα and IFNβ Stimulation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32679782
-|keywords=* aging
-* bone marrow
-* mesenchymal stromal cells
-* senescence
-* type 1 interferon
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7399891
-}}
-{{medline-entry
-|title=Facial rejuvenation using stem cell conditioned media combined with skin needling: A split-face comparative study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32623814
-|keywords=* amniotic fluid stem cells products
-* dermaroller
-* facial aging
-* skin needling
-|full-text-url=https://sci-hub.do/10.1111/jocd.13594
-}}
-{{medline-entry
-|title=Mesenchymal Stem Cell Senescence and Rejuvenation: Current Status and Challenges.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32582691
-|keywords=* autophagy
-* mesenchymal stem cells
-* mitochondrial
-* rejuvenation
-* senescence
-* telomere
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7283395
-}}
-{{medline-entry
-|title=The changing epigenetic landscape of Mesenchymal Stem/Stromal Cells during aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32445894
-|keywords=* Aging
-* DNA methylation
-* Epigenetics
-* Histome modifications
-* MSC
-* Mesenchymal Stem/Stromal Cells
-* Skeleton
-* miRNA
-|full-text-url=https://sci-hub.do/10.1016/j.bone.2020.115440
-}}
-{{medline-entry
-|title=Dual Role of Autophagy in Regulation of Mesenchymal Stem Cell Senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32391362
-|keywords=* SASP
-* general autophagy
-* mesenchymal stem cell
-* selective autophagy
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7193103
-}}
-{{medline-entry
-|title=Molecular Aspects of Adipose-Derived Stromal Cell Senescence in a Long-Term Culture: A Potential Role of Inflammatory Pathways.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32314614
-|keywords=* adipose-derived stromal/stem cell
-* aging
-* gene expression
-* long-term culture
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7586277
-}}
-{{medline-entry
-|title=Human Obesity Induces Dysfunction and Early Senescence in Adipose Tissue-Derived Mesenchymal Stromal/Stem Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32274385
-|keywords=* adipose tissue
-* cellular dysfunction
-* cellular senescence
-* mesenchymal stem cells
-* obesity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7113401
-}}
-{{medline-entry
-|title=miR-155-5p inhibition rejuvenates aged mesenchymal stem cells and enhances cardioprotection following infarction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32196916
-|keywords=* mesenchymal stem cells
-* miR-155-5p
-* myocardial infarction
-* rejuvenation
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189985
-}}
-{{medline-entry
-|title=Mesenchymal Stem Cell Derived Extracellular Vesicles in Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32154253
-|keywords=* aging
-* clinical translation
-* extracellular vesicles
-* mesenchymal stem cells
-* regenerative medicine
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7047768
-}}
-{{medline-entry
-|title=Molecular Mechanisms Contributing to Mesenchymal Stromal Cell Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32098040
-|keywords=* MSC senescence
-* in vitro aging
-* in vivo aging
-* mesenchymal stem/stromal cells (MSC)
-* rejuvenating strategies
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072652
-}}
-{{medline-entry
-|title=Inhibition of DNA Methyltransferase by RG108 Promotes Pluripotency-Related Character of Porcine Bone Marrow Mesenchymal Stem Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32125888
-|keywords=* RG108
-* apoptosis
-* pluripotency
-* porcine bone marrow mesenchymal stem cells
-* senescence
-|full-text-url=https://sci-hub.do/10.1089/cell.2019.0060
-}}
-{{medline-entry
-|title=Extracellular Vesicles of Stem Cells to Prevent BRONJ.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32119600
-|keywords=* bisphosphonate-associated osteonecrosis of the jaw
-* cellular senescence
-* exosomes
-* mesenchymal stem cells
-* wound healing
-* zoledronic acid
-|full-text-url=https://sci-hub.do/10.1177/0022034520906793
-}}
-{{medline-entry
-|title=Ginsenoside Rg1 as an Effective Regulator of Mesenchymal Stem Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32038244
-|keywords=* apoptosis
-* differentiation
-* ginsenoside Rg1
-* mesenchymal stem cells
-* preclinical study
-* proliferation
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6989539
-}}
-{{medline-entry
-|title=The Importance of Stem Cell Senescence in Regenerative Medicine.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32026416
-|keywords=* Aging
-* Mesenchymal stem cell
-* Regenerative medicine
-|full-text-url=https://sci-hub.do/10.1007/5584_2020_489
-}}
-{{medline-entry
-|title=Control of mesenchymal stem cell biology by histone modifications.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32025282
-|keywords=* Cell biology
-* Cell differentiation
-* Cellular senescence
-* Epigenetics
-* Histone modifications
-* Mesenchymal stem cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996187
-}}
-{{medline-entry
-|title=Impact of mesenchymal stem cell senescence on inflammaging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31964472
-|mesh-terms=* Aging
-* Cellular Senescence
-* Cytokines
-* Hematopoiesis
-* Humans
-* Immunomodulation
-* Immunosenescence
-* Inflammation
-* Macrophages
-* Mesenchymal Stem Cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7061209
-}}
-{{medline-entry
-|title=Late Rescue Therapy with Cord-Derived Mesenchymal Stromal Cells for Established Lung Injury in Experimental Bronchopulmonary Dysplasia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31918630
-|keywords=* COPD
-* aging
-* lung
-* newborn
-* regenerative medicine
-* stem cells
-|full-text-url=https://sci-hub.do/10.1089/scd.2019.0116
-}}
-{{medline-entry
-|title=Low-Level Radiofrequency Exposure Does Not Induce Changes in [[MSC]] Biology: An in vitro Study for the Prevention of NIR-Related Damage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31908499
-|keywords=* 169 MHz
-* CFU
-* senescence
-* stem cell
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6927227
-}}
-{{medline-entry
-|title=Macrophage migration inhibitory factor rejuvenates aged human mesenchymal stem cells and improves myocardial repair.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31881006
-|mesh-terms=* Adolescent
-* Aged
-* Aged, 80 and over
-* Aging
-* Animals
-* Animals, Newborn
-* Cellular Senescence
-* Humans
-* Macrophage Migration-Inhibitory Factors
-* Mesenchymal Stem Cell Transplantation
-* Mesenchymal Stem Cells
-* Myocardial Infarction
-* Myocardium
-* Myocytes, Cardiac
-* Rats
-* Rats, Sprague-Dawley
-* Young Adult
-|keywords=* macrophage migration inhibitory factor
-* mesenchymal stem cells
-* myocardial infarction
-* rejuvenation
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6949107
-}}
-{{medline-entry
-|title=Influence of olive oil and its components on mesenchymal stem cell biology.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31875868
-|keywords=* Aging
-* Cellular differentiation
-* Cellular niche
-* Mediterranean diet
-* Mesenchymal stem cells
-* Olive oil
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6904865
-}}
-{{medline-entry
-|title=Epigenetic Regulation of Mesenchymal Stem Cell Homeostasis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31866188
-|keywords=* aging
-* epigenetics
-* fate decision
-* mesenchymal stem cells
-* pathogenesis
-* regeneration
-|full-text-url=https://sci-hub.do/10.1016/j.tcb.2019.11.006
-}}
-{{medline-entry
-|title=Mesenchymal Stem Cells: Allogeneic [[MSC]] May Be Immunosuppressive but Autologous [[MSC]] Are Dysfunctional in Lupus Patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31799252
-|keywords=* dysfunction
-* immunoregulatory
-* mesenchymal stem cells
-* senescence
-* systemic lupus erythematosus
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6874144
-}}
-{{medline-entry
-|title=Effects of high glucose conditions on the expansion and differentiation capabilities of mesenchymal stromal cells derived from rat endosteal niche.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31752674
-|mesh-terms=* Adipogenesis
-* Animals
-* Biomarkers
-* Bone Regeneration
-* Bone and Bones
-* Cell Differentiation
-* Cell Proliferation
-* Cells, Cultured
-* Cellular Senescence
-* Diabetes Mellitus, Type 2
-* Glucose
-* Hyperglycemia
-* Male
-* Mesenchymal Stem Cells
-* Osteogenesis
-* Rats, Wistar
-|keywords=* Bone repair
-* Cellular senescence
-* Differentiation
-* Hyperglycaemia
-* Mesenchymal stromal cells; Endosteum
-* Type II diabetes
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6873668
-}}
-{{medline-entry
-|title=Autophagy inhibits the mesenchymal stem cell aging induced by D-galactose through ROS/JNK/p38 signalling.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31675454
-|keywords=* ROS/JNK/p38 signalling
-* autophagy
-* mesenchymal stem cells
-* senescence
-|full-text-url=https://sci-hub.do/10.1111/1440-1681.13207
-}}
-{{medline-entry
-|title=Enhancing survival, engraftment, and osteogenic potential of mesenchymal stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31692976
-|keywords=* Anoikis
-* Bioactive scaffolds
-* Bone regeneration
-* Engraftment
-* Homing
-* Hypoxia
-* Mesenchymal stem cells
-* Osteogenesis
-* Preconditioning
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6828596
-}}
-{{medline-entry
-|title=Mesenchymal stem cell senescence alleviates their intrinsic and seno-suppressive paracrine properties contributing to osteoarthritis development.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31644429
-|mesh-terms=* Animals
-* Cell Proliferation
-* Cells, Cultured
-* Cellular Senescence
-* Chondrocytes
-* Coculture Techniques
-* Collagenases
-* Etoposide
-* Gene Expression Regulation
-* Humans
-* Inflammation
-* Luciferases
-* Male
-* Mesenchymal Stem Cells
-* Mice
-* Mice, Inbred Strains
-* Mice, Transgenic
-* Osteoarthritis
-* Paracrine Communication
-|keywords=* mesenchymal stem cell
-* osteoarthritis
-* senescence
-* tissue homeostasis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834426
-}}
-{{medline-entry
-|title=Embryonic stem cell-derived extracellular vesicles enhance the therapeutic effect of mesenchymal stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31660081
-|mesh-terms=* Animals
-* Cell- and Tissue-Based Therapy
-* Cellular Senescence
-* Disease Models, Animal
-* Embryonic Stem Cells
-* Extracellular Vesicles
-* Humans
-* Insulin-Like Growth Factor I
-* Mesenchymal Stem Cell Transplantation
-* Mesenchymal Stem Cells
-* Mice
-* Mice, Inbred BALB C
-* Phosphatidylinositol 3-Kinases
-* Wounds and Injuries
-|keywords=* Cellular senescence
-* Embryonic stem cells
-* Extracellular vesicles
-* IGF1/PI3K/AKT pathway
-* Mesenchymal stem cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6815953
-}}
-{{medline-entry
-|title=Survival of aging CD264  and CD264  populations of human bone marrow mesenchymal stem cells is independent of colony-forming efficiency.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31612990
-|keywords=* aging
-* decoy TRAIL receptor 2 (CD264)
-* mesenchymal stem cells
-* survival
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6906265
-}}
-{{medline-entry
-|title=Differential effects of extracellular vesicles from aging and young mesenchymal stem cells in acute lung injury.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31575829
-|mesh-terms=* Acute Lung Injury
-* Age Factors
-* Animals
-* Disease Models, Animal
-* Extracellular Vesicles
-* Mesenchymal Stem Cell Transplantation
-* Mesenchymal Stem Cells
-* Mice
-* Treatment Outcome
-|keywords=* ARDS
-* acute lung injury
-* aging
-* extracellular vesicles
-* mesenchymal stem cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6781978
-}}
-{{medline-entry
-|title=Connexin43 is Dispensable for Early Stage Human Mesenchymal Stem Cell Adipogenic Differentiation But is Protective against Cell Senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31514306
-|mesh-terms=* Adipogenesis
-* Cell Differentiation
-* Cellular Senescence
-* Connexin 43
-* Gene Expression Regulation
-* Humans
-* Mesenchymal Stem Cells
-* Time Factors
-|keywords=* CRISPR-Cas9
-* adipogenesis
-* connexin43
-* gap junctional intercellular communication
-* mesenchymal stem cells
-* oculodentodigital dysplasia
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6770901
-}}
-{{medline-entry
-|title=Maintained Properties of Aged Dental Pulp Stem Cells for Superior Periodontal Tissue Regeneration.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31440385
-|keywords=* inflammation
-* mesenchymal stem cells
-* periodontitis
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6675537
-}}
-==MTHFR==
-{{medline-entry
-|title=One-carbon metabolism supplementation improves outcome after stroke in aged male [[MTHFR]]-deficient mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31525435
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Choline
-* Dietary Supplements
-* Male
-* Methylenetetrahydrofolate Reductase (NADPH2)
-* Mice
-* Mice, Inbred C57BL
-* Recovery of Function
-* Stroke
-* Tetrahydrofolates
-* Vitamin B 12
-|keywords=* Cerebral ischemia
-* Homocysteine
-* Methylenetetrahydrofolate reductase
-* Neurodegeneration
-* Sensorimotor cortex
-* Supplementation
-|full-text-url=https://sci-hub.do/10.1016/j.nbd.2019.104613
-}}
-==MTOR==
-{{medline-entry
-|title=The roles of [[MTOR]] and miRNAs in endothelial cell senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32246301
-|keywords=* Endothelium
-* MTOR
-* MicroRNAs
-* Senescence
-* Vascular aging
-|full-text-url=https://sci-hub.do/10.1007/s10522-020-09876-w
-}}
-{{medline-entry
-|title=Autophagy drives fibroblast senescence through [[MTOR]]C2 regulation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31931659
-|keywords=* Autophagy
-* MTORC2
-* myofibroblast
-* rapamycin
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7595590
-}}
-{{medline-entry
-|title=The GID ubiquitin ligase complex is a regulator of AMPK activity and organismal lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31795790
-|keywords=* AMPK
-* GID
-* autophagy
-* longevity
-* primary cilium
-* ubiquitination
-|full-text-url=https://sci-hub.do/10.1080/15548627.2019.1695399
-}}
-==MTR==
-{{medline-entry
-|title=Amide proton transfer-weighted magnetic resonance imaging of human brain aging at 3 Tesla.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32269932
-|keywords=* Aging
-* amide proton transfer imaging
-* biomarkers
-* chemical exchange saturation transfer (CEST)
-* molecular imaging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7136735
-}}
-==MUC7==
-{{medline-entry
-|title=Reduced Salivary Mucin Binding and Glycosylation in Older Adults Influences Taste in an In Vitro Cell Model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31554163
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aging
-* Cell Line
-* Epithelial Cells
-* Female
-* Glycosylation
-* Humans
-* Male
-* Middle Aged
-* Mucins
-* N-Acetylneuraminic Acid
-* Plasmids
-* Protein Binding
-* Rheology
-* Saliva
-* Taste
-* Young Adult
-|keywords=* ageing
-* mucin
-* rheology
-* saliva
-* taste
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6835954
-}}
-==MYB==
-{{medline-entry
-|title=Transcriptome profiling of postharvest shoots identifies PheNAP2- and PheNAP3-promoted shoot senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31595958
-|mesh-terms=* Arabidopsis
-* Arabidopsis Proteins
-* Gene Expression Profiling
-* Gene Expression Regulation, Plant
-* Plant Leaves
-* Transcriptome
-|keywords=*
-          Phyllostachys edulis
-* NAC
-* postharvest
-* regulatory factors
-* shoot senescence
-|full-text-url=https://sci-hub.do/10.1093/treephys/tpz100
-}}
-==MYC==
-{{medline-entry
-|title=Enhanced proliferative capacity of human preadipocytes achieved by an optimized cultivating method that induces transient activity of hTERT.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32703451
-|keywords=* Adipogenesis
-* Adipose-derived stromal cells
-* Senescence
-* hTERT
-* mTesR1
-|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2020.06.019
-}}
-==MYCN==
-{{medline-entry
-|title=Silencing of AURKA augments the antitumor efficacy of the AURKA inhibitor MLN8237 on neuroblastoma cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31920463
-|keywords=* Aurora kinase A
-* Cellular senescence
-* MLN8237
-* Neuroblastoma
-* Small interfering RNA
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6947931
-}}
-==MYSM1==
-{{medline-entry
-|title=[[MYSM1]] Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33240758
-|keywords=* DNA repair
-* Myb‐like, SWIRM, and MPN domains‐containing protein 1 (MYSM1)
-* aging
-* senescence
-* senescence‐associated secretory phenotype (SASP)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7675055
-}}
-==MYT1==
-{{medline-entry
-|title=ESC-sEVs Rejuvenate Aging Hippocampal NSCs by Transferring SMADs to Regulate the [[MYT1]]-Egln3-Sirt1 Axis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33038325
-|keywords=* ESC-sEVs
-* MYT1
-* aging
-* hippocampal NSCs
-* senescence
-|full-text-url=https://sci-hub.do/10.1016/j.ymthe.2020.09.037
-}}
-==NACA==
-{{medline-entry
-|title=Age and Sex Are Strongly Correlated to the Rate and Type of Mountain Injuries Requiring Search and Rescue Missions.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31699646
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Emergency Medical Services
-* Female
-* Humans
-* Male
-* Middle Aged
-* Mountaineering
-* Rescue Work
-* Sex Factors
-* Young Adult
-|keywords=* MRT
-* NACA ICAR
-* SAR
-* injury
-* mechanism
-|full-text-url=https://sci-hub.do/10.1016/j.wem.2019.06.016
-}}
-==NAMPT==
-{{medline-entry
-|title=Over-expression of Nicotinamide phosphoribosyltransferase in mouse cells confers protective effect against oxidative and ER stress-induced premature senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32533606
-|keywords=* ER stress
-* NAD+
-* NAMPT
-* oxidative stress
-* premature senescence
-|full-text-url=https://sci-hub.do/10.1111/gtc.12794
-}}
-{{medline-entry
-|title=Resistance training increases muscle NAD  and NADH concentrations as well as [[NAMPT]] protein levels and global sirtuin activity in middle-aged, overweight, untrained individuals.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32369778
-|keywords=* NAD +
-* NADH
-* aging
-* muscle
-* resistance training
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7288928
-}}
-{{medline-entry
-|title=Differential Expression of Human N-Alpha-Acetyltransferase 40 (hNAA40), Nicotinamide Phosphoribosyltransferase ([[NAMPT]]) and Sirtuin-1 (SIRT-1) Pathway in Obesity and T2DM: Modulation by Metformin and Macronutrient Intake.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31920356
-|keywords=* NAMPT
-* T2DM
-* hNAA40
-* nicotinamide phosphoribosyltransferase
-* obesity
-* senescence
-* sirtuin-1
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6938199
-}}
-==NDRG2==
-{{medline-entry
-|title=[[NDRG2]] Expression Correlates with Neurofibrillary Tangles and Microglial Pathology in the Ageing Brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31947996
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Alzheimer Disease
-* Antigens, CD
-* Antigens, Differentiation, Myelomonocytic
-* Astrocytes
-* Brain
-* DNA Damage
-* Excitatory Amino Acid Transporter 2
-* Gene Expression Regulation
-* Glial Fibrillary Acidic Protein
-* Glutamate-Ammonia Ligase
-* Humans
-* Microglia
-* Neurofibrillary Tangles
-* Tumor Suppressor Proteins
-* tau Proteins
-|keywords=* N-myc downstream regulated gene 2 (NDRG2)
-* ageing brain
-* astrocyte
-* neurofibrillary tangles
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6982267
-}}
-==NDUFS8==
-{{medline-entry
-|title=Mitochondrial Complex I Mutations Predispose Drosophila to Isoflurane Neurotoxicity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32773682
-|mesh-terms=* Aging
-* Anesthetics, Inhalation
-* Animals
-* Animals, Genetically Modified
-* Drosophila
-* Electron Transport Complex I
-* Isoflurane
-* Male
-* Mitochondria
-* Mutation
-* Sevoflurane
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7494633
-}}
-==NEDD8==
-{{medline-entry
-|title=Targeting Protein Neddylation for Cancer Therapy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31898235
-|mesh-terms=* Animals
-* Apoptosis
-* Autophagy
-* Cyclopentanes
-* Humans
-* NEDD8 Protein
-* Neoplasms
-* Pyrimidines
-* Ubiquitin-Protein Ligases
-* Ubiquitination
-|keywords=* Apoptosis
-* Autophagy
-* Cancer target
-* Inflammatory responses
-* Neddylation
-* Senescence
-|full-text-url=https://sci-hub.do/10.1007/978-981-15-1025-0_18
-}}
-{{medline-entry
-|title=Effective targeting of the ubiquitin-like modifier [[NEDD8]] for lung adenocarcinoma treatment.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31907687
-|keywords=* NEDD8
-* apoptosis
-* cullin-RING ligases
-* neddylation
-* senescence
-|full-text-url=https://sci-hub.do/10.1007/s10565-019-09503-6
-}}
-{{medline-entry
-|title=Pevonedistat targeted therapy inhibits canine melanoma cell growth through induction of DNA re-replication and senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31665821
-|keywords=* DNA re-replication
-* MLN4924
-* NAE-inhibitor
-* canine
-* melanoma
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7473101
-}}
-==NEO1==
-{{medline-entry
-|title=Neogenin-1 distinguishes between myeloid-biased and balanced [i]Hoxb5[/i]   mouse long-term hematopoietic stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31754028
-|mesh-terms=* Aging
-* Animals
-* Female
-* Hematopoietic Stem Cell Transplantation
-* Hematopoietic Stem Cells
-* Homeodomain Proteins
-* Membrane Proteins
-* Mice
-* Mice, Transgenic
-|keywords=* Neogenin-1
-* aging
-* hematopoietic stem cell
-* myeloid bias
-* transplantation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6911217
-}}
-==NES==
-{{medline-entry
-|title=Mini-review: Aging of the neuroendocrine system: Insights from nonhuman primate models.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31891735
-|keywords=* Aging
-* Neuroendocrine system
-* Nonhuman primate
-|full-text-url=https://sci-hub.do/10.1016/j.pnpbp.2019.109854
-}}
-==NFKB1==
-{{medline-entry
-|title=[[NFKB1]] gene single-nucleotide polymorphisms: implications for graft-versus-host disease in allogeneic hematopoietic stem cell transplantation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32002656
-|mesh-terms=* Adult
-* Allografts
-* Disease-Free Survival
-* Female
-* Graft vs Host Disease
-* Hematopoietic Stem Cell Transplantation
-* Humans
-* Male
-* Middle Aged
-* NF-kappa B p50 Subunit
-* Pilot Projects
-* Polymorphism, Single Nucleotide
-* Survival Rate
-|keywords=* Allogeneic hematopoietic stem cell transplantation
-* Cellular senescence
-* Graft-versus-host disease
-* NFKB1 gene
-* Senescence-associated secretory phenotype
-* Single-nucleotide polymorphism
-|full-text-url=https://sci-hub.do/10.1007/s00277-020-03935-5
-}}
-==NGF==
-{{medline-entry
-|title=Dietary fish hydrolysate supplementation containing n-3 LC-PUFAs and peptides prevents short-term memory and stress response deficits in aged mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32976934
-|keywords=* Aging
-* Anxiety-like behaviour
-* Cognitive decline
-* Hydrolysate
-* Low molecular weight peptides
-* Marine by-products
-* Memory
-* Navigation strategies
-* Neuroinflammation
-* Stress response
-* n-3 Long chain polyunsaturated fatty acids (n-3 LC-PUFAs)
-|full-text-url=https://sci-hub.do/10.1016/j.bbi.2020.09.022
-}}
-{{medline-entry
-|title=Imbalance of nerve growth factor metabolism in aging women with overactive bladder syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32870355
-|keywords=* Aging female
-* MMP-7
-* MMP-9
-* Nerve growth factor
-* Overactive bladder
-* proNGF
-|full-text-url=https://sci-hub.do/10.1007/s00345-020-03422-6
-}}
-{{medline-entry
-|title=Parity Attenuates Intraepithelial Corneal Sensory Nerve Loss in Female Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32708332
-|keywords=* aging
-* corneal epithelial cell proliferation
-* corneal sensitivity
-* corneal sensory nerves
-* mouse
-* parity
-* pregnancy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7404034
-}}
-{{medline-entry
-|title=Cholinergic System and [[NGF]] Receptors: Insights from the Brain of the Short-Lived Fish [i]Nothobranchius furzeri[/i].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32575701
-|keywords=* NTRK1/NTRKA
-* aging
-* cholinergic system
-* fish
-* p75/NGFR
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7348706
-}}
-{{medline-entry
-|title=Retrograde axonal transport of BDNF and pro[[NGF]] diminishes with age in basal forebrain cholinergic neurons.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31574357
-|mesh-terms=* Aging
-* Alzheimer Disease
-* Axonal Transport
-* Brain-Derived Neurotrophic Factor
-* Cholinergic Neurons
-* Humans
-* Nerve Growth Factor
-* Prosencephalon
-|keywords=* Alzheimer's disease
-* Axonal transport
-* Basal forebrain
-* Neurodegeneration
-* Neurotrophins
-* Trk receptors
-|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2019.07.018
-}}
-{{medline-entry
-|title=C-SH2 point mutation converts p85β regulatory subunit of phosphoinositide 3-kinase to an anti-aging gene.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31481652
-|mesh-terms=* Aging
-* Animals
-* Blood Glucose
-* Class I Phosphatidylinositol 3-Kinases
-* Class Ia Phosphatidylinositol 3-Kinase
-* Female
-* Forkhead Transcription Factors
-* Insulin
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Mice, Transgenic
-* Nerve Growth Factor
-* Oxidative Stress
-* PC12 Cells
-* Platelet-Derived Growth Factor
-* Point Mutation
-* Proto-Oncogene Proteins c-akt
-* Rats
-* src Homology Domains
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6722097
-}}
-==NHS==
-{{medline-entry
-|title=Telomerase Activation to Reverse Immunosenescence in Elderly Patients With Acute Coronary Syndrome: Protocol for a Randomized Pilot Trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32965237
-|keywords=* acute coronary syndrome
-* coronary heart disease
-* immunosenescence
-* telomerase activator
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7542409
-}}
-{{medline-entry
-|title=Factors associated with COVID-19-related death using OpenSAFELY.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32640463
-|mesh-terms=* Adolescent
-* Adult
-* African Continental Ancestry Group
-* Age Distribution
-* Age Factors
-* Aged
-* Aged, 80 and over
-* Aging
-* Asian Continental Ancestry Group
-* Asthma
-* Betacoronavirus
-* COVID-19
-* Cohort Studies
-* Coronavirus Infections
-* Diabetes Mellitus
-* Female
-* Humans
-* Hypertension
-* Male
-* Middle Aged
-* Pandemics
-* Pneumonia, Viral
-* Proportional Hazards Models
-* Risk Assessment
-* SARS-CoV-2
-* Sex Characteristics
-* Smoking
-* State Medicine
-* Young Adult
-|full-text-url=https://sci-hub.do/10.1038/s41586-020-2521-4
-}}
-{{medline-entry
-|title=Advanced ophthalmic nurse practitioners: the potential to improve outcomes for older people with cataracts.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32548985
-|keywords=* advanced practice
-* gerontology
-* older people
-* patient outcomes
-* patients
-* practice development
-* professional
-* professional issues
-* quality of life
-|full-text-url=https://sci-hub.do/10.7748/nop.2020.e1229
-}}
-{{medline-entry
-|title=Patient Satisfaction in the Spanish National Health Service: Partial Least Squares Structural Equation Modeling.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31817147
-|mesh-terms=* Cross-Sectional Studies
-* Gross Domestic Product
-* Health Care Rationing
-* Health Expenditures
-* Humans
-* Latent Class Analysis
-* Least-Squares Analysis
-* Life Expectancy
-* Patient Safety
-* Patient Satisfaction
-* Spain
-* State Medicine
-|keywords=* National Health Service
-* health policy
-* partial least squares structural equation modeling (PLS-SEM)
-* patient satisfaction
-* quality of healthcare
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6950388
-}}
-{{medline-entry
-|title=Heart failure with preserved ejection fraction (HFpEF) pathophysiology study (IDENTIFY-HF): does increased arterial stiffness associate with HFpEF, in addition to ageing and vascular effects of comorbidities? Rationale and design.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31748285
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Biomarkers
-* Comorbidity
-* Diabetes Mellitus
-* Echocardiography
-* Exercise Tolerance
-* Female
-* Heart Failure
-* Heart Ventricles
-* Humans
-* Hypertension
-* Male
-* Observational Studies as Topic
-* Prospective Studies
-* Pulse Wave Analysis
-* Research Design
-* Stroke Volume
-* Vascular Stiffness
-|keywords=* arterial stiffness
-* comorbidities
-* heart failure with preserved ejection fraction
-* pathophysiology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6886989
-}}
-{{medline-entry
-|title=Challenges to concordance: theories that explain variations in patient responses.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31604052
-|mesh-terms=* Aging
-* Benchmarking
-* Communication Barriers
-* Community Health Nursing
-* Humans
-* Nurse-Patient Relations
-* State Medicine
-* United Kingdom
-|keywords=* Concordance
-* Decision making
-* Person-centred care
-* Psychological theories
-* Self-management
-|full-text-url=https://sci-hub.do/10.12968/bjcn.2019.24.10.466
-}}
-{{medline-entry
-|title=Optimism is associated with exceptional longevity in 2 epidemiologic cohorts of men and women.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31451635
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Female
-* Health Behavior
-* Humans
-* Logistic Models
-* Longevity
-* Longitudinal Studies
-* Male
-* Middle Aged
-* Odds Ratio
-|keywords=* aging
-* longevity
-* longitudinal study
-* optimism
-* psychological well-being
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6744861
-}}
-==NKAP==
-{{medline-entry
-|title=[[NKAP]] Regulates Senescence and Cell Death Pathways in Hematopoietic Progenitors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31632967
-|keywords=* NKAP
-* apoptosis
-* cyclin dependent kinase inhibitor
-* hematopoiesis
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6783958
-}}
-==NKX6-1==
-{{medline-entry
-|title=The dynamic methylome of islets in health and disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31500828
-|mesh-terms=* Animals
-* Cell Differentiation
-* DNA Methylation
-* Diabetes Mellitus, Type 2
-* Epigenome
-* Humans
-* Insulin-Secreting Cells
-|keywords=* Aging
-* Beta cells
-* DNA methylation
-* Endocrine pancreas
-* Epigenetics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6768570
-}}
-==NLRC4==
-{{medline-entry
-|title=Hyperglycemia-induced inflamm-aging accelerates gingival senescence via [[NLRC4]] phosphorylation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31676687
-|mesh-terms=* Aging
-* Animals
-* Apoptosis Regulatory Proteins
-* Blotting, Western
-* Calcium-Binding Proteins
-* Cellular Senescence
-* Clustered Regularly Interspaced Short Palindromic Repeats
-* Gingiva
-* Glucose
-* Hyperglycemia
-* Immunohistochemistry
-* Inflammation
-* Interferon Regulatory Factors
-* Male
-* Mice
-* Mice, Inbred C57BL
-* RAW 264.7 Cells
-* Signal Transduction
-|keywords=* NLRC4
-* SASP
-* aging
-* cellular senescence
-* diabetes
-* gingiva
-* hyperglycemia
-* inflamm-aging
-* inflammasome
-* inflammation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6901307
-}}
-==NLRP12==
-{{medline-entry
-|title=Persistent DNA damage-induced [[NLRP12]] improves hematopoietic stem cell function.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32434992
-|keywords=* Aging
-* DNA repair
-* Hematology
-* Hematopoietic stem cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7259522
-}}
-==NLRP3==
-{{medline-entry
-|title=Innate and Adaptive Immunity in Aging and Longevity: The Foundation of Resilience.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33269094
-|keywords=* adaptive immunity
-* aging
-* innate immunity
-* longevity
-* resilience
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673842
-}}
-{{medline-entry
-|title=TET2-Loss-of-Function-Driven Clonal Hematopoiesis Exacerbates Experimental Insulin Resistance in Aging and Obesity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33113366
-|keywords=* CHIP
-* IL-1β
-* TET2
-* adipose tissue
-* aging
-* clonal hematopoiesis
-* diabetes
-* insulin resistance
-* obesity
-* somatic mutations
-|full-text-url=https://sci-hub.do/10.1016/j.celrep.2020.108326
-}}
-{{medline-entry
-|title=Repeated propofol exposure-induced neuronal damage and cognitive impairment in aged rats by activation of NF-κB pathway and [[NLRP3]] inflammasome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33115643
-|keywords=* Aging
-* Apoptosis
-* NOD-like receptor protein 3 inflammasome
-* Neuroinflammation
-* Postoperative cognitive dysfunction
-* Propofol
-|full-text-url=https://sci-hub.do/10.1016/j.neulet.2020.135461
-}}
-{{medline-entry
-|title=A Small Molecule Stabilizer of the MYC G4-Quadruplex Induces Endoplasmic Reticulum Stress, Senescence and Pyroptosis in Multiple Myeloma.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33066043
-|keywords=* ASC and pannexin 1
-* MYC G4-quadruplex stabilizer
-* NLRP3
-* caspase 1
-* endoplasmic reticulum stress
-* gasdermin D
-* inflammasome
-* pyroptosis
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7650714
-}}
-{{medline-entry
-|title=Interleukin-1β Drives Cellular Senescence of Rat Astrocytes Induced by Oligomerized Amyloid β Peptide and Oxidative Stress.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33013631
-|keywords=* Alzheimer's disease
-* amyloid β
-* astrocyte
-* interleukin-1β
-* neuroinflammation
-* senescence
-* tau
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7493674
-}}
-{{medline-entry
-|title=Mechanisms of [[NLRP3]] priming in inflammaging and age related diseases.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32883606
-|keywords=* Aging
-* Inflammaging
-* Inflammasome
-* NLRP3
-* Priming
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7571497
-}}
-{{medline-entry
-|title=Lamivudine Inhibits [i]Alu[/i] RNA-induced Retinal Pigment Epithelium Degeneration via Anti-inflammatory and Anti-senescence Activities.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32855848
-|keywords=* NLRP3 inflammasome
-* age-related macular degeneration
-* lamivudine
-* retinal pigment epithelium
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7422901
-}}
-{{medline-entry
-|title=The [[NLRP3]] Inflammasome: Metabolic Regulation and Contribution to Inflammaging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32751530
-|keywords=* NLRP3 inflammasome
-* aging
-* inflammation
-* metabolism
-* mitochondria
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7463618
-}}
-{{medline-entry
-|title=Aging aggravated liver ischemia and reperfusion injury by promoting STING-mediated [[NLRP3]] activation in macrophages.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32666684
-|keywords=* aging
-* and reperfusion injury
-* leucine-rich repeat containing protein 3
-* liver ischemia
-* macrophage immune response
-* nucleotide-binding domain
-* stimulator of interferon genes
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431827
-}}
-{{medline-entry
-|title=Targeting [[NLRP3]] Inflammasome Reduces Age-Related Experimental Alveolar Bone Loss.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32531176
-|keywords=* aging
-* inflammasomes
-* inflammation
-* macrophages
-* osteoclasts
-* periodontitis
-|full-text-url=https://sci-hub.do/10.1177/0022034520933533
-}}
-{{medline-entry
-|title=Korean Red Ginseng Suppresses the Expression of Oxidative Stress Response and [[NLRP3]] Inflammasome Genes in Aged C57BL/6 Mouse Ovaries.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32331214
-|keywords=* Korean ginseng extract
-* NLRP3 inflammasome
-* aging
-* ovary
-* oxidative stress response
-* subfertility
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7231237
-}}
-{{medline-entry
-|title=Cepharanthine promotes the effect of dexmedetomidine on the deposition of β-amyloid in the old age of the senile dementia rat model by regulating inflammasome expression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32337948
-|mesh-terms=* Aging
-* Animals
-* Benzylisoquinolines
-* Brain
-* Dexmedetomidine
-* Inflammasomes
-* Inflammation
-* Male
-* Mitochondria
-* Oxidative Stress
-* Rats, Sprague-Dawley
-* Reactive Oxygen Species
-|keywords=*  dementia
-*  dexmedetomidine
-*  inflammasomes
-*  β-amyloid
-* cepharanthine
-|full-text-url=https://sci-hub.do/10.5114/fn.2019.89855
-}}
-{{medline-entry
-|title=Ginsenoside Rg1 ameliorates glomerular fibrosis during kidney aging by inhibiting NOX4 and [[NLRP3]] inflammasome activation in SAMP8 mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32114413
-|keywords=* Ginsenoside Rg1
-* Kidney aging
-* NADPH oxidase 4 (NOX4)
-* NLRP3 inflammasome
-* Renal fibrosis
-|full-text-url=https://sci-hub.do/10.1016/j.intimp.2020.106339
-}}
-{{medline-entry
-|title=Blockade of the [[NLRP3]] inflammasome improves metabolic health and lifespan in obese mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31975052
-|keywords=* Aging
-* Autophagy
-* High-fat diet
-* Longevity
-* NLRP3 inflammasome
-* Obesity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7206474
-}}
-{{medline-entry
-|title=Autophagy and [[NLRP3]] inflammasome crosstalk in neuroinflammation in aged bovine brains.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31903559
-|keywords=* NLRP3 inflammasome
-* aging
-* autophagy
-* bovine
-* immunosenescence
-* neuroinflammation
-|full-text-url=https://sci-hub.do/10.1002/jcp.29426
-}}
-{{medline-entry
-|title=[[NLRP3]] Inflammasome Inhibition by MCC950 in Aged Mice Improves Health via Enhanced Autophagy and PPARα Activity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31603987
-|keywords=* Aging
-* Autophagy
-* MCC950
-* NLRP3 inflammasome
-* PPARα
-|full-text-url=https://sci-hub.do/10.1093/gerona/glz239
-}}
-{{medline-entry
-|title=[[NLRP3]] inflammasome suppression improves longevity and prevents cardiac aging in male mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31625260
-|keywords=* NLRP3-inflammasome
-* autophagy
-* cardiac aging
-* longevity
-* morbidity
-* mortality
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6974709
-}}
-{{medline-entry
-|title=Reduced NRF2 expression suppresses endothelial progenitor cell function and induces senescence during aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31494646
-|mesh-terms=* Aging
-* Animals
-* Cellular Senescence
-* Endothelial Progenitor Cells
-* Mice
-* NF-E2-Related Factor 2
-* NF-kappa B
-* NLR Family, Pyrin Domain-Containing 3 Protein
-* Neovascularization, Physiologic
-* Oxidative Stress
-|keywords=* NLRP3 inflammasome
-* NRF2
-* aging
-* endothelial progenitor cells
-* oxidative stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6756903
-}}
-{{medline-entry
-|title=Effect of Aging on Taurine Transporter (TauT) Expression in the Mouse Brain Cortex.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31468381
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Membrane Glycoproteins
-* Membrane Transport Proteins
-* Mice
-* Mice, Inbred C57BL
-* Taurine
-|keywords=* Age-related diseases
-* Glycine Transporter (GLYT)
-* NLRP3
-* Taurine Transporter (TauT)
-|full-text-url=https://sci-hub.do/10.1007/978-981-13-8023-5_1
-}}
-==NMI==
-{{medline-entry
-|title=Age-Dependent Control of Shoulder Muscles During a Reach-and-Lift Task.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31825888
-|keywords=* activity of daily living
-* aging
-* functional connectivity
-* motor variability
-* muscle fatigue
-|full-text-url=https://sci-hub.do/10.1123/japa.2019-0055
-}}
-==NMS==
-{{medline-entry
-|title=Uncontrolled Diabetes as an Associated Factor with Dynapenia in Adults Aged 50 Years or Older: Sex Differences.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31665234
-|keywords=* Aging
-* Dynapenia
-* Glycated hemoglobin
-* Hyperglycemia
-* Neuromuscular strength
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7243578
-}}
-==NMUR1==
-{{medline-entry
-|title=[Medicinal Chemistry Focused on Mid-sized Peptides Derived from Biomolecules].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31685733
-|mesh-terms=* Aging
-* Chemistry, Pharmaceutical
-* Drug Discovery
-* Humans
-* Life Style
-* Molecular Targeted Therapy
-* Muscle Weakness
-* Muscular Atrophy
-* Myostatin
-* Neuropeptides
-* Obesity
-* Peptides
-* Receptors, Neurotransmitter
-* Structure-Activity Relationship
-|keywords=* myostatin inhibitor
-* neuromedin U receptor-selective agonist
-* peptide
-|full-text-url=https://sci-hub.do/10.1248/yakushi.19-00149
-}}
-==NNT==
-{{medline-entry
-|title=Yoga, Health-Related Quality of Life and Mental Well-Being: A Re-analysis of a Meta-analysis Using the Quality Effects Model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31814012
-|keywords=* Outcomes
-* Physical activity
-* Successful aging
-* Systematic review
-|full-text-url=https://sci-hub.do/10.1093/gerona/glz284
-}}
-{{medline-entry
-|title=Statins After Myocardial Infarction in the Oldest: A Cohort Study in the Clinical Practice Research Datalink Database.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31647578
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Case-Control Studies
-* Databases, Factual
-* Female
-* Humans
-* Hydroxymethylglutaryl-CoA Reductase Inhibitors
-* Male
-* Myocardial Infarction
-* Proportional Hazards Models
-* Retrospective Studies
-* Risk Assessment
-* Secondary Prevention
-* Stroke
-|keywords=* geriatrics
-* myocardial infarction
-* secondary prevention
-* statin
-* time varying
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7028025
-}}
-==NOP10==
-{{medline-entry
-|title=Pseudouridylation defect due to [i]DKC1[/i] and [i][[NOP10]][/i] mutations causes nephrotic syndrome with cataracts, hearing impairment, and enterocolitis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32554502
-|mesh-terms=* Animals
-* Cataract
-* Cell Cycle Proteins
-* Child
-* Enterocolitis
-* Female
-* Genetic Predisposition to Disease
-* Hearing Loss, Sensorineural
-* Humans
-* Longevity
-* Male
-* Models, Molecular
-* Molecular Dynamics Simulation
-* Mutation
-* Nephrotic Syndrome
-* Nuclear Proteins
-* Pedigree
-* Protein Conformation
-* RNA, Ribosomal
-* Ribonucleoproteins, Small Nucleolar
-* Zebrafish
-|keywords=* H/ACA snoRNP
-* pediatrics
-* pseudouridylation
-* rRNA
-* telomere
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7334496
-}}
-==NOS1==
-{{medline-entry
-|title=Prepubertal overexposure to manganese induce precocious puberty through GABA  receptor/nitric oxide pathway in immature female rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31711775
-|mesh-terms=* Aging
-* Animals
-* Chlorides
-* Endocrine Disruptors
-* Female
-* Gonadotropin-Releasing Hormone
-* Manganese Compounds
-* Neurons
-* Nitric Oxide
-* Ovary
-* Preoptic Area
-* Rats
-* Rats, Sprague-Dawley
-* Receptors, GABA-A
-* Sexual Maturation
-* Signal Transduction
-* Uterus
-* Weaning
-|keywords=* GABA(A)R
-* GnRH
-* Manganese
-* Nitric oxide
-* Precocious puberty
-|full-text-url=https://sci-hub.do/10.1016/j.ecoenv.2019.109898
-}}
-==NOS3==
-{{medline-entry
-|title=Application of Oxidative Stress to a Tissue-Engineered Vascular Aging Model Induces Endothelial Cell Senescence and Activation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32455928
-|keywords=* endothelial cells
-* oxidative stress
-* senescence
-* tissue-engineered blood vessel
-* vascular smooth muscle cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7290800
-}}
-==NOTCH1==
-{{medline-entry
-|title=[How Does Aging Contribute to Cancer?]
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33130684
-|mesh-terms=* Aged
-* Aging
-* Carcinogenesis
-* Esophageal Neoplasms
-* Humans
-* Mutation
-}}
-{{medline-entry
-|title=H19 is not hypomethylated or upregulated with age or sex in the aortic valves of mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31609547
-|mesh-terms=* Aging
-* Animals
-* Aortic Valve
-* Aortic Valve Stenosis
-* Calcinosis
-* DNA Methylation
-* Female
-* Male
-* Mice
-* Mice, Inbred C57BL
-* RNA, Long Noncoding
-* Sex Factors
-* Up-Regulation
-|keywords=*
-H19
-* age
-* calcific aortic valve disease
-* epigenetics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6778597
-}}
-==NOTCH4==
-{{medline-entry
-|title=Age-dependent autophagy induction after injury promotes axon regeneration by limiting NOTCH.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31920157
-|keywords=* Aging
-* DLK
-* LC3
-* Notch signaling
-* autophagy
-* axon injury
-* axon regeneration
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7595581
-}}
-==NOX4==
-{{medline-entry
-|title=Sestrin2 Attenuates Cellular Senescence by Inhibiting NADPH Oxidase 4 Expression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33227845
-|keywords=* NOX4
-* Reactive oxygen species
-* Senescence
-* Sestrin2
-|full-text-url=https://sci-hub.do/10.4235/agmr.20.0051
-}}
-==NPM1==
-{{medline-entry
-|title=Flow cytometric identification and cell-line establishment of macrophages in naked mole-rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31784606
-|mesh-terms=* Animals
-* Cell Line
-* Cell Proliferation
-* Cell Separation
-* Culture Media
-* Flow Cytometry
-* Longevity
-* Macrophage Colony-Stimulating Factor
-* Macrophages
-* Mole Rats
-* Recombinant Proteins
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6884578
-}}
-==NPR1==
-{{medline-entry
-|title=The [[NPR1]]-WRKY46-WRKY6 signaling cascade mediates probenazole/salicylic acid-elicited leaf senescence in Arabidopsis thaliana.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33270345
-|keywords=* Leaf senescence
-* NPR1
-* Probenazole
-* Salicylic acid
-* WRKY46
-* WRKY6
-|full-text-url=https://sci-hub.do/10.1111/jipb.13044
-}}
-{{medline-entry
-|title=Loss of proton/calcium exchange 1 results in the activation of plant defense and accelerated senescence in Arabidopsis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32540002
-|keywords=* Early senescence
-* H(+)/Ca(2+)exchanger 1
-* Plant defense
-* Salicylic acid
-* Scopoletin
-|full-text-url=https://sci-hub.do/10.1016/j.plantsci.2020.110472
-}}
-==NPW==
-{{medline-entry
-|title=Novel information processing at work across time is associated with cognitive change in later life: A 14-year longitudinal study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32309980
-|mesh-terms=* Aged
-* Aging
-* Cognition
-* Cognitive Aging
-* Cognitive Dysfunction
-* Employment
-* Female
-* Humans
-* Longitudinal Studies
-* Male
-* Middle Aged
-* Retirement
-* Time
-|full-text-url=https://sci-hub.do/10.1037/pag0000468
-}}
-==NPY==
-{{medline-entry
-|title=Neuropeptide Y Enhances Progerin Clearance and Ameliorates the Senescent Phenotype of Human Hutchinson-Gilford Progeria Syndrome Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32012215
-|keywords=* Autophagy
-* Caloric restriction mimetic
-* Cellular senescence
-* Human aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7243588
-}}
-{{medline-entry
-|title=Effects of rikkunshito supplementation on resistance to oxidative stress and lifespan in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31855319
-|mesh-terms=* Animals
-* Caloric Restriction
-* Dietary Supplements
-* Drugs, Chinese Herbal
-* Female
-* Ghrelin
-* Longevity
-* Male
-* Mice
-* Mice, Knockout
-* Oxidative Stress
-|keywords=* calorie restriction
-* ghrelin
-* longevity
-* metabolism
-* oxidative stress
-|full-text-url=https://sci-hub.do/10.1111/ggi.13848
-}}
-==NRAS==
-{{medline-entry
-|title=Senescent cholangiocytes release extracellular vesicles that alter target cell phenotype via the epidermal growth factor receptor.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32558183
-|keywords=* biliary epithelial cell
-* cellular senescence
-* extracellular vesicles
-* primary sclerosing cholangitis
-* senescence-associated secretory phenotype
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7669612
-}}
-{{medline-entry
-|title=STAT3 Relays a Differential Response to Melanoma-Associated [i][[NRAS]][/i] Mutations.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31906480
-|keywords=* NRAS
-* STAT3
-* melanoma
-* mutation
-* oncogene-induced senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7016650
-}}
-{{medline-entry
-|title=Cooperation of Dnmt3a R878H with Nras G12D promotes leukemogenesis in knock-in mice: a pilot study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31703632
-|mesh-terms=* Animals
-* Apoptosis
-* Carcinogenesis
-* Cell Differentiation
-* DNA (Cytosine-5-)-Methyltransferases
-* Disease Models, Animal
-* Disease Progression
-* Gene Expression Regulation, Neoplastic
-* Gene Knock-In Techniques
-* Leukemia, Myeloid, Acute
-* Longevity
-* Mice
-* Mice, Inbred C57BL
-* Mice, Transgenic
-* Monomeric GTP-Binding Proteins
-* Mutation
-* Phenotype
-* Pilot Projects
-* Proto-Oncogene Proteins c-myc
-* RNA-Seq
-* Transcription, Genetic
-|keywords=* Acute myeloid leukemia
-* DNMT3A mutation
-* Myc activation
-* Nras G12D
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6842226
-}}
-==NRL==
-{{medline-entry
-|title=Development of a cyclophosphamide stress test to predict resilience to aging in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32613492
-|keywords=* Aging mice
-* Cyclophosphamide
-* Neutrophil lymphocyte ratio
-* Resilience to aging
-* Stress test
-* WBC count
-|full-text-url=https://sci-hub.do/10.1007/s11357-020-00222-z
-}}
-==NRM==
-{{medline-entry
-|title=Association between Clonal Hematopoiesis and Late Nonrelapse Mortality after Autologous Hematopoietic Cell Transplantation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31445185
-|mesh-terms=* Adult
-* Age Factors
-* Aged
-* Aging
-* Autografts
-* Female
-* Hematopoiesis
-* Hematopoietic Stem Cell Transplantation
-* Humans
-* Lymphoma, Non-Hodgkin
-* Male
-* Middle Aged
-* Multiple Myeloma
-* Retrospective Studies
-|keywords=* Autologous
-* Clonal hematopoiesis
-* Lymphoma
-* Multiple myeloma
-* Nonrelapse mortality
-* Survivors
-* Transplantation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7192097
-}}
-==NSF==
-{{medline-entry
-|title=Effects of air pollution on children from a socioecological perspective.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31727016
-|mesh-terms=* Air Pollution
-* Child Mortality
-* Child, Preschool
-* Environment
-* Humans
-* Income
-* Infant
-* Life Expectancy
-* Retrospective Studies
-* Socioeconomic Factors
-* Sociological Factors
-|keywords=* Deaths of children under age 5
-* Electrification rates
-* Income
-* Inequality in life expectancy
-* Natural resource depletion
-* Non-solid fuel
-* Outdoor and indoor air pollution
-* Socioecological perspective
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6857293
-}}
-==NT5E==
-{{medline-entry
-|title=The [[NT5E]] gene variant strongly affects the degradation rate of inosine 5'-monophosphate under postmortem conditions in Japanese Black beef.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31401370
-|mesh-terms=* 5'-Nucleotidase
-* Animals
-* Cattle
-* Diaphragm
-* Food Handling
-* Inosine Monophosphate
-* Muscle, Skeletal
-* Polymorphism, Single Nucleotide
-* Postmortem Changes
-* Red Meat
-* Taste
-|keywords=* Inosine 5′-monophosphate
-* Japanese Black beef
-* Meat quality
-* NT5E
-* Postmortem aging
-|full-text-url=https://sci-hub.do/10.1016/j.meatsci.2019.107893
-}}
-==NTHL1==
-{{medline-entry
-|title=Mitochondrial base excision repair positively correlates with longevity in the liver and heart of mammals.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31970600
-|keywords=* AP endonuclease
-* Aging
-* DNA glycosylases
-* DNA repair
-* Mitochondria
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7205949
-}}
-==NUCB2==
-{{medline-entry
-|title=Ontogenetic Pattern Changes of Nucleobindin-2/Nesfatin-1 in the Brain and Intestinal Bulb of the Short Lived African Turquoise Killifish.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31906085
-|keywords=* Nesf-1
-* Nothobranchius furzeri
-* aging
-* brain-gut axis
-* vertebrate
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7019235
-}}
-==OGA==
-{{medline-entry
-|title=NPGPx-Mediated Adaptation to Oxidative Stress Protects Motor Neurons from Degeneration in Aging by Directly Modulating O-GlcNAcase.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31747588
-|mesh-terms=* Aging
-* Amyotrophic Lateral Sclerosis
-* Animals
-* Female
-* Humans
-* Mice
-* Mice, Mutant Strains
-* Motor Neurons
-* Muscle Denervation
-* Oxidative Stress
-* Paralysis
-* beta-N-Acetylhexosaminidases
-|keywords=* ALS
-* NPGPx
-* O-GlcNAcylation
-* OGA
-* aging
-* motor neuron
-* oxidative stress
-|full-text-url=https://sci-hub.do/10.1016/j.celrep.2019.10.053
-}}
-==OGG1==
-{{medline-entry
-|title=Advanced Age Is Associated with Iron Dyshomeostasis and Mitochondrial DNA Damage in Human Skeletal Muscle.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31783583
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* DNA, Mitochondrial
-* Female
-* Homeostasis
-* Humans
-* Inflammation
-* Iron
-* Male
-* Mitochondria, Muscle
-* Quadriceps Muscle
-* Young Adult
-|keywords=* ZIP
-* ferritin
-* hepcidin
-* inflammation
-* iron overload
-* mitochondrial dysfunction
-* mtDNA
-* muscle aging
-* physical performance
-* transferrin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6953082
-}}
-==OGT==
-{{medline-entry
-|title=ELT-2 promotes O-GlcNAc transferase [[OGT]]-1 expression to modulate Caenorhabditis elegans lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32628333
-|keywords=* Caenorhabditis elegans
-* GATA factor ELT-2
-* OGT-1
-* lifespan
-|full-text-url=https://sci-hub.do/10.1002/jcb.29817
-}}
-{{medline-entry
-|title=Neuronal O-GlcNAcylation Improves Cognitive Function in the Aged Mouse Brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31588002
-|mesh-terms=* Acetylglucosamine
-* Acylation
-* Aging
-* Animals
-* Cognition
-* Male
-* Mice
-* Mice, Knockout
-* N-Acetylglucosaminyltransferases
-|keywords=* O-GlcNAcylation
-* OGT
-* aging
-* brain
-* cognition
-* hippocampus
-* rejuvenation
-* synaptic plasticity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7199460
-}}
-==OSM==
-{{medline-entry
-|title=Age Differences in Sexual Minority Stress and the Importance of Friendship in Later Life.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33143546
-|keywords=* LGBT
-* Sexual minorities
-* cohort differences
-* discrimination
-* friendship aging
-* internalized homonegativity
-* minority stress
-* outness
-* social support
-|full-text-url=https://sci-hub.do/10.1080/07317115.2020.1836107
-}}
-==OTC==
-{{medline-entry
-|title=Age and growth of stocked juvenile Shoal Bass in a tailwater: Environmental variation and accuracy of daily age estimates.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31644599
-|mesh-terms=* Aging
-* Animals
-* Bass
-* Ecosystem
-* Environmental Monitoring
-* Population Dynamics
-* Reproduction
-* Rivers
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6808449
-}}
-==P2RY12==
-{{medline-entry
-|title=Potential caveats of putative microglia-specific markers for assessment of age-related cerebrovascular neuroinflammation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33261619
-|keywords=* Aging
-* Brain infiltrating myeloid cells
-* CD45
-* Cerebral amyloid angiopathy
-* Microglia
-* Neuroinflammation
-* P2RY12
-* Stroke
-* Tmem119
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7709276
-}}
-{{medline-entry
-|title=Microglial changes in the early aging stage in a healthy retina and an experimental glaucoma model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32958210
-|keywords=* Aging
-* CD68
-* Glaucoma
-* Iba-1
-* Inflammation
-* MHCII
-* Microglia
-* Mouse
-* Ocular hypertension
-* P2RY12
-* Retina
-|full-text-url=https://sci-hub.do/10.1016/bs.pbr.2020.05.024
-}}
-{{medline-entry
-|title=Patterns of Expression of Purinergic Receptor [[P2RY12]], a Putative Marker for Non-Activated Microglia, in Aged and Alzheimer's Disease Brains.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31968618
-|mesh-terms=* Aging
-* Alzheimer Disease
-* Biomarkers
-* Brain
-* Humans
-* Immunohistochemistry
-* Inflammation
-* Macrophages
-* Microglia
-* Phenotype
-* Plaque, Amyloid
-* Receptors, Purinergic P2Y2
-|keywords=* Alzheimer’s disease
-* activation phenotypes
-* amyloid
-* immunohistochemistry
-* microglia
-* neuroinflammation
-* temporal cortex
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7014248
-}}
-==P4HA2==
-{{medline-entry
-|title=Expanding the Phenotypic and Genotypic Landscape of Nonsyndromic High Myopia: A Cross-Sectional Study in 731 Chinese Patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31560770
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Asian Continental Ancestry Group
-* Axial Length, Eye
-* Child
-* Child, Preschool
-* China
-* Cross-Sectional Studies
-* DNA Mutational Analysis
-* Female
-* Genetic Association Studies
-* Genotype
-* Humans
-* Male
-* Middle Aged
-* Myopia, Degenerative
-* Phenotype
-* Retinal Diseases
-* Vision, Low
-* Young Adult
-|full-text-url=https://sci-hub.do/10.1167/iovs.19-27921
-}}
-==P4HA3==
-{{medline-entry
-|title=Age-associated genes in human mammary gland drive human breast cancer progression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32539762
-|mesh-terms=* Adult
-* Age Factors
-* Aged
-* Aged, 80 and over
-* Animals
-* Biomarkers, Tumor
-* Breast
-* Breast Neoplasms
-* Disease Progression
-* Dyneins
-* Female
-* Gene Expression Regulation, Neoplastic
-* Heterografts
-* Humans
-* Mice
-* Mice, Inbred NOD
-* Mice, SCID
-* Middle Aged
-* Procollagen-Proline Dioxygenase
-* Prognosis
-* Survival Rate
-* Tumor Cells, Cultured
-|keywords=* ALX4
-* Aging
-* Breast cancer
-* DYNLT3
-* Gene expression
-* P4HA3
-* Relapse-free survival
-* Transcriptomics
-* Tumor progression
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7294649
-}}
-==PAH==
-{{medline-entry
-|title=Changes in light absorption by brown carbon in soot particles due to heterogeneous ozone aging in a smog chamber.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32771846
-|mesh-terms=* Aerosols
-* Biomass
-* Carbon
-* Ozone
-* Smog
-* Soot
-|keywords=* Absorption Ångström exponent
-* Brown carbon
-* Light absorption
-* Ozone aging
-* Soot particles
-|full-text-url=https://sci-hub.do/10.1016/j.envpol.2020.115273
-}}
-{{medline-entry
-|title=Factors associated with pulmonary arterial hypertension ([[PAH]]) in systemic sclerosis (SSc).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32659476
-|mesh-terms=* Aging
-* Humans
-* Natriuretic Peptide, Brain
-* Pulmonary Arterial Hypertension
-* Risk Factors
-* Scleroderma, Systemic
-|full-text-url=https://sci-hub.do/10.1016/j.autrev.2020.102602
-}}
-{{medline-entry
-|title=Potentially Avoidable Hospitalization among Long-Term Care Insurance Beneficiaries with Dementia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32316707
-|keywords=* Aging
-* Dementia
-* Long-Term Care
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7509129
-}}
-==PAM==
-{{medline-entry
-|title=Relationship between patient activation measurement and self-rated health in patients with chronic diseases.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33148185
-|keywords=* Aging population
-* Chronic diseases
-* Patient activation measurement
-* Primary health care
-* Self-rated health
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7643260
-}}
-{{medline-entry
-|title=Reversal of Age-Related Neuronal Atrophy by α5-GABAA Receptor Positive Allosteric Modulation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33068001
-|keywords=* GABA
-* aging
-* cognition
-* neurotrophic effect
-* positive allosteric modulator
-|full-text-url=https://sci-hub.do/10.1093/cercor/bhaa310
-}}
-{{medline-entry
-|title=The ratio of prematurely aging to non-prematurely aging mice cohabiting, conditions their behavior, immunity and lifespan.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32330742
-|mesh-terms=* Aging
-* Aging, Premature
-* Animals
-* Behavior, Animal
-* Female
-* Housing, Animal
-* Longevity
-* Lymphocytes
-* Macrophages
-* Mice
-* Oxidative Stress
-* Social Environment
-|keywords=* Behavior
-* Immunity
-* Mean lifespan
-* Prematurely aging mice
-* Social environmental strategy
-|full-text-url=https://sci-hub.do/10.1016/j.jneuroim.2020.577240
-}}
-==PAX8==
-{{medline-entry
-|title=Inadequate control of thyroid hormones sensitizes to hepatocarcinogenesis and unhealthy aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31518338
-|mesh-terms=* Aging
-* Animals
-* Fatty Liver
-* Insulin Resistance
-* Liver
-* Liver Neoplasms
-* Male
-* Mice
-* Mice, Knockout
-* PAX8 Transcription Factor
-* Thyroid Hormones
-|keywords=* glucose metabolism
-* healthspan
-* hyperthyroidism
-* hypothyroidism
-* lifespan
-* thyroid hormones
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6781991
-}}
-==PBX1==
-{{medline-entry
-|title=Internalization of the TAT-[[PBX1]] fusion protein significantly enhances the proliferation of human hair follicle-derived mesenchymal stem cells and delays their senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32436118
-|keywords=* AKT
-* Hair follicle mesenchymal stem cells
-* PBX1
-* Protein purification
-* Senescence
-* TAT
-|full-text-url=https://sci-hub.do/10.1007/s10529-020-02909-x
-}}
-==PC==
-{{medline-entry
-|title=Blended home-based exercise and dietary protein in community-dwelling older adults: a cluster randomized controlled trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33103379
-|keywords=* Aging
-* Behaviour change
-* Physical functioning
-* Protein
-* Sarcopenia
-* e-Health
-|full-text-url=https://sci-hub.do/10.1002/jcsm.12634
-}}
-{{medline-entry
-|title=Right ventricular diastolic function in aging: a head-to-head comparison between phase-contrast MRI and Doppler echocardiography.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32980983
-|keywords=* Aging
-* Diastolic function
-* Phase-contrast MRI
-* Right ventricle
-|full-text-url=https://sci-hub.do/10.1007/s10554-020-02040-y
-}}
-{{medline-entry
-|title=Pulse Width and Implantable Pulse Generator Longevity in Pallidal Deep Brain Stimulation for Dystonia: A Population-Based Comparative Effectiveness Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32668433
-|keywords=* Deep brain stimulation
-* Dystonia
-* Globus pallidus internus
-* Pulse generator longevity
-* Pulse width
-|full-text-url=https://sci-hub.do/10.1159/000508794
-}}
-{{medline-entry
-|title=Gemcitabine plus nab-paclitaxel with initial dose reduction for older patients with advanced pancreatic cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32576518
-|keywords=* Adverse events
-* Chemotherapy
-* Gemcitabine
-* Geriatrics
-* Nab-paclitaxel
-* Pancreatic cancer
-|full-text-url=https://sci-hub.do/10.1016/j.jgo.2020.06.017
-}}
-{{medline-entry
-|title=Protective effects of 17-β-oestradiol and phytoestrogen on age-induced oxidative stress and inhibition of surfactant synthesis in rat type II pneumocytes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32314935
-|keywords=* 17-β-Oestradiol
-* aging
-* oxidative stress
-* phytoestrogen
-* surfactant
-* type ii pneumocytes
-|full-text-url=https://sci-hub.do/10.1080/09637486.2020.1757044
-}}
-{{medline-entry
-|title=Pacing During 200-m Competitive Masters Swimming.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32271289
-|mesh-terms=* Adult
-* Age Factors
-* Aged
-* Aged, 80 and over
-* Aging
-* Athletes
-* Athletic Performance
-* Competitive Behavior
-* Female
-* Humans
-* Male
-* Middle Aged
-* Sex Factors
-* Swimming
-|full-text-url=https://sci-hub.do/10.1519/JSC.0000000000003621
-}}
-{{medline-entry
-|title=Prostate cancer in Pennsylvania: The role of older age at diagnosis, aggressiveness, and environmental risk factors on treatment and mortality using data from the Pennsylvania Cancer Registry.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32212232
-|keywords=* aging
-* behavioral risk factors
-* geriatric oncology
-* healthy aging
-* prostate cancer survivorship
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7221418
-}}
-{{medline-entry
-|title=Extracranial versus intracranial hydro-hemodynamics during aging: a [[PC]]-MRI pilot cross-sectional study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31931818
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Brain
-* Cerebral Ventricles
-* Cerebrospinal Fluid
-* Cerebrovascular Circulation
-* Cross-Sectional Studies
-* Female
-* Hemodynamics
-* Humans
-* Magnetic Resonance Imaging
-* Male
-* Middle Aged
-|keywords=* Aging
-* Arterial cerebral blood flow
-* CSF flow
-* PC-MRI
-* Pulsatility
-* Venous cerebral blood flow
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6958565
-}}
-{{medline-entry
-|title=Age-specific health-related quality of life in disease-free long-term prostate cancer survivors versus male population controls-results from a population-based study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31736000
-|mesh-terms=* Adult
-* Age Factors
-* Aged
-* Aging
-* Cancer Survivors
-* Case-Control Studies
-* Disease-Free Survival
-* Germany
-* Humans
-* Male
-* Middle Aged
-* Prostatic Neoplasms
-* Quality of Life
-* Surveys and Questionnaires
-* Young Adult
-|keywords=* Health-related quality of life
-* Long-term survivor
-* Population-based
-* Prostate cancer
-|full-text-url=https://sci-hub.do/10.1007/s00520-019-05120-5
-}}
-{{medline-entry
-|title=Cross-Linked Polyphenol-Based Drug Nano-Self-Assemblies Engineered to Blockade Prostate Cancer Senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31553876
-|mesh-terms=* Animals
-* Antineoplastic Agents
-* Apoptosis
-* Cell Line, Tumor
-* Cellular Senescence
-* Docetaxel
-* Forkhead Box Protein O1
-* Humans
-* Male
-* Mice
-* Mice, Nude
-* Nanostructures
-* Polyphenols
-* Prostatic Neoplasms
-* Receptor, Transforming Growth Factor-beta Type I
-* Signal Transduction
-* Tannins
-* Transplantation, Heterologous
-|keywords=* DSAs
-* apoptosis
-* docetaxel
-* nanoassemblies
-* prostate cancer
-* senescence
-|full-text-url=https://sci-hub.do/10.1021/acsami.9b14738
-}}
-{{medline-entry
-|title=An Immersive Virtual Reality Platform for Assessing Spatial Navigation Memory in Predementia Screening: Feasibility and Usability Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31482851
-|keywords=* cognition
-* dementia
-* healthy aging
-* memory
-* virtual reality
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6751096
-}}
-==PCNA==
-{{medline-entry
-|title=Impairment of Pol β-related DNA Base-excision Repair Leads to Ovarian Aging in Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33223510
-|keywords=* BER
-* Pol β
-* menopause
-* oocytes
-* ovarian aging
-|full-text-url=https://sci-hub.do/10.18632/aging.104123
-}}
-{{medline-entry
-|title=[Heat shock protein 90 (HSP90) in age-dependent changes in the number of fibroblasts in human skin.]
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32362082
-|mesh-terms=* Adolescent
-* Adult
-* Aging
-* Child
-* Child, Preschool
-* Dermis
-* Female
-* Fibroblasts
-* HSP90 Heat-Shock Proteins
-* Humans
-* Infant
-* Infant, Newborn
-* Middle Aged
-* Pregnancy
-* Young Adult
-|keywords=* HSP90
-* PCNA
-* aging
-* fibroblasts
-* skin
-}}
-{{medline-entry
-|title=A Higher Frequency Administration of the Nontoxic Cycloartane-Type Triterpene Argentatin A Improved Its Anti-Tumor Activity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32295227
-|keywords=* Argentatin A
-* PCNA
-* antiproliferative
-* antitumor
-* apoptosis
-* cell senescence
-* colon cancer
-* xenografts
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7221627
-}}
-{{medline-entry
-|title=[Mechanosensitive protein of Hippo regulatory pathway - transcription coactivator with PZD-binding motif (TAZ) in human skin during aging.]
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32145162
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Child
-* Child, Preschool
-* Dermis
-* Female
-* Fibroblasts
-* Humans
-* Infant
-* Infant, Newborn
-* Middle Aged
-* Pregnancy
-* Protein-Serine-Threonine Kinases
-* Skin Aging
-* Trans-Activators
-* Young Adult
-|keywords=* CD31
-* PCNA
-* TAZ
-* aging
-* blood vessels
-* fibroblasts
-* skin
-}}
-{{medline-entry
-|title=[Mechanosensitive Yes-associated protein in human skin during aging.]
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31800177
-|mesh-terms=* Adaptor Proteins, Signal Transducing
-* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Dermis
-* Endothelial Cells
-* Female
-* Fibroblasts
-* Humans
-* Middle Aged
-* Pregnancy
-* Skin Aging
-* Transcription Factors
-|keywords=* CD31
-* PCNA
-* YAP
-* aging
-* blood vessels
-* fibroblasts
-* skin
-}}
-{{medline-entry
-|title=[Role of mechanosensitive protein Piezo1 in human age-dependent changes in the number of fibroblasts and blood vessels in human skin.]
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31512421
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aged, 80 and over
-* Blood Vessels
-* Child
-* Child, Preschool
-* Dermis
-* Female
-* Fibroblasts
-* Humans
-* Infant
-* Ion Channels
-* Male
-* Middle Aged
-* Platelet Endothelial Cell Adhesion Molecule-1
-* Pregnancy
-* Proliferating Cell Nuclear Antigen
-* Skin Aging
-|keywords=* CD31
-* PCNA
-* Piezo1
-* aging
-* blood vessels
-* fibroblasts
-* skin
-}}
-==PCSK9==
-{{medline-entry
-|title=Lipoprotein removal mechanisms and aging: implications for the cardiovascular health of the elderly.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32011347
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Apolipoproteins B
-* Atherosclerosis
-* Cardiovascular Diseases
-* Cardiovascular System
-* Cholesterol
-* Humans
-* Lipid Metabolism
-* Lipoproteins
-* Lipoproteins, LDL
-* Risk Factors
-|full-text-url=https://sci-hub.do/10.1097/MED.0000000000000529
-}}
-{{medline-entry
-|title=The role of proprotein convertase subtilisin-kexin type 9 ([[PCSK9]]) in the vascular aging process - is there a link?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31708986
-|keywords=* PCSK9
-* atherosclerosis
-* cholesterol
-* inflammation
-* vascular aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6836637
-}}
-==PDCD4==
-{{medline-entry
-|title=Petal abscission in roses is associated with the activation of a truncated version of the animal [[PDCD4]] homologue, RbPCD1.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31521226
-|mesh-terms=* Amino Acid Sequence
-* Arabidopsis
-* Gene Expression Regulation, Plant
-* Plant Proteins
-* Plants, Genetically Modified
-* Programmed Cell Death 1 Receptor
-* Rosa
-* Sequence Alignment
-* Transcription Factors
-|keywords=* Ethylene
-* Heat shock
-* Inflorescence
-* MA3 domain
-* PDCD4
-* Repression
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.plantsci.2019.110242
-}}
-==PDE2A==
-{{medline-entry
-|title=TAK-915, a phosphodiesterase 2A inhibitor, ameliorates the cognitive impairment associated with aging in rodent models.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31521738
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Cognition
-* Cognition Disorders
-* Cognitive Dysfunction
-* Cyclic AMP
-* Cyclic GMP
-* Cyclic Nucleotide Phosphodiesterases, Type 2
-* Male
-* Memory Disorders
-* Memory, Episodic
-* Phosphodiesterase Inhibitors
-* Pyrazines
-* Pyridines
-* Rats
-* Rats, Inbred F344
-* Rats, Long-Evans
-* Rats, Sprague-Dawley
-|keywords=* Aging
-* Cognition
-* PDE2A
-* TAK-915
-|full-text-url=https://sci-hub.do/10.1016/j.bbr.2019.112192
-}}
-==PDE4D==
-{{medline-entry
-|title=Phosphodiesterase [[PDE4D]] Is Decreased in Frontal Cortex of Aged Rats and Positively Correlated With Working Memory Performance and Inversely Correlated With PKA Phosphorylation of Tau.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33192469
-|keywords=* Alzheimer’s disease
-* PDE4D
-* aging
-* tau
-* working memory
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7655962
-}}
-==PDE5A==
-{{medline-entry
-|title=Repurposing erectile dysfunction drugs tadalafil and vardenafil to increase bone mass.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32513693
-|mesh-terms=* Aging
-* Animals
-* Bone Density
-* Bone and Bones
-* Brain
-* Cell Differentiation
-* Cyclic Nucleotide Phosphodiesterases, Type 5
-* Drug Repositioning
-* Erectile Dysfunction
-* Humans
-* Male
-* Mice
-* Middle Aged
-* Models, Animal
-* Models, Molecular
-* Neurons
-* Osteoblasts
-* Osteoclasts
-* Osteogenesis
-* Osteoporosis
-* Osteoporotic Fractures
-* Phosphodiesterase 5 Inhibitors
-* Primary Cell Culture
-* Tadalafil
-* Vardenafil Dihydrochloride
-|keywords=* PDE5 inhibitor
-* computational modeling
-* cyclic GMP
-* osteoporosis
-* resorption
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7321982
-}}
-==PDK1==
-{{medline-entry
-|title=Inhibition of 3-phosphoinositide-dependent protein kinase 1 ([[PDK1]]) can revert cellular senescence in human dermal fibroblasts.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33229519
-|keywords=* PDK1
-* cellular senescence
-* network modeling
-* skin aging
-* systems biology
-|full-text-url=https://sci-hub.do/10.1073/pnas.1920338117
-}}
-{{medline-entry
-|title=The Impact of the PI3K/Akt Signaling Pathway in Anxiety and Working Memory in Young and Middle-Aged [[PDK1]] K465E Knock-In Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32457586
-|keywords=* PI3K/Akt
-* RDoC
-* aging
-* animal model
-* anxiety
-* cognition
-* fine tuning
-* signaling pathway
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7225327
-}}
-==PER1==
-{{medline-entry
-|title=Quercetin, caffeic acid and resveratrol regulate circadian clock genes and aging-related genes in young and old human lung fibroblast cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31773385
-|mesh-terms=* ARNTL Transcription Factors
-* Age Factors
-* Aging
-* CLOCK Proteins
-* Caffeic Acids
-* Cell Line
-* Circadian Clocks
-* Circadian Rhythm
-* Fibroblasts
-* Humans
-* NF-E2-Related Factor 2
-* Polyphenols
-* Quercetin
-* Receptors, Glucocorticoid
-* Resveratrol
-* Sirtuin 1
-|keywords=* Caffeic acid
-* Circadian clock genes
-* NR1D1
-* NRF2
-* Quercetin
-* Resveratrol
-|full-text-url=https://sci-hub.do/10.1007/s11033-019-05194-8
-}}
-==PER2==
-{{medline-entry
-|title=NAD  Controls Circadian Reprogramming through [[PER2]] Nuclear Translocation to Counter Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32369735
-|mesh-terms=* ARNTL Transcription Factors
-* Age Factors
-* Aging
-* Animals
-* CLOCK Proteins
-* Circadian Clocks
-* Circadian Rhythm
-* Cytokines
-* Female
-* HEK293 Cells
-* Humans
-* Male
-* Mice
-* Mice, Inbred C57BL
-* NAD
-* Period Circadian Proteins
-* Sirtuin 1
-* Sirtuins
-|keywords=* NAD(+)
-* SIRT1
-* aging
-* circadian
-* clock
-* heat shock factor 1
-* liver
-* nicotinamide mononucleotide
-* nicotinamide riboside
-* transcriptomics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7275919
-}}
-==PEX19==
-{{medline-entry
-|title=A genome-wide screen identifies genes that suppress the accumulation of spontaneous mutations in young and aged yeast cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31854076
-|mesh-terms=* Amino Acid Transport Systems, Basic
-* Cellular Senescence
-* DNA Replication
-* Flap Endonucleases
-* Gene Ontology
-* Genetic Techniques
-* Genomic Instability
-* Membrane Proteins
-* Mutagenesis
-* Mutation
-* Mutation Accumulation
-* Mutation Rate
-* Nuclear Pore Complex Proteins
-* Saccharomyces cerevisiae
-* Saccharomyces cerevisiae Proteins
-* Single-Strand Specific DNA and RNA Endonucleases
-|keywords=* genome stability
-* high-throughput screen
-* mutagenesis
-* mutation rate
-* replicative aging
-* yeast
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996960
-}}
-==PEX5==
-{{medline-entry
-|title=Aging lowers [[PEX5]] levels in cortical neurons in male and female mouse brains.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32777345
-|keywords=* Aging brain
-* PEX5
-* Peroxisomal protein
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7484460
-}}
-==PFAS==
-{{medline-entry
-|title=Associations between serum concentrations of perfluoroalkyl substances and DNA methylation in women exposed through drinking water: A pilot study in Ronneby, Sweden.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33007577
-|keywords=* EPIC chip
-* Environmental pollutant
-* Epigenetic aging
-* Epigenetics
-* PFAS
-* Perfluoroalkyl substance
-|full-text-url=https://sci-hub.do/10.1016/j.envint.2020.106148
-}}
-{{medline-entry
-|title=Perfluorinated alkyl substances impede growth, reproduction, lipid metabolism and lifespan in Daphnia magna.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32521362
-|mesh-terms=* Alkanesulfonic Acids
-* Animals
-* Caprylates
-* Daphnia
-* Fatty Acids
-* Fluorocarbons
-* Humans
-* Lipid Metabolism
-* Longevity
-* Reproduction
-|keywords=* Fatty acid
-* Fecundity
-* Gene expression
-* PFAS toxicity
-* Perfluorooctane sulfonate (PFOS)
-* Perfluorooctanoic acid (PFOA)
-|full-text-url=https://sci-hub.do/10.1016/j.scitotenv.2020.139682
-}}
-{{medline-entry
-|title=The effect of weathering on per- and polyfluoroalkyl substances ([[PFAS]]s) from durable water repellent (DWR) clothing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32062207
-|mesh-terms=* Acrylates
-* Alcohols
-* Clothing
-* Environmental Monitoring
-* Fluorocarbon Polymers
-* Fluorocarbons
-* Humidity
-* Models, Chemical
-* Textiles
-* Water
-* Water Pollutants, Chemical
-* Weather
-|keywords=* Aging
-* Durable water repellency
-* Outdoor clothing
-* Per- and polyfluoroalkyl substances
-* Textile
-* Weathering
-|full-text-url=https://sci-hub.do/10.1016/j.chemosphere.2020.126100
-}}
-==PGC==
-{{medline-entry
-|title=The Aging Stress Response and Its Implication for AMD Pathogenesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33266495
-|keywords=* AMD
-* DNA damage response
-* PGC-1α
-* SIRT1
-* age-related macular degeneration
-* aging
-* autophagy
-* insulin/IGF-1
-* mitochondrial quality control
-* the aging stress response
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7700335
-}}
-{{medline-entry
-|title=Constitutive [[PGC]]-1α Overexpression in Skeletal Muscle Does Not Contribute to Exercise-Induced Neurogenesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33200398
-|keywords=* Aging
-* Hippocampal neurogenesis
-* Immunohistochemistry
-* PGC-1α
-* Transgenic mice
-* Voluntary running
-|full-text-url=https://sci-hub.do/10.1007/s12035-020-02189-6
-}}
-{{medline-entry
-|title=Dysregulated Autophagy Mediates Sarcopenic Obesity and Its Complications via AMPK and [[PGC]]1α Signaling Pathways: Potential Involvement of Gut Dysbiosis as a Pathological Link.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32961822
-|keywords=* AMPK signaling pathway
-* PGC-1α signaling pathway
-* aging
-* autophagy
-* gut axis
-* inflammation
-* insulin resistance
-* sarcopenic obesity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7555990
-}}
-{{medline-entry
-|title=Resemblance and differences in dietary restriction nephroprotective mechanisms in young and old rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32970613
-|keywords=* aging
-* caloric restriction
-* ischemia/reperfusion
-* kidney injury
-* mitochondria
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7585108
-}}
-{{medline-entry
-|title=Acute and chronic effects of resistance training on skeletal muscle markers of mitochondrial remodeling in older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32748504
-|keywords=* aging
-* mitochondrial dynamics
-* mitochondrial function
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7399374
-}}
-{{medline-entry
-|title=[[PGC]]-1α-mediated regulation of mitochondrial function and physiological implications.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32516539
-|keywords=* aging
-* exercise metabolism
-* insulin resistance
-* mitochondrial metabolism
-* muscle metabolism
-* muscle physiology
-* métabolisme mitochondrial
-* métabolisme musculaire
-* métabolisme à l’effort
-* physiologie musculaire
-* résistance à l’insuline
-* vieillissement
-|full-text-url=https://sci-hub.do/10.1139/apnm-2020-0005
-}}
-{{medline-entry
-|title=Targeting Mitochondrial Network Architecture in Down Syndrome and Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32365535
-|keywords=* Down syndrome
-* PGC-1α/PPARGC1A
-* aging
-* mTOR
-* mitochondrial dynamics
-* mitochondrial function
-* mitochondrial network
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7247689
-}}
-{{medline-entry
-|title=Colchicine treatment impairs skeletal muscle mitochondrial function and insulin sensitivity in an age-specific manner.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32372536
-|keywords=* ADP sensitivity
-* ROS
-* aging
-* autophagy
-|full-text-url=https://sci-hub.do/10.1096/fj.201903113RR
-}}
-{{medline-entry
-|title=A novel dipeptide from potato protein hydrolysate augments the effects of exercise training against high-fat diet-induced damages in senescence-accelerated mouse-prone 8 by boosting pAMPK / SIRT1/ [[PGC]]-1α/ pFOXO3 pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32335547
-|keywords=* alcalase
-* bioactive peptides
-* cardio-protection
-* hepato-protection
-* longevity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7202530
-}}
-{{medline-entry
-|title=Mitochondrial nucleoid remodeling and biogenesis are regulated by the p53-p21 -PKCζ pathway in p16 -silenced cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32330121
-|keywords=* mitochondria
-* nucleoid remodeling
-* p16INK4a silence
-* p53-p21-PKCζ activation
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7202532
-}}
-{{medline-entry
-|title=[Metabolic Alteration in Aging Process: Metabolic Remodeling in White Adipose Tissue by Caloric Restriction].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115557
-|mesh-terms=* Adipose Tissue, White
-* Aging
-* Animals
-* Caloric Restriction
-* Gene Expression
-* Humans
-* Longevity
-* Mice
-* Organelle Biogenesis
-* Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
-* Sirtuin 3
-* Sterol Regulatory Element Binding Protein 1
-* Up-Regulation
-|keywords=* caloric restriction (CR)
-* fatty acid biosynthesis
-* mitochondria
-* white adipose tissue (WAT)
-|full-text-url=https://sci-hub.do/10.1248/yakushi.19-00193-2
-}}
-{{medline-entry
-|title=Kynurenine aminotransferase isoforms display fiber-type specific expression in young and old human skeletal muscle.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32068089
-|keywords=* Aging
-* Kynurenine aminotransferases
-* Mitochondria
-* Muscle fiber-type
-* Skeletal muscle
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110880
-}}
-{{medline-entry
-|title=Ubiquinol-10 delays postovulatory oocyte aging by improving mitochondrial renewal in pigs.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31958774
-|keywords=* mitochondria
-* oxidative stress
-* pig
-* postovulatory aging
-* ubiquinol-10
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053629
-}}
-{{medline-entry
-|title=Mitochondrial oxidative capacity and NAD  biosynthesis are reduced in human sarcopenia across ethnicities.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31862890
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Biopsy
-* Case-Control Studies
-* Energy Metabolism
-* Humans
-* Jamaica
-* Male
-* Middle Aged
-* Mitochondria
-* Muscle, Skeletal
-* NAD
-* Oxidation-Reduction
-* Oxidative Phosphorylation
-* Oxidative Stress
-* Proteostasis
-* Sarcopenia
-* Singapore
-* United Kingdom
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6925228
-}}
-{{medline-entry
-|title=MicroRNA-34a (miR-34a) Mediates Retinal Endothelial Cell Premature Senescence through Mitochondrial Dysfunction and Loss of Antioxidant Activities.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31443378
-|keywords=* diabetic retinopathy
-* miR-34a
-* mitochondrial dysfunction
-* vascular senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6769710
-}}
-{{medline-entry
-|title=Constitutive [[PGC]]-1α overexpression in skeletal muscle does not protect from age-dependent decline in neurogenesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31444397
-|mesh-terms=* Aging
-* Animals
-* Blood Proteins
-* Cytokines
-* Female
-* Hippocampus
-* Male
-* Mice, Inbred C57BL
-* Mice, Transgenic
-* Muscle, Skeletal
-* Neurogenesis
-* Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
-* Reproducibility of Results
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6707251
-}}
-==PGK2==
-{{medline-entry
-|title=Arsenic influences spermatogenesis by disorganizing the elongation of spermatids in adult male mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31472347
-|mesh-terms=* Aging
-* Animals
-* Arsenic
-* Cell Cycle Proteins
-* DEAD-box RNA Helicases
-* Gene Expression Profiling
-* Male
-* Mice
-* RNA, Messenger
-* Spermatids
-* Spermatogenesis
-* Spermatozoa
-|keywords=* Arsenic
-* Elongation of spermatids
-* Male reproduction
-* Spermatogenesis
-|full-text-url=https://sci-hub.do/10.1016/j.chemosphere.2019.124650
-}}
-==PGLS==
-{{medline-entry
-|title=547 transcriptomes from 44 brain areas reveal features of the aging brain in non-human primates.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31779658
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Carboxylic Ester Hydrolases
-* Macaca mulatta
-* Male
-* Mice
-* Transcriptome
-|keywords=* Brain aging
-* Multiple brain regions
-* PGLS
-* Rhesus macaques
-* Transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6883628
-}}
-==PIEZO1==
-{{medline-entry
-|title=Niche stiffness underlies the ageing of central nervous system progenitor cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31413369
-|mesh-terms=* Adult Stem Cells
-* Aging
-* Animals
-* Animals, Newborn
-* Cell Count
-* Central Nervous System
-* Extracellular Matrix
-* Female
-* Humans
-* Membrane Proteins
-* Multipotent Stem Cells
-* Oligodendroglia
-* Rats
-* Stem Cell Niche
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7025879
-}}
-==PINK1==
-{{medline-entry
-|title=Spermidine inhibits neurodegeneration and delays aging via the [[PINK1]]-PDR1-dependent mitophagy pathway in [i]C. elegans[/i].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32902411
-|keywords=* aging
-* caenorhabditis elegans
-* mitophagy
-* neurodegenerative diseases
-* spermidine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7521492
-}}
-{{medline-entry
-|title=Female mice are resilient to age-related decline of substantia nigra dopamine neuron firing parameters.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32846275
-|keywords=* Aging
-* Dopamine
-* Electrophysiology
-* Firing
-* Mouse
-* Substantia nigra
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7606778
-}}
-{{medline-entry
-|title=Attenuation of epigenetic regulator SMARCA4 and ERK-ETS signaling suppresses aging-related dopaminergic degeneration.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32749068
-|keywords=*
-Drosophila
-* MAPK-ERK-ETS signaling
-* Parkinson's disease
-* SMARCA4/Brahma
-* aging
-* neurodegeneration
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7511865
-}}
-{{medline-entry
-|title=SIRT1 alleviates high-magnitude compression-induced senescence in nucleus pulposus cells via [[PINK1]]-dependent mitophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32687063
-|keywords=* SIRT1
-* compression
-* mitophagy
-* nucleus pulposus
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7485741
-}}
-{{medline-entry
-|title=Synergistic action of propolis with levodopa in the management of Parkinsonism in Drosophila melanogaster.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32386191
-|keywords=* Drosophila melanogaster
-* Levodopa induced dyskinesia
-* PINK1B9
-* Parkinsonism
-* Parkinson’s disease
-* aging
-* antioxidant activity
-* catalase
-* climbing index
-* lifespan
-* oxidative stress
-* propolis
-|full-text-url=https://sci-hub.do/10.1515/jcim-2019-0136
-}}
-{{medline-entry
-|title=Compression-induced senescence of nucleus pulposus cells by promoting mitophagy activation via the [[PINK1]]/PARKIN pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32281308
-|keywords=* PARKIN pathway
-* PINK1
-* compression
-* intervertebral disc
-* mitophagy
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7214186
-}}
-{{medline-entry
-|title=Doxorubicin-induced normal breast epithelial cellular aging and its related breast cancer growth through mitochondrial autophagy and oxidative stress mitigated by ginsenoside Rh2.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32100342
-|mesh-terms=* Autophagy
-* Breast Neoplasms
-* Cell Culture Techniques
-* Cell Line, Tumor
-* Doxorubicin
-* Drugs, Chinese Herbal
-* Female
-* Ginsenosides
-* Humans
-* Mitochondria
-* Oxidative Stress
-|keywords=* ROS
-* cancer growth
-* cellular senescence
-* chemotherapy
-* ginsenoside Rh2
-* mitophagy
-|full-text-url=https://sci-hub.do/10.1002/ptr.6636
-}}
-{{medline-entry
-|title=Mitochondrial DNA heteroplasmy rises in substantial nigra of aged [[PINK1]] KO mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31727366
-|mesh-terms=* Aging
-* Animals
-* Brain
-* DNA Copy Number Variations
-* DNA, Mitochondrial
-* Gene Frequency
-* Mice, Knockout
-* Mutation Rate
-* Protein Kinases
-* Substantia Nigra
-|keywords=* PINK1
-* Parkin
-* Parkinson’s disease
-* mtDNA heteroplasmy
-|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2019.10.112
-}}
-==PIP==
-{{medline-entry
-|title=Potentially inappropriate prescriptions according to explicit and implicit criteria in patients with multimorbidity and polypharmacy. MULTIPAP: A cross-sectional study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32785232
-|mesh-terms=* Aged
-* Cross-Sectional Studies
-* Female
-* Geriatrics
-* Humans
-* Inappropriate Prescribing
-* Independent Living
-* Male
-* Multimorbidity
-* Polypharmacy
-* Potentially Inappropriate Medication List
-* Prevalence
-* Primary Health Care
-* Risk
-* Spain
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7423095
-}}
-{{medline-entry
-|title=Quality of prescribing predicts hospitalisation in octogenarians: life and living in advanced age: a cohort study in New Zealand (LiLACS NZ).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31856733
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Cohort Studies
-* Drug Prescriptions
-* Female
-* Follow-Up Studies
-* Forecasting
-* Hospitalization
-* Humans
-* Inappropriate Prescribing
-* Longitudinal Studies
-* Male
-* New Zealand
-* Patient Discharge
-* Potentially Inappropriate Medication List
-|keywords=* Appropriate prescribing
-* Ethnicity
-* Longitudinal study
-* Older people
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6921419
-}}
-==PLIN2==
-{{medline-entry
-|title=Cardiac overexpression of perilipin 2 induces atrial steatosis, connexin 43 remodeling, and atrial fibrillation in aged mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31661297
-|mesh-terms=* Animals
-* Atrial Fibrillation
-* Connexin 43
-* Gene Knock-In Techniques
-* Heart Atria
-* Isolated Heart Preparation
-* Lipid Droplets
-* Mice
-* Mice, Transgenic
-* Microscopy, Electron
-* Myocytes, Cardiac
-* Perilipin-2
-* Sterol Esterase
-* Triglycerides
-* Voltage-Sensitive Dye Imaging
-|keywords=* aging
-* cardiac steatosis
-* gap junction
-* lipid droplets
-* lipotoxic arrhythmia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6957375
-}}
-==PLK4==
-{{medline-entry
-|title=A novel lncRNA [[PLK4]] up-regulated by talazoparib represses hepatocellular carcinoma progression by promoting YAP-mediated cell senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32243714
-|keywords=* Yes-associated protein
-* cellular senescence
-* hepatocellular carcinoma
-* polo-like kinase 4 associated lncRNA
-* talazoparib
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7205816
-}}
-{{medline-entry
-|title=Differential expression of AURKA/[[PLK4]] in quiescence and senescence of osteosarcoma U2OS cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32200684
-|keywords=* AURKA
-* Osteosarcoma
-* PLK4
-* quiescence
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217361
-}}
-==PLN==
-{{medline-entry
-|title=An analysis of the costs of treating aged patients in a large clinical hospital in Poland under the pressure of recent demographic trends.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32399116
-|keywords=* Polish health care system
-* ageing society
-* gerontology
-* healthcare
-* hospital costs
-* length and cost of hospitalization
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7212232
-}}
-==PML==
-{{medline-entry
-|title=Progressive multifocal leukoencephalopathy in dimethyl fumarate-treated multiple sclerosis patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32808554
-|keywords=* Multiple sclerosis
-* PML
-* fumarate
-* immunosenescence
-* lymphopenia
-|full-text-url=https://sci-hub.do/10.1177/1352458520949158
-}}
-{{medline-entry
-|title=[[PML]]2-mediated thread-like nuclear bodies mark late senescence in Hutchinson-Gilford progeria syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32351002
-|keywords=* HGPS
-* PML2
-* senescence
-* thread-like PML NBs
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7294779
-}}
-==PNN==
-{{medline-entry
-|title=Hyaluronan degradation and release of a hyaluronan-aggrecan complex from perineuronal nets in the aged mouse brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33253804
-|keywords=* Brain aging
-* Chondroitin sulfate proteoglycan
-* Extracellular matrix
-* Hyaluronan
-* Perineuronal net
-|full-text-url=https://sci-hub.do/10.1016/j.bbagen.2020.129804
-}}
-==PNP==
-{{medline-entry
-|title=Temporal Discrimination Thresholds and Proprioceptive Performance: Impact of Age and Nerve Conduction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31803012
-|keywords=* TDMT
-* aging
-* kinesthesia
-* pointing task
-* position estimation
-* somatosensory temporal discrimination
-* temporal discrimination threshold
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6877661
-}}
-==POLL==
-{{medline-entry
-|title=Temporal trends in loss of life expectancy after a cancer diagnosis among the Australian population.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32062407
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Australia
-* Cancer Survivors
-* Cohort Studies
-* Female
-* Humans
-* Life Expectancy
-* Male
-* Middle Aged
-* Neoplasms
-|keywords=* Australia
-* Cancer
-* Life expectancy
-* Survival
-* Temporal
-|full-text-url=https://sci-hub.do/10.1016/j.canep.2020.101686
-}}
-==POLR3A==
-{{medline-entry
-|title=Nucleolar disruption, activation of P53 and premature senescence in [[POLR3A]]-mutated Wiedemann-Rautenstrauch syndrome fibroblasts.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32976914
-|keywords=* Cell senescence
-* DNA damage
-* Nucleolus
-* Nucleus
-* RNA polymerase III subunit A (POLR3A)
-* Wiedemann-Rautenstrauch syndrome
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2020.111360
-}}
-==POMC==
-{{medline-entry
-|title=Gpr17 deficiency in [[POMC]] neurons ameliorates the metabolic derangements caused by long-term high-fat diet feeding.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31611548
-|mesh-terms=* Aging
-* Animals
-* Body Weight
-* Brain
-* Diet, High-Fat
-* Energy Metabolism
-* Female
-* Homeostasis
-* Insulin Resistance
-* Liver
-* Male
-* Mice
-* Mice, Knockout
-* Motor Activity
-* Nerve Tissue Proteins
-* Neurons
-* Pro-Opiomelanocortin
-* Receptors, G-Protein-Coupled
-* Sex Factors
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6791877
-}}
-==POR==
-{{medline-entry
-|title=The Ventricular System Enlarges Abnormally in the Seventies, Earlier in Men, and First in the Frontal Horn: A Study Based on More Than 3,000 Scans.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31749695
-|keywords=* Evans’ index
-* aging
-* brain
-* enlargement
-* hydrocephalus
-* normal pressure
-* ventricular system
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6848156
-}}
-==POT1==
-{{medline-entry
-|title=MiR-185 targets [[POT1]] to induce telomere dysfunction and cellular senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32687062
-|keywords=* aging
-* cellular senescence
-* miR-185
-* protection of telomere 1
-* telomere dysfunction
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7425516
-}}
-{{medline-entry
-|title=Seryl tRNA synthetase cooperates with [[POT1]] to regulate telomere length and cellular senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31815007
-|keywords=* Cancer genomics
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6882858
-}}
-==POU5F1==
-{{medline-entry
-|title=Cell quality evaluation with gene expression analysis of spheroids (3D) and adherent (2D) adipose stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33148459
-|keywords=* ALDH family
-* Adipose stem cells
-* Aging
-* Shelterin complex
-* Spheroid
-* Telomere length
-|full-text-url=https://sci-hub.do/10.1016/j.gene.2020.145269
-}}
-==PPID==
-{{medline-entry
-|title=Relationships of inflamm-aging with circulating nutrient levels, body composition, age, and pituitary pars intermedia dysfunction in a senior horse population.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32058159
-|mesh-terms=* Aging
-* Animals
-* Body Composition
-* Cytokines
-* Female
-* Folic Acid
-* Horse Diseases
-* Horses
-* Inflammation
-* Male
-* Nutrients
-* Pituitary Diseases
-* Pituitary Gland, Intermediate
-|keywords=* Horse
-* Inflamm-aging
-* Muscle
-* Nutrition
-* Pituitary pars intermedia dysfunction
-* Senior
-|full-text-url=https://sci-hub.do/10.1016/j.vetimm.2020.110013
-}}
-==PRDM8==
-{{medline-entry
-|title=[[PRDM8]] reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32819411
-|keywords=* Aging
-* Aplastic anemia
-* DNA methylation
-* Dyskeratosis congenita
-* Epigenetic clock
-* Hematopoietic differentiation
-* Neuronal differentiation
-* PRDM8
-* Telomere
-* iPSC
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7439574
-}}
-==PRDX1==
-{{medline-entry
-|title=Active vitamin D supplementation alleviates initiation and progression of nonalcoholic fatty liver disease by repressing the p53 pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31756344
-|mesh-terms=* Animals
-* Apoptosis
-* Cellular Senescence
-* Diet, High-Fat
-* Dietary Supplements
-* Fas Ligand Protein
-* Hepatocytes
-* Metabolic Networks and Pathways
-* Mice, Knockout
-* Non-alcoholic Fatty Liver Disease
-* Oxidative Stress
-* Proteins
-* Steroid Hydroxylases
-* Tumor Suppressor Protein p53
-* Vitamin D
-* fas Receptor
-|keywords=* Active vitamin D
-* Apoptosis
-* Nonalcoholic fatty liver disease
-* Oxidative stress
-* Senescence
-* p53 pathway
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2019.117086
-}}
-==PRDX3==
-{{medline-entry
-|title=Proteomic analyses reveal that ginsenoside Rg3([i]S[/i]) partially reverses cellular senescence in human dermal fibroblasts by inducing peroxiredoxin.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32148389
-|keywords=* Ginsenoside Rg3(S)
-* Human dermal fibroblast
-* Label-free quantitative proteomics
-* Restoration
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7033328
-}}
-==PRDX6==
-{{medline-entry
-|title=Dentate Gyrus Peroxiredoxin 6 Levels Discriminate Aged Unimpaired From Impaired Rats in a Spatial Memory Task.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31417400
-|keywords=* PRDX6
-* aging
-* dentate gyrus
-* hippocampus
-* hole-board
-* peroxiredoxin
-* proteomics
-* spatial memory
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6684764
-}}
-==PRKDC==
-{{medline-entry
-|title=DNA-PKcs modulates progenitor cell proliferation and fibroblast senescence in idiopathic pulmonary fibrosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31464599
-|mesh-terms=* Animals
-* Cell Line
-* Cell Proliferation
-* Cellular Senescence
-* Chromones
-* DNA Damage
-* DNA Repair
-* DNA-Activated Protein Kinase
-* DNA-Binding Proteins
-* Female
-* Fibroblasts
-* Humans
-* Idiopathic Pulmonary Fibrosis
-* Lung
-* Mesenchymal Stem Cells
-* Mice
-* Mice, SCID
-* Morpholines
-|keywords=* DNA-PKcs
-* IPF
-* Mesenchymal progenitor cells
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6716822
-}}
-==PRL==
-{{medline-entry
-|title=Mechanism of [[PRL]]2 phosphatase-mediated PTEN degradation and tumorigenesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32788364
-|mesh-terms=* Animals
-* Carcinogenesis
-* Female
-* HEK293 Cells
-* Humans
-* Immediate-Early Proteins
-* Longevity
-* Male
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Nedd4 Ubiquitin Protein Ligases
-* PTEN Phosphohydrolase
-* Protein Tyrosine Phosphatases
-* Proto-Oncogene Proteins c-akt
-* Ubiquitination
-|keywords=* NEDD4
-* PRL2
-* PTEN
-* protein tyrosine phosphatases
-* ubiquitination
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7456095
-}}
-{{medline-entry
-|title=Prolactin mitigates deficiencies of retinal function associated with aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31698287
-|mesh-terms=* Aging
-* Animals
-* Apoptosis
-* Electroretinography
-* Mice, Inbred C57BL
-* Nerve Growth Factors
-* Neuroglia
-* Prolactin
-* Retina
-* Retinal Degeneration
-|keywords=* Aging
-* Apoptosis
-* Glia activation
-* Hormone
-* Mesotopic and photopic electroretinogram
-* Retina
-|full-text-url=https://sci-hub.do/10.1016/j.neurobiolaging.2019.10.002
-}}
-{{medline-entry
-|title=A Spontaneous Aggressive ERα+ Mammary Tumor Model Is Driven by Kras Activation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31390566
-|mesh-terms=* Aging
-* Animals
-* Carcinogenesis
-* Datasets as Topic
-* Estrogen Receptor alpha
-* Female
-* Gene Expression Profiling
-* Humans
-* Mammary Neoplasms, Experimental
-* Mice
-* Prolactin
-* Proto-Oncogene Proteins p21(ras)
-* Rats
-* Signal Transduction
-* Transgenes
-|keywords=* ER+ breast cancer
-* Ras mutations
-* breast cancer
-* genomic analyses
-* mouse models
-* prolactin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6713291
-}}
-==PRNP==
-{{medline-entry
-|title=Spontaneous generation of prions and transmissible PrP amyloid in a humanised transgenic mouse model of A117V GSS.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32516343
-|mesh-terms=* Adult
-* Aging
-* Amyloid
-* Animals
-* Brain
-* Codon
-* Heterozygote
-* Homozygote
-* Humans
-* Mice, Transgenic
-* Middle Aged
-* Prions
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7282622
-}}
-==PROC==
-{{medline-entry
-|title=Does midlife aging impact women's sleep duration, continuity, and timing?: A longitudinal analysis from the Study of Women's Health Across the Nation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31633180
-|keywords=* actigraphy
-* aging
-* sleep duration
-* sleep in women
-* sleep quality
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7157190
-}}
-==PSD==
-{{medline-entry
-|title=Quantitative Immunoblotting Analyses Reveal that the Abundance of Actin, Tubulin, Synaptophysin and EEA1 Proteins is Altered in the Brains of Aged Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32652177
-|keywords=* aging
-* brain
-* cortex
-* glutamate receptor
-* synapse
-* vesicle
-|full-text-url=https://sci-hub.do/10.1016/j.neuroscience.2020.06.044
-}}
-{{medline-entry
-|title=Exercise Attenuates Brain Aging by Rescuing Down-Regulated Wnt/β-Catenin Signaling in Aged Rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32390823
-|keywords=* DKK-1
-* Wnt
-* brain aging
-* exercise
-* β-catenin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7192222
-}}
-{{medline-entry
-|title=Concurrent nicotine exposure to prenatal alcohol consumption alters the hippocampal and cortical neurotoxicity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31938742
-|keywords=* Aging
-* Mitochondrial function
-* Neuroscience
-* Oxidative stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6953639
-}}
-==PSEN2==
-{{medline-entry
-|title=Accelerated brain aging towards transcriptional inversion in a zebrafish model of the K115fs mutation of human [[PSEN2]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31978074
-|mesh-terms=* Aging
-* Alternative Splicing
-* Alzheimer Disease
-* Animals
-* Animals, Genetically Modified
-* Brain
-* Datasets as Topic
-* Disease Models, Animal
-* Down-Regulation
-* Female
-* Frameshift Mutation
-* Gene Editing
-* Gene Regulatory Networks
-* Heterozygote
-* Humans
-* Microglia
-* Presenilin-1
-* Presenilin-2
-* Protein Isoforms
-* Proteomics
-* RNA-Seq
-* Up-Regulation
-* Zebrafish
-* Zebrafish Proteins
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6980398
-}}
-{{medline-entry
-|title=Loss of presenilin 2 age-dependently alters susceptibility to acute seizures and kindling acquisition.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31862541
-|keywords=* Aging
-* Alzheimer's
-* Carbamazepine
-* Corneal kindling
-* Diazepam
-* Epilepsy
-* Lamotrigine
-* Levetiracetam
-* Presenilin
-* Seizures
-* Valproic acid
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7462087
-}}
-==PSMD11==
-{{medline-entry
-|title=The effect and mechanism of 19S proteasome [[PSMD11]]/Rpn6 subunit in D-Galactose induced mimetic aging models.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32450067
-|keywords=* Age-related hearing loss
-* Aging
-* D-galactose
-* PSMD11
-* Proteasome
-|full-text-url=https://sci-hub.do/10.1016/j.yexcr.2020.112093
-}}
-==PSMD14==
-{{medline-entry
-|title=Upregulation of deubiquitinase [[PSMD14]] in lung adenocarcinoma (LUAD) and its prognostic significance.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32226511
-|keywords=* PMSD14
-* apoptosis
-* deubiquitinating enzyme
-* lung adenocarcinoma
-* prognosis
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7086243
-}}
-==PTEN==
-{{medline-entry
-|title=Senescence Reprogramming by TIMP1 Deficiency Promotes Prostate Cancer Metastasis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33186519
-|keywords=* FGF1
-* GDF-15
-* MMPs
-* PTEN
-* TIMP1
-* docetaxel
-* prostate cancer metastasis
-* senescence
-* senescence-associated secretory phenotype (SASP)
-* senolytic therapy
-|full-text-url=https://sci-hub.do/10.1016/j.ccell.2020.10.012
-}}
-{{medline-entry
-|title=Alterations in Mitochondrial Dynamic-related Genes in the Peripheral Blood of Alzheimer's Disease Patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33023448
-|keywords=* Alzheimer's disease
-* DRP1
-* FIS1
-* aging
-* mitochondrial dynamics
-* mitophagy
-|full-text-url=https://sci-hub.do/10.2174/1567205017666201006162538
-}}
-{{medline-entry
-|title=Human ESC-sEVs alleviate age-related bone loss by rejuvenating senescent bone marrow-derived mesenchymal stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32944188
-|keywords=* Extracellular vesicle
-* bone loss
-* bone marrow MSCs
-* cellular senescence
-* embryonic stem cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7480439
-}}
-{{medline-entry
-|title=The precursor of PI(3,4,5)P  alleviates aging by activating daf-18(Pten) and independent of daf-16.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32901024
-|mesh-terms=* Aging
-* Animals
-* Animals, Genetically Modified
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* Cell Line, Tumor
-* Female
-* Forkhead Transcription Factors
-* Inositol
-* Locomotion
-* Longevity
-* Metabolic Networks and Pathways
-* Metabolomics
-* Mice
-* Mitophagy
-* Models, Animal
-* PTEN Phosphohydrolase
-* Phosphatidylinositol Phosphates
-* Protein Kinases
-* Protein-Serine-Threonine Kinases
-* RNA Interference
-* RNA-Seq
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7479145
-}}
-{{medline-entry
-|title=Quercetin alleviates kidney fibrosis by reducing renal tubular epithelial cell senescence through the SIRT1/PINK1/mitophagy axis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32702447
-|mesh-terms=* Animals
-* Antioxidants
-* Cell Line
-* Cellular Senescence
-* Epithelium
-* Fibrosis
-* Flow Cytometry
-* Kidney
-* Kidney Tubules, Proximal
-* Mitophagy
-* Protein Kinases
-* Quercetin
-* Rats
-* Sirtuin 1
-|keywords=* Fibrosis
-* Mitochondria
-* Mitophagy
-* Quercetin
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2020.118116
-}}
-{{medline-entry
-|title=Downregulation of [[PTEN]] mediates bleomycin-induced premature senescence in lung cancer cells by suppressing autophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32436415
-|keywords=* PI3K/Akt/mTOR pathway
-* PTEN
-* autophagy
-* bleomycin
-* cancer cell
-* premature senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7287201
-}}
-{{medline-entry
-|title=miR-155 inhibits mitophagy through suppression of BAG5, a partner protein of PINK1.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31948758
-|mesh-terms=* Adaptor Proteins, Signal Transducing
-* Aging
-* Animals
-* Cell Line
-* Cells, Cultured
-* Down-Regulation
-* Humans
-* Male
-* Mesenchymal Stem Cells
-* Mice, Inbred C57BL
-* MicroRNAs
-* Mitophagy
-* Protein Interaction Maps
-* Protein Kinases
-* Up-Regulation
-|keywords=* Aging
-* Bone marrow MSCs
-* Mitophagy
-* miR-155
-|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2020.01.022
-}}
-{{medline-entry
-|title=Environmental Exposures and Asthma Development: Autophagy, Mitophagy, and Cellular Senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31849968
-|mesh-terms=* Airway Remodeling
-* Asthma
-* Autophagy
-* Cellular Senescence
-* Disease Susceptibility
-* Environmental Exposure
-* Humans
-* Mitophagy
-* Oxidative Stress
-* Respiratory Mucosa
-|keywords=* asthma
-* autophagy
-* mitophagy
-* oxidative stress
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6896909
-}}
-{{medline-entry
-|title=[[PTEN]] loss regulates alveolar epithelial cell senescence in pulmonary fibrosis depending on Akt activation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31527305
-|mesh-terms=* Aging
-* Cellular Senescence
-* Epithelial Cells
-* Humans
-* Idiopathic Pulmonary Fibrosis
-* PTEN Phosphohydrolase
-* Proto-Oncogene Proteins c-akt
-* Pulmonary Alveoli
-* Respiratory Mucosa
-|keywords=* aging
-* cellular senescence
-* phosphatase and tension homolog deleted on chromosome ten
-* protein kinase B
-* pulmonary fibrosis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6781970
-}}
-==PTH==
-{{medline-entry
-|title=Vitamin D Receptor Polymorphisms in Sex-Frailty Paradox.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32899460
-|keywords=* aging
-* frailty
-* vitamin D
-* vitamin D receptor
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7551757
-}}
-{{medline-entry
-|title=Parathyroid hormone ameliorates temporomandibular joint osteoarthritic-like changes related to age.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32154622
-|mesh-terms=* Aging
-* Animals
-* Calcium-Regulating Hormones and Agents
-* Cells, Cultured
-* Disease Models, Animal
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Osteoarthritis
-* Osteogenesis
-* Parathyroid Hormone
-* Temporomandibular Joint
-|keywords=* cellular senescence
-* cyclin-dependent kinase inhibitor P16INK4A
-* marrow mesenchymal stem cells
-* osteoarthritis
-* temporomandibular joint disorders
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7162802
-}}
-==PTP4A3==
-{{medline-entry
-|title=Transcriptional and Functional Changes of the Human Microvasculature during Physiological Aging and Alzheimer Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32402127
-|keywords=* 3D microvascular network
-* blood-brain barrier
-* endothelium
-* human serum
-* vascular aging
-|full-text-url=https://sci-hub.do/10.1002/adbi.202000044
-}}
-==PTPN11==
-{{medline-entry
-|title=Fine mapping genetic variants associated with age at puberty and sow fertility using SowPro90 genotyping array.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32888012
-|keywords=*
-          SowPro90
-* Bayes interval mapping
-* custom genotyping array
-* gilts
-* puberty
-* reproductive longevity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7568434
-}}
-==PTTG1==
-{{medline-entry
-|title=[Down-regulated [[PTTG1]] expression promotes the senescence of human prostate cancer LNCaP-AI].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32216239
-|mesh-terms=* Cell Line, Tumor
-* Cell Proliferation
-* Humans
-* Male
-* Prostatic Neoplasms, Castration-Resistant
-* RNA, Small Interfering
-* Securin
-* beta-Galactosidase
-|keywords=*  LNCaP-AI cell
-*  castration-resistant prostate cancer
-*  cellular senescence
-*  pituitary tumor-transforming gene-1
-* prostate cancer
-}}
-==PTX3==
-{{medline-entry
-|title=Aerobic Training Down-Regulates Pentraxin 3 and Pentraxin 3/Toll-Like Receptor 4 Ratio, Irrespective of Oxidative Stress Response, in Elderly Subjects.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32012711
-|keywords=* aging
-* endurance training
-* exercise
-* inflammation
-* oxidative stress
-* pentraxin 3
-* toll-like receptor 4
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7070734
-}}
-{{medline-entry
-|title=Sex Differences in the Association Between Pentraxin 3 and Cognitive Decline: The Cardiovascular Health Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31808814
-|keywords=* Biomarkers
-* Cognitive aging
-* Inflammation
-* Sex differences
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7357589
-}}
-==PUM1==
-{{medline-entry
-|title=Identification of reference genes for RT-qPCR data normalisation in aging studies.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31562345
-|mesh-terms=* Aging
-* Algorithms
-* Gene Expression Profiling
-* Genes, Essential
-* Humans
-* Real-Time Polymerase Chain Reaction
-* Software
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6764958
-}}
-==RACK1==
-{{medline-entry
-|title=Invariable stoichiometry of ribosomal proteins in mouse brain tissues with aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31636180
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Female
-* Gene Expression Regulation, Developmental
-* Male
-* Mice
-* Proteomics
-* Ribosomal Proteins
-|keywords=* aging
-* mass spectrometry
-* neuronal tissues
-* ribosome
-* translation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6842600
-}}
-==RAF1==
-{{medline-entry
-|title=Circular [i]ANRIL[/i] isoforms switch from repressors to activators of [i]p15/CDKN2B[/i] expression during [[RAF1]] oncogene-induced senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32862732
-|keywords=*  INK4 locus
-* Non-coding RNAs
-* Polycomb proteins
-* circular RNAs
-* gene expression regulation
-* oncogene-induced senescence
-|full-text-url=https://sci-hub.do/10.1080/15476286.2020.1812910
-}}
-==RAG1==
-{{medline-entry
-|title=T cell senescence accelerates Angiotensin II-induced target organ damage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32049355
-|keywords=* T cell
-* angiotensin II
-* cardiorenal dysfunction
-* senescence
-|full-text-url=https://sci-hub.do/10.1093/cvr/cvaa032
-}}
-==RAG2==
-{{medline-entry
-|title=Phosphate Transporter Profiles in Murine and Human Thymi Identify Thymocytes at Distinct Stages of Differentiation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32793218
-|keywords=* aging
-* glucose transporters
-* human
-* metabolism
-* mice
-* phosphate transporters
-* thymus
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7387685
-}}
-==RAN==
-{{medline-entry
-|title=Rapid automatized naming ([[RAN]]): effects of aging on a predictor of reading skill.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32799742
-|keywords=* Aging
-* RAN
-* individual differences
-* naming
-* reading
-|full-text-url=https://sci-hub.do/10.1080/13825585.2020.1806987
-}}
-==RELB==
-{{medline-entry
-|title=New control of the senescence barrier in breast cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32158912
-|keywords=* CEBPB
-* Cellular senescence
-* PAK4
-* RELB
-* p21-activated kinase
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7051141
-}}
-==REST==
-{{medline-entry
-|title=[Brain and Neuronal Aging: Aged Brain Controls via Gene Expression Fidelity and Master Regulatory Factors].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115559
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Animals
-* Brain
-* Gene Expression
-* Gene Expression Regulation, Developmental
-* Humans
-* Neurodegenerative Diseases
-* Protein Biosynthesis
-* Repressor Proteins
-* Ribosomes
-|keywords=* aging
-* brain
-* gene expression
-* neurodegeneration
-* ribosome
-* translational fidelity
-|full-text-url=https://sci-hub.do/10.1248/yakushi.19-00193-4
-}}
-{{medline-entry
-|title=Effect of 9 - PAHSA on cognitive dysfunction in diabetic mice and its possible mechanism.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32014256
-|mesh-terms=* Aging
-* Animals
-* Behavior, Animal
-* Blood Glucose
-* Body Weight
-* Brain
-* Brain-Derived Neurotrophic Factor
-* Cognitive Dysfunction
-* Diabetes Mellitus, Experimental
-* Exploratory Behavior
-* Male
-* Memory Disorders
-* Mice
-* Palmitic Acid
-* Repressor Proteins
-* Social Behavior
-* Spatial Memory
-* Stearic Acids
-|keywords=* 9-PAHSA
-* BDNF
-* Diabetes mellitus
-* REST
-|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2020.01.071
-}}
-{{medline-entry
-|title=Increased [[REST]] to Optimize Life Span?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31762373
-|mesh-terms=* Animals
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* Homeostasis
-* Longevity
-* Repressor Proteins
-* Signal Transduction
-|keywords=* life span
-* neuronal activity
-* neurotoxicity
-|full-text-url=https://sci-hub.do/10.1089/rej.2019.2287
-}}
-==RET==
-{{medline-entry
-|title=Effects of resistance exercise training on redox homeostasis in older adults. A systematic review and meta-analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32615210
-|keywords=* Aging
-* Antioxidants
-* Exercise
-* Oxidative stress
-* Resistance exercise training
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.111012
-}}
-{{medline-entry
-|title=Effects of an 8-week resistance training intervention on plantar flexor muscle quality and functional capacity in older women: A randomised controlled trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32562747
-|keywords=* Aging
-* Muscle echo intensity
-* Muscle quality
-* Physical function
-* Resistance training
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.111003
-}}
-{{medline-entry
-|title=Resistance exercise training promotes fiber type-specific myonuclear adaptations in older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32134710
-|keywords=* aging
-* hypertrophy
-* myonuclear domain
-* skeletal muscle
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191507
-}}
-{{medline-entry
-|title=Low skeletal muscle capillarization limits muscle adaptation to resistance exercise training in older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31518665
-|mesh-terms=* Adaptation, Physiological
-* Aged
-* Capillaries
-* Citrate (si)-Synthase
-* Exercise
-* Female
-* Humans
-* Hypertrophy
-* Male
-* Muscle Fibers, Skeletal
-* Muscle Proteins
-* Muscle, Skeletal
-* Resistance Training
-* Sarcopenia
-* Ubiquitin-Protein Ligases
-|keywords=* Aging
-* Capillary
-* Fiber cross-sectional area
-* Muscle hypertrophy
-* Muscle protein synthesis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6904952
-}}
-==REV1==
-{{medline-entry
-|title=[[REV1]] inhibitor JH-RE-06 enhances tumor cell response to chemotherapy by triggering senescence hallmarks.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33168727
-|keywords=* Rev1
-* cell death
-* chemotherapy
-* senescence
-* translesion synthesis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7682577
-}}
-==RHEB==
-{{medline-entry
-|title=The Rheb-TORC1 signaling axis functions as a developmental checkpoint.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32041790
-|mesh-terms=* Animals
-* Animals, Genetically Modified
-* Autophagy
-* CRISPR-Cas Systems
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* Life Cycle Stages
-* Longevity
-* Mechanistic Target of Rapamycin Complex 1
-* Phosphotransferases (Alcohol Group Acceptor)
-* RNA Interference
-* RNA, Small Interfering
-* Ras Homolog Enriched in Brain Protein
-* Signal Transduction
-|keywords=* MTOR
-* MTORC1
-* Ral
-* RalGAP
-* TSC
-* Tuberous sclerosis complex
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7063671
-}}
-==RHO==
-{{medline-entry
-|title=Conditional reprogramming: next generation cell culture.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32963937
-|keywords=* 3T3-J2 fibroblast
-* AACR, American Association for Cancer Research
-* ACC, adenoid cystic carcinoma
-* AR, androgen receptor
-* CFTR, cystic fibrosis transmembrane conductance regulators
-* CR, conditional reprogramming
-* CYPs, cytochrome P450 enzymes
-* Conditional reprogramming
-* DCIS, ductal carcinoma in situ
-* ECM, extracellular matrix
-* ESC, embryonic stem cell
-* HCMI, human cancer model initiatives
-* HGF, hepatocyte growth factor
-* HNE, human nasal epithelial
-* HPV, human papillomaviruses
-* ICD, intracellular domain
-* LECs, limbal epithelial cells
-* NCI, National Cancer Institute
-* NGFR, nerve growth factor receptor
-* NSCLC, non-small cell lung cancer
-* NSG, NOD/SCID/gamma
-* PDAC, pancreatic ductal adenocarcinoma
-* PDX, patient derived xenograft
-* PP2A, protein phosphatase 2A
-* RB, retinoblastoma-associated protein
-* ROCK
-* ROCK, Rho kinase
-* SV40, simian virus 40 large tumor antigen
-* Senescence
-* UVB, ultraviolet radiation b
-* Y-27632
-* dECM, decellularized extracellular matrix
-* hASC, human adipose stem cells
-* hTERT, human telomerase reverse transcriptase
-* iPSCs, induction of pluripotent stem cells
-* ΔNP63α, N-terminal truncated form of P63α
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7488362
-}}
-{{medline-entry
-|title=SARS-CoV-2 receptor ACE2 and TMPRSS2 are primarily expressed in bronchial transient secretory cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32246845
-|mesh-terms=* Adult
-* Aging
-* Angiotensin-Converting Enzyme 2
-* Bronchi
-* COVID-19
-* Cells, Cultured
-* Chronic Disease
-* Coronavirus Infections
-* Epithelial Cells
-* Female
-* Gene Expression
-* Gene Expression Profiling
-* Germany
-* Goblet Cells
-* Humans
-* Lung
-* Male
-* Middle Aged
-* Pandemics
-* Peptidyl-Dipeptidase A
-* Pneumonia, Viral
-* Reference Standards
-* Sequence Analysis, RNA
-* Serine Endopeptidases
-* Sex Characteristics
-* Single-Cell Analysis
-* Smoking
-* Tissue Banks
-|keywords=*
-FURIN
-* COVID-19
-* Human Cell Atlas
-* epithelial differentiation
-* respiratory tract
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7232010
-}}
-==RICTOR==
-{{medline-entry
-|title=Endothelial senescence-associated secretory phenotype (SASP) is regulated by Makorin-1 ubiquitin E3 ligase.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31476350
-|mesh-terms=* Cellular Senescence
-* Endothelial Cells
-* Human Umbilical Vein Endothelial Cells
-* Humans
-* MicroRNAs
-* Nerve Tissue Proteins
-* Phosphorylation
-* Protein Binding
-* Rapamycin-Insensitive Companion of mTOR Protein
-* Ribonucleoproteins
-* Telomeric Repeat Binding Protein 2
-* Ubiquitin-Protein Ligases
-|keywords=* Inflammation
-* MKRN1
-* Senescence
-* Senescence-associated secretory phenotype (SASP)
-* Telomeric repeat binding factor 2-interacting protein (TERF2IP)
-* p90RSK
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059097
-}}
-==RIF1==
-{{medline-entry
-|title=53BP1 Enforces Distinct Pre- and Post-resection Blocks on Homologous Recombination.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31653568
-|mesh-terms=* Aging
-* Animals
-* BRCA1 Protein
-* DNA Breaks, Double-Stranded
-* DNA Damage
-* Genomic Instability
-* Homologous Recombination
-* Mice
-* Mutation
-* Poly(ADP-ribose) Polymerase Inhibitors
-* Rad51 Recombinase
-* Tumor Suppressor p53-Binding Protein 1
-* Ubiquitin-Protein Ligases
-|keywords=* 53BP1
-* BRCA1
-* PARPi
-* aging
-* cancer
-* homologous recombination
-* resection
-* shieldin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6993210
-}}
-==RIPK1==
-{{medline-entry
-|title=Casein kinase 1G2 suppresses necroptosis-promoted testis aging by inhibiting receptor-interacting kinase 3.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33206046
-|keywords=* aging
-* cell biology
-* mouse
-* necroptosis
-* protein kinase
-* reproductivity
-* testis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673785
-}}
-{{medline-entry
-|title=Crucial role of the terminal complement complex in chondrocyte death and hypertrophy after cartilage trauma.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31981738
-|keywords=* Aurintricarboxylic acid
-* Cartilage trauma
-* Hypertrophy
-* Regulated cell death
-* Senescence
-* Terminal complement complex
-|full-text-url=https://sci-hub.do/10.1016/j.joca.2020.01.004
-}}
-==RIPK3==
-{{medline-entry
-|title=Metformin mediates cardioprotection against aging-induced ischemic necroptosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31944526
-|mesh-terms=* Aging
-* Animals
-* Autophagy
-* GTPase-Activating Proteins
-* Humans
-* Hypoglycemic Agents
-* Imidazoles
-* Indoles
-* Male
-* Metformin
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Myocardium
-* Myocytes, Cardiac
-* Necroptosis
-* Protein Binding
-* RNA, Small Interfering
-* Receptor-Interacting Protein Serine-Threonine Kinases
-* Reperfusion Injury
-* Sequestosome-1 Protein
-|keywords=* aging
-* autophagy defect
-* cardioprotection
-* ischemia/reperfusion injury
-* metformin
-* myocardial necroptosis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996959
-}}
-==RNF10==
-{{medline-entry
-|title=Reduced RING finger protein 10 expression in macrophages is associated with aging-related inflammation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33249776
-|keywords=* E3 ubiquitin ligase
-* RNF10
-* immunosenescence
-* inflammation
-* macrophages
-|full-text-url=https://sci-hub.do/10.1002/2211-5463.13049
-}}
-==RNF13==
-{{medline-entry
-|title=The effects of environmental stressors on candidate aging associated genes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32344118
-|keywords=* Aging
-* Candidate genes
-* Environmental factors
-* Epigenetic
-* Hypo/hyper methylated (methylation)
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110952
-}}
-==ROCK2==
-{{medline-entry
-|title=Physical exercise increases ROCK activity in the skeletal muscle of middle-aged rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32032622
-|keywords=* Aging
-* Insulin resistance
-* Physical exercise
-* Rho-kinase (ROCK)
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2020.111213
-}}
-==RPE==
-{{medline-entry
-|title=Transcriptomic Profiling of Human Pluripotent Stem Cell-derived Retinal Pigment Epithelium over Time.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33307245
-|keywords=* Aging
-* Human embryonic stem cell
-* Human pluripotent stem cell
-* Retinal pigment epithelium
-* Single-cell RNA sequencing
-|full-text-url=https://sci-hub.do/10.1016/j.gpb.2020.08.002
-}}
-{{medline-entry
-|title=Relationship between Oxygen Uptake, Heart Rate, and Perceived Effort in an Aquatic Incremental Test in Older Women.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33187067
-|keywords=* aging
-* cardiorespiratory
-* maximum test
-* rate of perceived exertion
-* water aerobics
-* water-based exercises
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7697777
-}}
-{{medline-entry
-|title=Photoreceptor Degeneration in Homozygous Male Per2  Mice During Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33135952
-|keywords=* Per2luc
-* aging
-* circadian
-* mice
-* photoreceptors
-* retinal pigment epithelium
-|full-text-url=https://sci-hub.do/10.1177/0748730420965285
-}}
-{{medline-entry
-|title=An In-Vitro Cell Model of Intracellular Protein Aggregation Provides Insights into [[RPE]] Stress Associated with Retinopathy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32932802
-|keywords=* AMD
-* RPE
-* aging
-* autofluorescence
-* autophagy
-* diet
-* lysosomes
-* oxidized POS
-* proteolysis
-* retina
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7555953
-}}
-{{medline-entry
-|title=Short-Term Effect of Self-Selected Training Intensity on Ambulatory Blood Pressure in Hypertensive Older Women: A Randomized Controlled Trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32904579
-|keywords=* aging
-* exercise
-* hypertension
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7457386
-}}
-{{medline-entry
-|title=Correlation between brain volume and retinal photoreceptor outer segment volume in normal aging and neurodegenerative diseases.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32881874
-|mesh-terms=* Aged
-* Aging
-* Brain
-* Female
-* Humans
-* Linear Models
-* Magnetic Resonance Imaging
-* Male
-* Middle Aged
-* Multivariate Analysis
-* Neurodegenerative Diseases
-* Organ Size
-* Retinal Photoreceptor Cell Outer Segment
-* Retinal Pigment Epithelium
-* Tomography, Optical Coherence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7470418
-}}
-{{medline-entry
-|title=Oxidative stress in the retina and retinal pigment epithelium ([[RPE]]): Role of aging, and DJ-1.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32826201
-|keywords=* Aging
-* DJ-1
-* Oxidative stress
-* Retina
-* Retinal pigment epithelium
-* Sodium iodate
-|full-text-url=https://sci-hub.do/10.1016/j.redox.2020.101623
-}}
-{{medline-entry
-|title=Direct-Coupled Electroretinogram (DC-ERG) for Recording the Light-Evoked Electrical Responses of the Mouse Retinal Pigment Epithelium.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32744516
-|mesh-terms=* Aging
-* Animals
-* Electrophysiological Phenomena
-* Electroretinography
-* Light
-* Mice
-* Retinal Pigment Epithelium
-|full-text-url=https://sci-hub.do/10.3791/61491
-}}
-{{medline-entry
-|title=High-density lipoproteins are a potential therapeutic target for age-related macular degeneration.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32737203
-|keywords=* age-related macular degeneration
-* aging
-* apolipoprotein
-* complement
-* complement factor H
-* glycosaminoglycan
-* heparan sulfate
-* heparan sulfate proteoglycans
-* high-density lipoprotein (HDL)
-* lipoprotein
-* oligosaccharide
-* retinal degeneration
-* retinal pigmented epithelium
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7521644
-}}
-{{medline-entry
-|title=MTOR-initiated metabolic switch and degeneration in the retinal pigment epithelium.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32721041
-|keywords=* AMD
-* Mtor
-* aging
-* lipid
-* metabolism
-|full-text-url=https://sci-hub.do/10.1096/fj.202000612R
-}}
-{{medline-entry
-|title=[i]Lactobacillus paracasei[/i] KW3110 Suppresses Inflammatory Stress-Induced Premature Cellular Senescence of Human Retinal Pigment Epithelium Cells and Reduces Ocular Disorders in Healthy Humans.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32708511
-|keywords=* cellular senescence
-* eye fatigue
-* inflammation
-* lactic acid bacteria
-* probiotics
-* retina
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7403967
-}}
-{{medline-entry
-|title=Retinal pigment epithelium transcriptome analysis in chronic smoking reveals a suppressed innate immune response and activation of differentiation pathways.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32634473
-|keywords=* Age-related macular degeneration
-* Aging
-* Differentiation
-* Innate immunity
-* RNA sequencing
-* Smoking
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7434665
-}}
-{{medline-entry
-|title=Differences in Intraretinal Pigment Migration Across Inherited Retinal Dystrophies.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32442431
-|mesh-terms=* Adult
-* Aging
-* Cell Movement
-* Female
-* Follow-Up Studies
-* Humans
-* Male
-* Ophthalmoscopy
-* Retinal Dystrophies
-* Retinal Pigment Epithelium
-* Retrospective Studies
-* Slit Lamp Microscopy
-* Tomography, Optical Coherence
-|full-text-url=https://sci-hub.do/10.1016/j.ajo.2020.05.010
-}}
-{{medline-entry
-|title=Exosomal MiRNA Transfer between Retinal Microglia and [[RPE]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32429541
-|keywords=* RPE
-* aging
-* exosome
-* inflammation
-* microglia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7279010
-}}
-{{medline-entry
-|title=Functionally validated imaging endpoints in the Alabama study on early age-related macular degeneration 2 (ALSTAR2): design and methods.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32429847
-|keywords=* Age-related macular degeneration
-* Aging
-* Cones
-* Dark adaptation
-* Light sensitivity
-* Macula
-* Quantitative autofluorescence
-* Retina
-* Rods
-* Spectral domain optical coherence tomography
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7236516
-}}
-{{medline-entry
-|title=Mechanisms of mitochondrial dysfunction and their impact on age-related macular degeneration.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32298788
-|keywords=* Age-related macular degeneration
-* Aggregation
-* Aging
-* Autophagy
-* Clearance
-* Degeneration
-* Mitochondria
-* Mitophagy
-* Retina
-* Retinal pigment epithelium
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7650008
-}}
-{{medline-entry
-|title=CSF1R blockade induces macrophage ablation and results in mouse choroidal vascular atrophy and [[RPE]] disorganization.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32234210
-|keywords=* RPE disorganization
-* aging
-* choroid
-* choroidal macrophage
-* choroidal vasculature
-* immunology
-* inflammation
-* mouse
-* neuroscience
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156269
-}}
-{{medline-entry
-|title=Extracellular microparticles exacerbate oxidative damage to retinal pigment epithelial cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32173468
-|keywords=* Extracellular vesicles
-* Oxidative stress
-* Phagocytosis
-* RPE cell Dysfunction
-* RPE cell-Derived microparticles (RMPs)
-* Retinal pigment epithelial cell (RPE)
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.yexcr.2020.111957
-}}
-{{medline-entry
-|title=Water-based continuous and interval training in older women: Cardiorespiratory and neuromuscular outcomes (WATER study).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32145293
-|keywords=* Aerobic capacity
-* Aerobic training
-* Aging
-* Aquatic exercise
-* Interval exercise
-* Muscle echo intensity
-* Muscle strength
-* Muscle thickness
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110914
-}}
-{{medline-entry
-|title=Retrieval Practice Improves Recollection-Based Memory Over a Seven-Day Period in Younger and Older Adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32038382
-|keywords=* aging
-* recollection and familiarity
-* retrieval practice
-* temporal dynamics
-* testing effect
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6990689
-}}
-{{medline-entry
-|title=A Comparison of Heart Rate Training Load and Perceptual Effort Between Masters and Young Cyclists
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32000141
-|mesh-terms=* Adult
-* Aging
-* Bicycling
-* Heart Rate
-* High-Intensity Interval Training
-* Humans
-* Middle Aged
-* Perception
-* Physical Exertion
-|keywords=* age
-* endurance training
-* high-intensity interval training
-* older athlete
-|full-text-url=https://sci-hub.do/10.1123/ijspp.2019-0413
-}}
-{{medline-entry
-|title=Retinal Pigment Epithelial Cells: The Unveiled Component in the Etiology of Prpf Splicing Factor-Associated Retinitis Pigmentosa.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31884616
-|mesh-terms=* Animals
-* Circadian Rhythm
-* Epithelial Cells
-* Eye Proteins
-* Humans
-* Mice
-* Phagocytosis
-* Photoreceptor Cells, Vertebrate
-* RNA Splicing Factors
-* Retinal Pigment Epithelium
-* Retinitis Pigmentosa
-|keywords=* Aging
-* Cellular stress
-* Circadian rhythm
-* Metabolism
-* PRPF
-* Phagocytosis
-* Retinal pigment epithelium
-* Retinitis pigmentosa
-* Splicing factors
-|full-text-url=https://sci-hub.do/10.1007/978-3-030-27378-1_37
-}}
-{{medline-entry
-|title=AMPK May Play an Important Role in the Retinal Metabolic Ecosystem.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31884657
-|mesh-terms=* AMP-Activated Protein Kinases
-* Animals
-* DNA Damage
-* DNA, Mitochondrial
-* Disease Models, Animal
-* Gene Dosage
-* Metformin
-* Mice
-* Oxidative Stress
-* Retina
-* Retinal Degeneration
-* Retinitis Pigmentosa
-|keywords=* AMPK
-* Adenosine monophosphate-activated protein kinase
-* Aging
-* Glycolysis
-* Metabolism
-* Neuroprotection
-* Retina
-|full-text-url=https://sci-hub.do/10.1007/978-3-030-27378-1_78
-}}
-{{medline-entry
-|title=Stem cell-derived retinal pigment epithelium from patients with age-related macular degeneration exhibit reduced metabolism and matrix interactions.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31840941
-|keywords=* Bruch's membrane
-* age-related macular degeneration
-* aging
-* induced pluripotent stem cells
-* nonenzymatic nitration
-* retinal pigment epithelium
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031648
-}}
-{{medline-entry
-|title=Elovanoids counteract oligomeric β-amyloid-induced gene expression and protect photoreceptors.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31712409
-|mesh-terms=* Amyloid beta-Peptides
-* Animals
-* Apoptosis
-* Autophagy
-* Cells, Cultured
-* Docosahexaenoic Acids
-* Extracellular Matrix
-* Fatty Acids, Omega-3
-* Gene Expression Regulation
-* Humans
-* Male
-* Mice, Inbred C57BL
-* Mice, Transgenic
-* Photoreceptor Cells
-* Retina
-* Retinal Pigment Epithelium
-* Young Adult
-|keywords=* SASP
-* age-related macular degeneration
-* p16
-* retinal pigment epithelial cells
-* senescence gene program
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6883841
-}}
-{{medline-entry
-|title=Genetic LAMP2 deficiency accelerates the age-associated formation of basal laminar deposits in the retina.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31699817
-|mesh-terms=* Aging
-* Animals
-* Basement Membrane
-* Bruch Membrane
-* Exocytosis
-* Humans
-* Lysosomal-Associated Membrane Protein 2
-* Lysosomes
-* Macular Degeneration
-* Mice
-* Mice, Knockout
-* Phagocytosis
-* Retina
-* Retinal Pigment Epithelium
-|keywords=* LAMP2
-* aging
-* lysosome
-* retinal degeneration
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6876195
-}}
-{{medline-entry
-|title=Age, lipofuscin and melanin oxidation affect fundus near-infrared autofluorescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31648994
-|mesh-terms=* Age Factors
-* Animals
-* Biomarkers
-* Choroid
-* Disease Models, Animal
-* Female
-* Fluorescein Angiography
-* Fundus Oculi
-* Humans
-* Lipofuscin
-* Macular Degeneration
-* Male
-* Melanins
-* Melanosomes
-* Mice
-* Mice, Knockout
-* Optical Imaging
-* Oxidation-Reduction
-* Oxidative Stress
-* Protein Transport
-* Retinal Pigment Epithelium
-* Tomography, Optical Coherence
-|keywords=* Aging
-* Lipofuscin
-* Melanin
-* Melanolipofuscin
-* Oxidative stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6838394
-}}
-{{medline-entry
-|title=Relevance of working memory for reinforcement learning in older adults varies with timescale of learning.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31544587
-|keywords=* Aging
-* computational modeling
-* individual differences
-* reinforcement learning
-* working memory
-|full-text-url=https://sci-hub.do/10.1080/13825585.2019.1664389
-}}
-{{medline-entry
-|title=Expression and Function of Mas-Related G Protein-Coupled Receptor D and Its Ligand Alamandine in Retina.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31392515
-|mesh-terms=* Aging
-* Angiotensin II
-* Animals
-* Cells, Cultured
-* Electroretinography
-* Humans
-* Ligands
-* Lipopolysaccharides
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Oligopeptides
-* Rats
-* Reactive Oxygen Species
-* Receptors, G-Protein-Coupled
-* Retina
-|keywords=* Alamandine
-* Angiotensin-(1–7)
-* Mas-related G protein-coupled receptor D
-* Rennin-angiotensin system
-* Retina
-|full-text-url=https://sci-hub.do/10.1007/s12035-019-01716-4
-}}
-==RPIA==
-{{medline-entry
-|title=Suppression of p16 Induces mTORC1-Mediated Nucleotide Metabolic Reprogramming.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31433975
-|mesh-terms=* Aldose-Ketose Isomerases
-* Animals
-* Cell Line
-* Cellular Senescence
-* Cyclin-Dependent Kinase Inhibitor p16
-* Gene Knockdown Techniques
-* Humans
-* Male
-* Mechanistic Target of Rapamycin Complex 1
-* Mice, SCID
-* Nucleotides
-* Pentose Phosphate Pathway
-* Protein Biosynthesis
-|keywords=* BRAF
-* cancer metabolism
-* cell cycle
-* melanoma
-* nevi
-* pancreatic cancer
-* pentose phosphate pathway
-* ribonucleotide reductase M2
-* ribose-5-phosphate isomerase A
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6716532
-}}
-==RPS19BP1==
-{{medline-entry
-|title=Material basis, effect, and mechanism of ethanol extract of Pinellia ternata tubers on oxidative stress-induced cell senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32659678
-|keywords=* Oxidative stress
-* Pinellia ternata
-* SIRT1
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.phymed.2020.153275
-}}
-==RTEL1==
-{{medline-entry
-|title=Telomere length and aging-related outcomes in humans: A Mendelian randomization study in 261,000 older participants.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31444995
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Aging
-* Cohort Studies
-* Female
-* Humans
-* Male
-* Mendelian Randomization Analysis
-* Middle Aged
-* Risk Factors
-* Telomere Homeostasis
-|keywords=* TERT
-* UK Biobank
-* anti-aging
-* cellular senescence
-* centenarians
-* frailty
-* longevity
-* sarcopenia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826144
-}}
-==RXFP3==
-{{medline-entry
-|title=The [[RXFP3]] receptor is functionally associated with cellular responses to oxidative stress and DNA damage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31794429
-|mesh-terms=* Camptothecin
-* Computational Biology
-* DNA Damage
-* Felodipine
-* GTPase-Activating Proteins
-* Gene Expression Regulation
-* Gene Regulatory Networks
-* HEK293 Cells
-* Humans
-* Oxidative Stress
-* RNA, Messenger
-* Receptors, G-Protein-Coupled
-* Topoisomerase I Inhibitors
-|keywords=* DNA damage
-* GPCR
-* aging
-* relaxin 3
-* relaxin family peptide 3 receptor
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6932917
-}}
-==S100A4==
-{{medline-entry
-|title=Protective role of mesenchymal stem cells and mesenchymal stem cell-derived exosomes in cigarette smoke-induced mitochondrial dysfunction in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31678243
-|mesh-terms=* Alarmins
-* Animals
-* Cytokines
-* Exosomes
-* Lung
-* Mesenchymal Stem Cells
-* Mice
-* Mitochondria
-* Mitophagy
-* Oxidative Phosphorylation
-* Smoke
-* Tobacco
-|keywords=* COPD
-* Cellular Senescence
-* Exosomes
-* Mesenchymal stem cells
-* Mitochondria
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6894395
-}}
-==S100A9==
-{{medline-entry
-|title=Cigarette smoke induction of [[S100A9]] contributes to chronic obstructive pulmonary disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32964723
-|keywords=* Cigarette smoke
-* S100A9
-* aging
-* kinase
-* pulmonary function
-|full-text-url=https://sci-hub.do/10.1152/ajplung.00207.2020
-}}
-{{medline-entry
-|title=Modulation of KDM1A with vafidemstat rescues memory deficit and behavioral alterations.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32469975
-|mesh-terms=* Aging
-* Alzheimer Disease
-* Animals
-* Behavior, Animal
-* Brain
-* Disease Models, Animal
-* Enzyme Inhibitors
-* Epigenesis, Genetic
-* Female
-* Gene Expression
-* Hippocampus
-* Histone Demethylases
-* Humans
-* Male
-* Memory Disorders
-* Mice
-* Mice, Inbred C57BL
-* Mice, Mutant Strains
-* Monoamine Oxidase Inhibitors
-* Oxadiazoles
-* Rats
-* Rats, Sprague-Dawley
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7259601
-}}
-{{medline-entry
-|title=Cellular senescence induced by [[S100A9]] in mesenchymal stromal cells through NLRP3 inflammasome activation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31727865
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aged, 80 and over
-* Calgranulin B
-* Case-Control Studies
-* Cell Line
-* Cells, Cultured
-* Cellular Reprogramming
-* Cellular Senescence
-* Female
-* Humans
-* Inflammasomes
-* Interleukin-1beta
-* Male
-* Mesenchymal Stem Cells
-* Middle Aged
-* Myelodysplastic Syndromes
-* NLR Family, Pyrin Domain-Containing 3 Protein
-* Reactive Oxygen Species
-* Signal Transduction
-* Stem Cell Niche
-* Toll-Like Receptor 4
-* Up-Regulation
-* Young Adult
-|keywords=* NLRP3
-* S100A9
-* cellular senescence
-* mesenchymal stromal cells
-* myelodysplastic syndromes
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6874461
-}}
-{{medline-entry
-|title=[[S100A9]] extends lifespan in insulin deficiency.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31391467
-|mesh-terms=* Animals
-* Calgranulin B
-* Diabetes Mellitus, Experimental
-* Diphtheria Toxin
-* Fatty Acids
-* Humans
-* Hyperglycemia
-* Insulin
-* Leptin
-* Liver
-* Longevity
-* Male
-* Mice
-* Mice, Knockout
-* Oxidation-Reduction
-* Signal Transduction
-* Streptozocin
-* Toll-Like Receptor 4
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6686003
-}}
-==S100B==
-{{medline-entry
-|title=Aging protects rat cortical slices against to oxygen-glucose deprivation induced damage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32064981
-|keywords=* Aging
-* LDH
-* S100B
-* edema
-* oxygen-glucose deprivation
-|full-text-url=https://sci-hub.do/10.1080/00207454.2020.1730830
-}}
-==S1PR1==
-{{medline-entry
-|title=Aging Suppresses Sphingosine-1-Phosphate Chaperone ApoM in Circulation Resulting in Maladaptive Organ Repair.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32544390
-|keywords=* aging
-* endothelial cell
-* fibrosis
-* kidney repair
-* lipoprotein
-* lung regeneration
-* sphingosine-1-phosphate receptor
-* vascular barrier
-* vascular niche
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7607448
-}}
-==SAG==
-{{medline-entry
-|title=WRKY42 transcription factor positively regulates leaf senescence through modulating SA and ROS synthesis in Arabidopsis thaliana.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32634860
-|keywords=*
-WRKY42
-* Arabidopsis
-* leaf senescence
-* reactive oxygen species
-* salicylic acid
-|full-text-url=https://sci-hub.do/10.1111/tpj.14914
-}}
-{{medline-entry
-|title=Neurogenesis in the inner ear: the zebrafish statoacoustic ganglion provides new neurons from a Neurod/Nestin-positive progenitor pool well into adulthood.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32165493
-|mesh-terms=* Adult Stem Cells
-* Aging
-* Animals
-* Animals, Genetically Modified
-* Basic Helix-Loop-Helix Transcription Factors
-* Cell Differentiation
-* Ear, Inner
-* Embryo, Nonmammalian
-* Ganglia, Sensory
-* Gene Expression Regulation, Developmental
-* Hair Cells, Auditory
-* Larva
-* Nerve Tissue Proteins
-* Nestin
-* Neural Stem Cells
-* Neurogenesis
-* Sensory Receptor Cells
-* Stem Cell Niche
-* Zebrafish
-|keywords=* Inner ear
-* Neuronal stem cells
-* PNS
-* Zebrafish
-|full-text-url=https://sci-hub.do/10.1242/dev.176750
-}}
-==SAT1==
-{{medline-entry
-|title=Triethylenetetramine (trientine): a caloric restriction mimetic with a new mode of action.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32544364
-|keywords=* Acetylation
-* SAT1
-* aging
-* autophagy
-* copper
-* metabolomics
-* obesity
-* spermidine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7469548
-}}
-==SATB1==
-{{medline-entry
-|title=Loss of [[SATB1]] Induces p21-Dependent Cellular Senescence in Post-mitotic Dopaminergic Neurons.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31543366
-|mesh-terms=* Aging
-* Animals
-* Cells, Cultured
-* Cellular Senescence
-* Cyclin-Dependent Kinase Inhibitor p21
-* Dopaminergic Neurons
-* Epigenetic Repression
-* Gene Knockdown Techniques
-* Humans
-* Matrix Attachment Region Binding Proteins
-* Mice
-* Mice, Knockout
-* Mitosis
-* Parkinson Disease
-* Protein Binding
-|keywords=* Parkinson’s disease
-* SATB1
-* cellular senescence
-* dopamine
-* neurodegeneration
-* neuroinflammation
-* p21
-* senolytics
-* stem cells
-* transcriptomics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7493192
-}}
-==SCD==
-{{medline-entry
-|title=Cognitive training and brain stimulation in prodromal Alzheimer's disease (AD-Stim)-study protocol for a double-blind randomized controlled phase IIb (monocenter) trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33160420
-|keywords=* Aging
-* Decision-making
-* Mild cognitive impairment
-* Subjective cognitive decline
-* Transcranial direct current stimulation
-* Transfer
-* Working memory
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7648990
-}}
-{{medline-entry
-|title=Blood Pressure in Different Dementia Disorders, Mild Cognitive Impairment, and Subjective Cognitive Decline.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33110409
-|keywords=* Alzheimer’s disease
-* aging
-* blood pressure
-* mild cognitive impairment
-* subjective cognitive decline
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7488384
-}}
-{{medline-entry
-|title=Known-Groups and Convergent Validity of the Telephone Rey Auditory Verbal Learning Test total Learning Scores for Distinguishing Between Older Adults With Amnestic Cognitive Impairment and Subjective Cognitive Decline.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33067996
-|keywords=* aging
-* cognitive impairment
-* neuropsychological assessment
-|full-text-url=https://sci-hub.do/10.1093/arclin/acaa085
-}}
-{{medline-entry
-|title=Subjective cognitive decline as a predictor of future cognitive decline: a systematic review.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32973979
-|keywords=* Alzheimer disease.
-* aging
-* cognition
-* cognitive dysfunction
-* dementia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7500809
-}}
-{{medline-entry
-|title=Geriatric assessment for older adults with sickle cell disease: protocol for a prospective cohort pilot study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32974042
-|keywords=* Aging
-* Functional assessment
-* Geriatric assessment
-* Geriatrics
-* Older adults
-* Sickle cell
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7495855
-}}
-{{medline-entry
-|title=Prevalence and psychosocial correlates of subjectively perceived decline in five cognitive domains: Results from a population-based cohort study in Germany.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32510658
-|keywords=* Germany
-* cognitive aging
-* cognitive complaints
-* cohort study
-* prevalence
-* subjective cognitive decline
-|full-text-url=https://sci-hub.do/10.1002/gps.5359
-}}
-{{medline-entry
-|title=SC411 treatment can enhance survival in a mouse model of sickle cell disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32447175
-|keywords=* Aging
-* Cerebral blood flow
-* Docosahexaenoic acid
-* Neuroinflammation
-* Sickle cell disease
-* Working memory
-|full-text-url=https://sci-hub.do/10.1016/j.plefa.2020.102110
-}}
-{{medline-entry
-|title=DNA fragmentation of human spermatozoa: Simple assessment of single- and double-strand DNA breaks and their respective dynamic behavioral response.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32416007
-|keywords=* DNA longevity
-* sperm DNA damage
-* sperm DNA dynamics
-* sperm DNA fragmentation
-* sperm chromatin dispersion test
-|full-text-url=https://sci-hub.do/10.1111/andr.12819
-}}
-{{medline-entry
-|title=Psychometric Cognitive Decline Precedes the Advent of Subjective Cognitive Decline in the Evolution of Alzheimer's Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32388509
-|keywords=* Alzheimer’s disease
-* Brain aging
-* Cognitive decline
-* Cognitive testing
-* Longitudinal studies
-* Psychometric cognition
-|full-text-url=https://sci-hub.do/10.1159/000507286
-}}
-{{medline-entry
-|title=Serum alkaline phosphatase is elevated and inversely correlated with cognitive functions in subjective cognitive decline: results from the ReGAl 2.0 project.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32363431
-|keywords=* Aging
-* Biochemistry
-* Cognition
-* Dementia
-* Geriatric medicine
-|full-text-url=https://sci-hub.do/10.1007/s40520-020-01572-6
-}}
-{{medline-entry
-|title=Changes in Activity Participation Among Older Adults With Subjective Cognitive Decline or Objective Cognitive Deficits.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32010049
-|keywords=* activity participation
-* aging
-* daily functioning
-* metamemory
-* subjective cognitive decline
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6974583
-}}
-{{medline-entry
-|title=Age, gender and drug therapy influences on Tpeak-tend interval and on electrical risk score.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32023499
-|keywords=* Aging
-* Electrical risk score
-* Gender
-* Mortality
-* QTc
-* Repolarization phase
-* T peak-tend interval
-|full-text-url=https://sci-hub.do/10.1016/j.jelectrocard.2020.01.009
-}}
-{{medline-entry
-|title=Comorbid Chronic Conditions Among Older Adults with Subjective Cognitive Decline, United States, 2015-2017.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31915725
-|keywords=* Aging
-* Chronic disease
-* Cognitive dysfunction
-* Dementia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6938465
-}}
-{{medline-entry
-|title=Resting State BOLD Variability Is Linked to White Matter Vascular Burden in Healthy Aging but Not in Older Adults With Subjective Cognitive Decline.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31920589
-|keywords=* Alzheimer’s disease
-* aging
-* biomarkers
-* cerebrovascular health
-* signal variability
-* subjective cognitive decline
-* white matter
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6936515
-}}
-{{medline-entry
-|title=Estimated Life Expectancy and Income of Patients With Sickle Cell Disease Compared With Those Without Sickle Cell Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31730182
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Anemia, Sickle Cell
-* Child
-* Child, Preschool
-* Cohort Studies
-* Female
-* Forecasting
-* Humans
-* Income
-* Infant
-* Life Expectancy
-* Male
-* Middle Aged
-* Models, Statistical
-* Quality-Adjusted Life Years
-* United States
-* Young Adult
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6902797
-}}
-{{medline-entry
-|title=Does Empirically Derived Classification of Individuals with Subjective Cognitive Complaints Predict Dementia?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31703450
-|keywords=* Compostela aging study
-* cluster analysis
-* cognitive aging
-* dementia
-* mild cognitive impairment
-* screening and diagnosis
-* subjective cognitive complaints
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6895967
-}}
-{{medline-entry
-|title=Spatiotemporal Oscillatory Patterns During Working Memory Maintenance in Mild Cognitive Impairment and Subjective Cognitive Decline.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31522594
-|mesh-terms=* Aged
-* Aging
-* Brain Waves
-* Cerebral Cortex
-* Cognitive Dysfunction
-* Cortical Synchronization
-* Female
-* Humans
-* Magnetoencephalography
-* Male
-* Memory, Short-Term
-* Task Performance and Analysis
-|keywords=* Alzheimer’s disease (AD)
-* Induced oscillatory activity
-* magnetoencephalography (MEG)
-* mild cognitive impairment (MCI)
-* subjective cognitive decline (SCD)
-* working memory (WM)
-|full-text-url=https://sci-hub.do/10.1142/S0129065719500199
-}}
-{{medline-entry
-|title=Microstructural Correlates and Laterality Effect of Prospective Memory in Non-Demented Adults with Memory Complaints.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31466053
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Corpus Callosum
-* Diffusion Tensor Imaging
-* Female
-* Frontal Lobe
-* Functional Laterality
-* Humans
-* Magnetic Resonance Imaging
-* Male
-* Memory Disorders
-* Middle Aged
-* Nerve Fibers
-* Neuropsychological Tests
-* Retrospective Studies
-* Surveys and Questionnaires
-* Taiwan
-|keywords=* Aging
-* Alzheimer’s disease
-* Cognitive complaints
-* Diffusion tensor imaging
-* Lateralization
-* Prospective memory
-* Tract-based spatial statistics
-|full-text-url=https://sci-hub.do/10.1159/000501366
-}}
-==SCN2A==
-{{medline-entry
-|title=Na 1.2 haploinsufficiency in Scn2a knock-out mice causes an autistic-like phenotype attenuated with age.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31501495
-|mesh-terms=* Aging
-* Animals
-* Autism Spectrum Disorder
-* Gene Knockout Techniques
-* Haploinsufficiency
-* Memory
-* Mice
-* NAV1.2 Voltage-Gated Sodium Channel
-* Phenotype
-* Spatial Learning
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6733925
-}}
-==SCN2B==
-{{medline-entry
-|title=MicroRNA‑449a regulates the progression of brain aging by targeting [[SCN2B]] in SAMP8 mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32124967
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Gene Expression Regulation
-* Male
-* Mice
-* Mice, Transgenic
-* MicroRNAs
-* Voltage-Gated Sodium Channel beta-2 Subunit
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053848
-}}
-==SCO1==
-{{medline-entry
-|title=Real-Time PCR Analysis of Metabolism-Related Genes in a Long-Lived Model of C. elegans.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32219749
-|keywords=* Caenorhabditis elegans
-* Energy metabolism
-* Longevity
-* TaqMan real-time PCR
-* p53/CEP-1
-|full-text-url=https://sci-hub.do/10.1007/978-1-0716-0471-7_12
-}}
-==SDC1==
-{{medline-entry
-|title=Olmesartan alleviates bleomycin-mediated vascular smooth muscle cell senescence via the miR-665/[[SDC1]] axis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33042414
-|keywords=* Atherosclerosis
-* MiR-665
-* SDC1
-* olmesartan
-* vascular smooth muscle cell senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7540088
-}}
-{{medline-entry
-|title=Sulfated syndecan 1 is critical to preventing cellular senescence by modulating fibroblast growth factor receptor endocytosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32530114
-|keywords=* FGFR1
-* SDC1
-* cellular senescence
-* endocytosis
-* heparan sulfation
-|full-text-url=https://sci-hub.do/10.1096/fj.201902714R
-}}
-==SDHB==
-{{medline-entry
-|title=Mitochondrial Signatures in Circulating Extracellular Vesicles of Older Adults with Parkinson's Disease: Results from the EXosomes in PArkiNson's Disease (EXPAND) Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32059608
-|keywords=* aging
-* biomarkers
-* exosomes
-* mitochondrial dynamics
-* mitochondrial quality control
-* mitochondrial-derived vesicles
-* mitochondrial-lysosomal axis
-* mitophagy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7074517
-}}
-==SDS==
-{{medline-entry
-|title=Semiautomatic morphometric analysis of skeletal muscle obtained by needle biopsy in older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32946050
-|keywords=* Aging skeletal muscle
-* Morphometric analysis
-* Myosin heavy chain
-* Semiautomatic muscle analysis
-* Skeletal muscle
-|full-text-url=https://sci-hub.do/10.1007/s11357-020-00266-1
-}}
-{{medline-entry
-|title=Effects of late-onset dietary intake of salidroside on insulin/insulin-like growth factor-1 (IGF-1) signaling pathway of the annual fish Nothobranchius guentheri.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32858432
-|keywords=* Aging
-* Annual fish
-* Lifespan
-* Nothobranchius
-* Salidroside
-|full-text-url=https://sci-hub.do/10.1016/j.archger.2020.104233
-}}
-{{medline-entry
-|title=Quantification of Insoluble Protein Aggregation in Caenorhabditis elegans during Aging with a Novel Data-Independent Acquisition Workflow.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32831297
-|mesh-terms=* Aging
-* Animals
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* Longevity
-* Protein Aggregates
-* Proteome
-* Proteomics
-* Workflow
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7519758
-}}
-{{medline-entry
-|title=Skeletal Muscle Myofibrillar Protein Abundance Is Higher in Resistance-Trained Men, and Aging in the Absence of Training May Have an Opposite Effect.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31936810
-|keywords=* aging
-* myofibrillar protein
-* proteomics
-* resistance training
-* sarcoplasmic protein
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7022975
-}}
-{{medline-entry
-|title=Characterization, evaluation of nutritional parameters of Radix isatidis protein and its antioxidant activity in D-galactose induced ageing mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31694618
-|mesh-terms=* Aging
-* Animals
-* Antioxidants
-* Catalase
-* Drugs, Chinese Herbal
-* Galactose
-* Humans
-* Kidney
-* Liver
-* Male
-* Malondialdehyde
-* Mice
-* Mice, Inbred ICR
-* Molecular Weight
-* Oxidative Stress
-* Plant Proteins
-* Plant Roots
-* Superoxide Dismutase
-|keywords=* Antioxidant activity
-* D-galactose
-* Oxidative damage
-* Protein composition
-* Radix isatidis protein
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6836523
-}}
-{{medline-entry
-|title=[Effects of silver nanoparticles on pupation, eclosion, life span, apoptosis and protein expression in Drosophila melanogaster].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31621246
-|mesh-terms=* Animals
-* Apoptosis
-* Drosophila melanogaster
-* Longevity
-* Metal Nanoparticles
-* Oregon
-* Silver
-|keywords=* Drosophila melanogaster
-* apoptosis
-* protein expression
-* silver nanoparticles
-|full-text-url=https://sci-hub.do/10.13287/j.1001-9332.201910.036
-}}
-{{medline-entry
-|title=Does an Age-Specific Treatment Program Augment the Efficacy of a Cognitive-Behavioral Weight Loss Program in Adolescence and Young Adulthood? Results from a Controlled Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31480678
-|mesh-terms=* Adolescent
-* Aging
-* Behavior Therapy
-* Cognitive Behavioral Therapy
-* Female
-* Humans
-* Male
-* Weight Loss
-* Weight Reduction Programs
-* Young Adult
-|keywords=* adolescents
-* behavioral weight loss
-* controlled trial
-* emerging adults
-* obesity
-* quality of life
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6769959
-}}
-==SELENBP1==
-{{medline-entry
-|title=A Caenorhabditis elegans ortholog of human selenium-binding protein 1 is a pro-aging factor protecting against selenite toxicity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31557719
-|mesh-terms=* Animals
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* Cytoplasm
-* Drug Resistance
-* Gene Expression Regulation
-* Humans
-* Longevity
-* Membrane Proteins
-* Oxidative Stress
-* Paraquat
-* Selenious Acid
-* Selenium-Binding Proteins
-* Structural Homology, Protein
-|keywords=* Caenorhabditis elegans
-* Lifespan
-* Selenium-binding protein
-* Stress signaling
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6812014
-}}
-==SELENOK==
-{{medline-entry
-|title=Dietary selenium deficiency and supplementation differentially modulate the expression of two ER-resident selenoproteins (selenoprotein K and selenoprotein M) in the ovaries of aged mice: Preliminary data.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32736983
-|keywords=* Female fertility
-* Ovarian aging
-* Selenium
-* Selenoprotein K
-* Selenoprotein M
-|full-text-url=https://sci-hub.do/10.1016/j.repbio.2020.07.006
-}}
-==SENP6==
-{{medline-entry
-|title=Molecular signature for senile and complicated cataracts derived from analysis of sumoylation enzymes and their substrates in human cataract lenses.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32827359
-|keywords=* Pax6
-* SUMO1
-* SUMO2/3
-* aging
-* apoptosis
-* cataract
-* de-sumoylation enzymes (SENPs)
-* sumoylation ligases
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7576240
-}}
-==SERPINE1==
-{{medline-entry
-|title=Elevated circulating HtrA4 in preeclampsia may alter endothelial expression of senescence genes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32056555
-|keywords=* Endothelial aging
-* Endothelial cells
-* HtrA4
-* Preeclampsia
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.placenta.2019.12.012
-}}
-==SESN2==
-{{medline-entry
-|title=Copy Number Alterations in Papillary Thyroid Carcinomas: Does Loss of [i][[SESN2]][/i] Have a Role in Age-related Different Prognoses?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32859642
-|keywords=* Papillary thyroid cancer
-* SESN2
-* aCGH
-* deletion
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7472442
-}}
-==SFN==
-{{medline-entry
-|title=The phytoprotective agent sulforaphane prevents inflammatory degenerative diseases and age-related pathologies via Nrf2-mediated hormesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33160067
-|keywords=* Aging
-* Hormesis
-* Inflammation
-* Neuroprotection
-* Nrf2
-* Sulforaphane
-|full-text-url=https://sci-hub.do/10.1016/j.phrs.2020.105283
-}}
-{{medline-entry
-|title=Multi-Omic Analysis Reveals Different Effects of Sulforaphane on the Microbiome and Metabolome in Old Compared to Young Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33003447
-|keywords=* aging
-* biomarkers
-* gut microbiome
-* metabolome
-* sulforaphane
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7599699
-}}
-{{medline-entry
-|title=Sulforaphane controls the release of paracrine factors by keratinocytes and thus mitigates particulate matter-induced premature skin aging by suppressing melanogenesis and maintaining collagen homeostasis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32659677
-|keywords=* Coculture system
-* Collagen homeostasis
-* Melanogenesis
-* Particulate matter 2.5
-* Premature skin aging
-* Sulforaphane
-|full-text-url=https://sci-hub.do/10.1016/j.phymed.2020.153276
-}}
-{{medline-entry
-|title=Sulforaphane Inhibits Autophagy and Induces Exosome-Mediated Paracrine Senescence via Regulating mTOR/TFE3.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32476238
-|keywords=* ROS
-* autophagy
-* exosome
-* senescence
-* sulforaphane
-|full-text-url=https://sci-hub.do/10.1002/mnfr.201901231
-}}
-==SFPQ==
-{{medline-entry
-|title=Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32267831
-|keywords=* IL-8
-* NORAD
-* cell apoptosis
-* cell senescence
-* ox-LDL
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185106
-}}
-==SGK1==
-{{medline-entry
-|title=Epigenetic Regulation of KL (Klotho) via H3K27me3 (Histone 3 Lysine [K] 27 Trimethylation) in Renal Tubule Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32223380
-|keywords=* AKT
-* EZH2
-* aging
-* mTOR
-* p53
-|full-text-url=https://sci-hub.do/10.1161/HYPERTENSIONAHA.120.14642
-}}
-==SHBG==
-{{medline-entry
-|title=Endogenous Testosterone Levels and the Risk of Incident Cardiovascular Events in Elderly Men: The MrOS Prospective Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32337470
-|keywords=* aging
-* cardiovascular events
-* men
-* testosterone
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7173399
-}}
-{{medline-entry
-|title=Associations of Endogenous Sex Hormones with Carotid Plaque Burden and Characteristics in Midlife Women.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31900485
-|keywords=* aging
-* atherosclerosis
-* carotid artery
-* hormones
-* women
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7077951
-}}
-{{medline-entry
-|title=Analysis of the Relationship between the Levels of Androgens and Biochemical Bone Markers in Men Aged 60-75 Years.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31877849
-|mesh-terms=* Absorptiometry, Photon
-* Aged
-* Aging
-* Androgens
-* Biomarkers
-* Bone Density
-* Bone Remodeling
-* Bone and Bones
-* Collagen Type I
-* Dehydroepiandrosterone Sulfate
-* Estradiol
-* Humans
-* Male
-* Middle Aged
-* Parathyroid Hormone
-* Peptide Fragments
-* Peptides
-* Procollagen
-* Sex Hormone-Binding Globulin
-* Testosterone
-|keywords=* aging men
-* biochemical bone markers
-* levels of androgens
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6982106
-}}
-{{medline-entry
-|title=Testosterone and Estrone Increase From the Age of 70 Years: Findings From the Sex Hormones in Older Women Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31408149
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Biomarkers
-* Community-Based Participatory Research
-* Cross-Sectional Studies
-* Dehydroepiandrosterone
-* Estrone
-* Female
-* Follow-Up Studies
-* Humans
-* Obesity
-* Overweight
-* Prognosis
-* Testosterone
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6830527
-}}
-==SHD==
-{{medline-entry
-|title=Does self-reported hearing difficulty decrease older adults' cognitive and physical functioning? The mediating role of social isolation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33036703
-|mesh-terms=* Activities of Daily Living
-* Aged
-* Aged, 80 and over
-* Cognition
-* Cognitive Dysfunction
-* Cohort Studies
-* Disabled Persons
-* Female
-* Health Status
-* Hearing Loss
-* Humans
-* Longevity
-* Longitudinal Studies
-* Male
-* Mental Status and Dementia Tests
-* Odds Ratio
-* Self Report
-* Social Isolation
-|keywords=* Cognitive impairment
-* Older people
-* Physical disability
-* Self-reported hearing difficulty
-* Social isolation
-|full-text-url=https://sci-hub.do/10.1016/j.maturitas.2020.06.011
-}}
-==SHH==
-{{medline-entry
-|title=Recent advances in [[SHH]] medulloblastoma progression: tumor suppressor mechanisms and the tumor microenvironment.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31700613
-|mesh-terms=* Animals
-* Cerebellar Neoplasms
-* Cerebellum
-* Hedgehog Proteins
-* Humans
-* Medulloblastoma
-* Mice
-* Tumor Microenvironment
-|keywords=* Medulloblastoma
-* Sonic hedgehog
-* cell senescence
-* tumor microenvironment
-* tumor progression
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6820827
-}}
-==SI==
-{{medline-entry
-|title=Microarray Profiling Reveals Distinct Circulating miRNAs in Aged Male and Female Mice Subjected to Post-stroke Social Isolation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33074466
-|keywords=* Aging
-* Biomarkers
-* Sex differences
-* Social isolation
-* Stroke
-* miRNAs
-|full-text-url=https://sci-hub.do/10.1007/s12017-020-08622-2
-}}
-{{medline-entry
-|title=Is Heart Rate a Confounding Factor for Photoplethysmography Markers? A Systematic Review.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32290168
-|mesh-terms=* Aging
-* Cardiovascular Diseases
-* Diabetes Mellitus, Type 2
-* Female
-* Fingers
-* Heart Rate
-* Humans
-* Male
-* Microcirculation
-* Photoplethysmography
-* Vascular Stiffness
-|keywords=* cardiovascular disease
-* heart rate
-* photoplethysmography
-* reflection index
-* second derivative of photoplethysmography
-* stiffness index
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7177218
-}}
-{{medline-entry
-|title=Survival time after marked reduction in oral intake in terminally ill noncancer patients: A retrospective study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32161695
-|keywords=* elderly
-* geriatrics
-* palliative medicine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7060293
-}}
-{{medline-entry
-|title=Adherence to Mediterranean diet moderates the association between multimorbidity and depressive symptoms in older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109694
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Cohort Studies
-* Depression
-* Diet, Mediterranean
-* Healthy Aging
-* Humans
-* Multimorbidity
-* Surveys and Questionnaires
-|keywords=* Aging
-* Depressive symptoms
-* Mediterranean diet
-* Mental health
-* Multimorbidity
-|full-text-url=https://sci-hub.do/10.1016/j.archger.2020.104022
-}}
-{{medline-entry
-|title=Loneliness, Social Isolation, and Objectively Measured Physical Activity in Rural-Living Older Adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31860831
-|keywords=* accelerometry
-* aging
-* health
-* social well-being
-* volunteering
-|full-text-url=https://sci-hub.do/10.1123/japa.2019-0027
-}}
-{{medline-entry
-|title=The associations between social support and negative social interaction with suicidal ideation in US Chinese older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31650846
-|keywords=* Chinese American
-* Social support
-* aging
-* negative social interaction
-* suicidal ideation
-|full-text-url=https://sci-hub.do/10.1080/13607863.2019.1680953
-}}
-{{medline-entry
-|title=Cell Senescence and Cerebral Small Vessel Disease in the Brains of People Aged 80 Years and Older.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31553444
-|mesh-terms=* Aged, 80 and over
-* Aging
-* Brain
-* Cellular Senescence
-* Cerebral Arteries
-* Cerebral Small Vessel Diseases
-* Female
-* Humans
-* Male
-* White Matter
-|keywords=* Brain aging
-* Cerebrovascular disease
-* Senescence
-* Small vessel disease
-|full-text-url=https://sci-hub.do/10.1093/jnen/nlz088
-}}
-==SIK3==
-{{medline-entry
-|title=Quantitative and Qualitative Role of Antagonistic Heterogeneity in Genetics of Blood Lipids.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31566214
-|keywords=* Age-related phenotypes
-* Aging
-* Genome-wide association studies
-* Health span
-* Life span
-* Pleiotropy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7518561
-}}
-==SIRT1==
-{{medline-entry
-|title=Anthocyanins attenuate endothelial dysfunction through regulation of uncoupling of nitric oxide synthase in aged rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33274583
-|keywords=* NO
-* SIRT1
-* anthocyanins
-* eNOS deacetylation
-* senescence
-|full-text-url=https://sci-hub.do/10.1111/acel.13279
-}}
-{{medline-entry
-|title=Sirtuins and Their Implications in Neurodegenerative Diseases from a Drug Discovery Perspective.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33280374
-|keywords=* Aging
-* neurodegenerative diseases
-* neuroprotective
-* sirtuin
-* sirtuin activators
-* sirtuin inhibitors
-|full-text-url=https://sci-hub.do/10.1021/acschemneuro.0c00696
-}}
-{{medline-entry
-|title=Effects of alpha-mangostin on memory senescence induced by high glucose in human umbilical vein endothelial cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33149857
-|keywords=* Cellular senescence
-* Diabetes
-* Diabetes complications
-* Endothelial cells
-* Garcinia mangostana
-* Hyperglycemia
-* Mangostin
-* Metabolic syndrome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7585532
-}}
-{{medline-entry
-|title=[[SIRT1]] Activation Using CRISPR/dCas9 Promotes Regeneration of Human Corneal Endothelial Cells through Inhibiting Senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33158256
-|keywords=* CRISPR/dCas9
-* SIRT1
-* corneal endothelial cells
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7694272
-}}
-{{medline-entry
-|title=Histone Deacetylase [[SIRT1]], Smooth Muscle Cell Function, and Vascular Diseases.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33117155
-|keywords=* SIRT1
-* SIRT1 activators
-* calorie restriction
-* senescence
-* vascular diseases
-* vascular smooth muscle cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7573826
-}}
-{{medline-entry
-|title=6,4'-dihydroxy-7-methoxyflavanone protects against H O -induced cellular senescence by inducing [[SIRT1]] and inhibiting phosphatidylinositol 3-kinase/Akt pathway activation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33111210
-|keywords=* 6,4′-dihydroxy-7-methoxyflavanone
-* Akt
-* Oxidative stress
-* Premature senescence
-* SIRT1
-|full-text-url=https://sci-hub.do/10.1007/s11010-020-03951-z
-}}
-{{medline-entry
-|title=Isoparvifuran isolated from Dalbergia odorifera attenuates H O -induced senescence of BJ cells through [[SIRT1]] activation and AKT/mTOR pathway inhibition.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33010892
-|keywords=* AKT/mTOR signaling pathway
-* Antioxidant: SIRT1
-* Cellular senescence
-* Isoparvifuran
-|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2020.09.096
-}}
-{{medline-entry
-|title=[[SIRT1]] Is the Target Gene for 2,3,5,4'-Tetrahydroxystilbene-2-O-β-D-Glucoside Alleviating the HUVEC Senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33013385
-|keywords=* 2,3,5,4’-tetrahydroxystilbene-2-O-β-d-glucoside
-* SIRT1
-* human umbilical vein cells
-* hydrogen peroxide
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7508177
-}}
-{{medline-entry
-|title=The Role of Sirtuins in Kidney Diseases.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32932720
-|keywords=* acute kidney injury
-* aging kidney
-* chronic kidney disease
-* diabetic nephropathy
-* kidney
-* sirtuins
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7555196
-}}
-{{medline-entry
-|title=The effect of 12-week resistance exercise training on serum levels of cellular aging process parameters in elderly men.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32919015
-|keywords=* Cellular senescence
-* Elderly
-* Resistance training
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.111090
-}}
-{{medline-entry
-|title=Virus-Induced Asthma Exacerbations: [[SIRT1]] Targeted Approach.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32823491
-|keywords=* SIRT1
-* asthma
-* cellular senescence
-* exacerbations
-* virus infection
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7464235
-}}
-{{medline-entry
-|title=Novel resveratrol derivatives have diverse effects on the survival, proliferation and senescence of primary human fibroblasts.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32793997
-|keywords=* Resveratrol
-* SIRT1
-* Senescence
-* Toxicity
-|full-text-url=https://sci-hub.do/10.1007/s10522-020-09896-6
-}}
-{{medline-entry
-|title=Glucose restriction delays senescence and promotes proliferation of HUVECs via the AMPK/[[SIRT1]]-FOXA3-Beclin1 pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32768436
-|keywords=* Beclin1
-* Endothelial cells
-* FOXA3
-* Glucose restriction
-* Proliferation
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.111053
-}}
-{{medline-entry
-|title=Therapeutic Effects of SRT2104 on Lung Injury in Rats with Emphysema via Reduction of Type II Alveolar Epithelial Cell Senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32722945
-|keywords=* Sirtuin 1
-* alveolar epithelial cells
-* cellular senescence
-* chronic obstructive pulmonary disease
-* cigarette smoking
-|full-text-url=https://sci-hub.do/10.1080/15412555.2020.1797657
-}}
-{{medline-entry
-|title=Latifolin Inhibits Oxidative Stress-Induced Senescence via Upregulation of [[SIRT1]] in Human Dermal Fibroblasts.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32404543
-|keywords=* human dermal fibroblast
-* latifolin
-* mammalian target of rapamycin
-* oxidative stress
-* senescence
-* silent information regulator 1
-|full-text-url=https://sci-hub.do/10.1248/bpb.b20-00094
-}}
-{{medline-entry
-|title=SRT1720-induced activation of [[SIRT1]] alleviates vascular smooth muscle cell senescence through PKA-dependent phosphorylation of AMPKα at Ser485.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32421926
-|keywords=* SIRT1
-* SRT1720
-* VSMC senescence
-* p-AMPK (Ser485)
-* telomere length
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7327920
-}}
-{{medline-entry
-|title=miR-128 plays a critical role in murine osteoclastogenesis and estrogen deficiency-induced bone loss.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32292498
-|keywords=* PMOP
-* aging
-* inflammation
-* miR-128
-* osteoclastogenesis
-* ovariectomy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7150474
-}}
-{{medline-entry
-|title=Lymphocyte senescence in COPD is associated with decreased sirtuin 1 expression in steroid resistant pro-inflammatory lymphocytes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32270742
-|keywords=* CD28nullCD8+ T and NKT-like cells
-* COPD
-* IFNγ and TNFα
-* SIRT1
-* lymphocyte senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7153179
-}}
-{{medline-entry
-|title=Therapeutic effects of hydro-alcoholic leaf extract of Withania somnifera on age-induced changes in daily rhythms of Sirt1, Nrf2 and Rev-erbα in the SCN of male Wistar rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32249404
-|keywords=* Aging
-* Ashwagandha
-* Circadian clock
-* NRF2
-* SCN
-* SIRT1
-|full-text-url=https://sci-hub.do/10.1007/s10522-020-09875-x
-}}
-{{medline-entry
-|title=The Serum Concentration of Anti-Aging Proteins, Sirtuin1 and αKlotho in Patients with End-Stage Kidney Disease on Maintenance Hemodialysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32214805
-|mesh-terms=* Age Factors
-* Aged
-* Aging
-* Biomarkers
-* Blood Pressure
-* Cardiovascular Diseases
-* Case-Control Studies
-* Diabetes Complications
-* Echocardiography
-* Female
-* Glucuronidase
-* Heart Ventricles
-* Humans
-* Kidney
-* Kidney Failure, Chronic
-* Male
-* Middle Aged
-* Renal Dialysis
-* Sirtuin 1
-* Stroke Volume
-|keywords=* chronic kidney disease
-* hemodialysis
-* sirtuin1
-* αKlotho
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7084123
-}}
-{{medline-entry
-|title=Small extracellular vesicles deliver miR-21 and miR-217 as pro-senescence effectors to endothelial cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32158519
-|keywords=* Cellular senescence
-* DNMT1
-* SIRT1
-* extracellular vesicles
-* microRNAs
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7048230
-}}
-{{medline-entry
-|title=Spatiotemporal gating of [[SIRT1]] functions by O-GlcNAcylation is essential for liver metabolic switching and prevents hyperglycemia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32152092
-|mesh-terms=* Acetylglucosamine
-* Aging
-* Animals
-* Fasting
-* Gluconeogenesis
-* Glycosylation
-* HEK293 Cells
-* Homeostasis
-* Humans
-* Hyperglycemia
-* Insulin Resistance
-* Liver
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Obesity
-* Phosphorylation
-* Protein Processing, Post-Translational
-* Sirtuin 1
-* Spatio-Temporal Analysis
-|keywords=* PGC1α
-* fed–fast cycle
-* gluconeogenesis
-* insulin signaling
-* ubiquitinylation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7104039
-}}
-{{medline-entry
-|title=Hydrogen Sulfide Inhibits Homocysteine-Induced Neuronal Senescence by Up-Regulation of [[SIRT1]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32132865
-|keywords=* SIRT1
-* cell senescence
-* homocysteine
-* hydrogen sulfide
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053352
-}}
-{{medline-entry
-|title=[[SIRT1]] and aging related signaling pathways.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32084459
-|keywords=* Aging
-* Deacetylate
-* NAD(+)
-* SIRT1
-* Signaling pathways
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2020.111215
-}}
-{{medline-entry
-|title=Tropisetron protects against brain aging via attenuating oxidative stress, apoptosis and inflammation: The role of [[SIRT1]] signaling.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32088214
-|mesh-terms=* Aging
-* Animals
-* Antioxidants
-* Apoptosis
-* Brain
-* Drug Administration Schedule
-* Galactose
-* Gene Expression Regulation
-* Inflammation
-* Injections, Intraperitoneal
-* Injections, Subcutaneous
-* Interleukin-6
-* Male
-* Mice
-* Mitochondria
-* Neurons
-* Nitric Oxide
-* Oxidative Stress
-* Proto-Oncogene Proteins c-bcl-2
-* Reactive Oxygen Species
-* Serotonin 5-HT3 Receptor Antagonists
-* Sirtuin 1
-* Tropisetron
-* Tumor Necrosis Factor-alpha
-* bcl-2-Associated X Protein
-|keywords=* Aging
-* Brain
-* Neurotoxicity
-* Sirtuin 1
-* Tropisetron
-* d-galactose
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2020.117452
-}}
-{{medline-entry
-|title=Nicotinamide mononucleotide (NMN) supplementation promotes neurovascular rejuvenation in aged mice: transcriptional footprint of [[SIRT1]] activation, mitochondrial protection, anti-inflammatory, and anti-apoptotic effects.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32056076
-|keywords=* Aging
-* Geroscience
-* Mitochondria dysfunction
-* Transcriptomics
-* Vascular cognitive impairment
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7206476
-}}
-{{medline-entry
-|title=Deacetylation of MRTF-A by [[SIRT1]] defies senescence induced down-regulation of collagen type I in fibroblast cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32061777
-|mesh-terms=* Acetylation
-* Animals
-* Benzamides
-* Carbazoles
-* Cellular Senescence
-* Collagen Type I
-* Down-Regulation
-* Embryo, Mammalian
-* Fibroblasts
-* HEK293 Cells
-* Heterocyclic Compounds, 4 or More Rings
-* Humans
-* Mice
-* Mutation
-* Naphthols
-* Primary Cell Culture
-* Promoter Regions, Genetic
-* RNA, Small Interfering
-* Resveratrol
-* Sirtuin 1
-* Trans-Activators
-|keywords=* Collagen type I
-* Fibroblast
-* Lysine deacetylation
-* Post-translational modification
-* Senescence
-* Transcriptional regulation
-|full-text-url=https://sci-hub.do/10.1016/j.bbadis.2020.165723
-}}
-{{medline-entry
-|title=Chronic Polyphenon-60 or Catechin Treatments Increase Brain Monoamines Syntheses and Hippocampal [[SIRT1]] Levels Improving Cognition in Aged Rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31991916
-|mesh-terms=* Age Factors
-* Animals
-* Behavior, Animal
-* Biogenic Monoamines
-* Catechin
-* Cognition
-* Cognitive Aging
-* Corpus Striatum
-* Hippocampus
-* Male
-* Memory, Episodic
-* Memory, Short-Term
-* Neuroprotective Agents
-* Rats, Sprague-Dawley
-* Sirtuin 1
-* Time Factors
-|keywords=* NF-κB
-* RBAP46/48
-* SIRT1
-* brain aging
-* brain monoamine synthesis
-* catechin
-* green tea
-* memory
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7071257
-}}
-{{medline-entry
-|title=Duck Oil-loaded Nanoemulsion Inhibits Senescence of Angiotensin II-treated Vascular Smooth Muscle Cells by Upregulating [[SIRT1]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31970335
-|keywords=* SIRT1
-* angiotensin II
-* duck oil
-* nanoemulsion
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6957441
-}}
-{{medline-entry
-|title=Two novel [[SIRT1]] activators, SCIC2 and SCIC2.1, enhance [[SIRT1]]-mediated effects in stress response and senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31942817
-|keywords=* Sirtuins
-* drug discovery
-* epigenetic modulators
-* senescence
-* stress response
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7574383
-}}
-{{medline-entry
-|title=Hydrogen sulfide attenuates mitochondrial dysfunction-induced cellular senescence and apoptosis in alveolar epithelial cells by upregulating sirtuin 1.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31881011
-|mesh-terms=* A549 Cells
-* Alveolar Epithelial Cells
-* Apoptosis
-* Cellular Senescence
-* Humans
-* Hydrogen Sulfide
-* Mitochondria
-* Oxidative Stress
-* Sirtuin 1
-* Smoke
-* Tobacco
-* Up-Regulation
-|keywords=* alveolar epithelial cell
-* cigarette smoke extract
-* hydrogen sulfide
-* mitochondria injury
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6949053
-}}
-{{medline-entry
-|title=The protective role of omentin-1 in IL-1β-induced chondrocyte senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31852248
-|mesh-terms=* Adipokines
-* Caveolin 1
-* Cell Line, Tumor
-* Cellular Senescence
-* Chondrocytes
-* Cyclin-Dependent Kinase Inhibitor p21
-* Cytoprotection
-* G1 Phase Cell Cycle Checkpoints
-* Humans
-* Interleukin-1beta
-* Plasminogen Activator Inhibitor 1
-* Sirtuin 1
-* Transcriptional Activation
-|keywords=* IL-1β
-* Omentin-1
-* SIRT-1
-* chondrocyte senescence
-|full-text-url=https://sci-hub.do/10.1080/21691401.2019.1699803
-}}
-{{medline-entry
-|title=The Lifespan Extension Ability of Nicotinic Acid Depends on Whether the Intracellular NAD  Level Is Lower than the Sirtuin-Saturating Concentrations.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31878234
-|mesh-terms=* Animals
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* Caloric Restriction
-* Cell Line
-* Humans
-* NAD
-* Niacin
-* Sirtuins
-* beta-Galactosidase
-|keywords=* C. elegans
-* Hs68 cells
-* NAD+
-* calorie restriction mimetic
-* lifespan
-* nicotinic acid
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6982340
-}}
-{{medline-entry
-|title=Alpha-mangostin decreased cellular senescence in human umbilical vein endothelial cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31792920
-|keywords=* Alpha-mangostin
-* Diabetes
-* HUVEC
-* High glucose
-* SIRT1
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7214571
-}}
-{{medline-entry
-|title=Central nervous system [[SIRT1]] expression is required for cued and contextual fear conditioning memory responses in aging mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31763496
-|keywords=* Fear conditioning
-* SIRT1
-* aging
-* classically conditioned memory
-* hippocampus
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6839599
-}}
-{{medline-entry
-|title=Does education level protect us from rapid ageing? Sirtuin expression versus age and level of education.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31785216
-|mesh-terms=* Adolescent
-* Adult
-* Age Factors
-* Aging
-* Aging, Premature
-* Educational Status
-* Epigenesis, Genetic
-* Female
-* Gene Expression Regulation, Enzymologic
-* Histones
-* Humans
-* Learning
-* Male
-* Middle Aged
-* Sirtuins
-* Young Adult
-}}
-{{medline-entry
-|title=CO ameliorates endothelial senescence induced by 5-fluorouracil through [[SIRT1]] activation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31704100
-|mesh-terms=* Antioxidants
-* Carbon Monoxide
-* Cellular Senescence
-* Down-Regulation
-* Fluorouracil
-* Heme Oxygenase-1
-* Human Umbilical Vein Endothelial Cells
-* Humans
-* Nitric Oxide Synthase Type III
-* Reactive Oxygen Species
-* Sirtuin 1
-|keywords=* 5-Fluorouracil
-* Carbon monoxide
-* Endothelial senescence
-* Reactive oxygen species
-* SIRT1
-|full-text-url=https://sci-hub.do/10.1016/j.abb.2019.108185
-}}
-{{medline-entry
-|title=Long noncoding RNA GAS5 inhibits cell proliferation and fibrosis in diabetic nephropathy by sponging miR-221 and modulating [[SIRT1]] expression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31631065
-|mesh-terms=* Aging
-* Animals
-* Argonaute Proteins
-* Cell Proliferation
-* Diabetes Mellitus, Experimental
-* Diabetic Nephropathies
-* Fibrosis
-* Gene Deletion
-* Gene Expression Regulation
-* Glucose
-* Male
-* Mesangial Cells
-* Mice
-* MicroRNAs
-* RAW 264.7 Cells
-* RNA, Long Noncoding
-* Rats
-* Rats, Sprague-Dawley
-* Sirtuin 1
-|keywords=* diabetic nephropathy
-* fibrosis
-* lncRNA GAS5
-* proliferation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834398
-}}
-{{medline-entry
-|title=The Role of Sirtuin1 in Regulating Endothelial Function, Arterial Remodeling and Vascular Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31572218
-|keywords=* PVAT
-* SIRT1
-* eNOS
-* vascular aging
-* vascular remodeling
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6751260
-}}
-{{medline-entry
-|title=Deacetylation of LAMP1 drives lipophagy-dependent generation of free fatty acids by Abrus agglutinin to promote senescence in prostate cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31544977
-|keywords=* Abrus agglutinin
-* LAMP1
-* SIRT1
-* free fatty acid
-* lipophagy
-* reactive oxygen species
-* senescence
-|full-text-url=https://sci-hub.do/10.1002/jcp.29182
-}}
-{{medline-entry
-|title=Plasma exosomes in OSA patients promote endothelial senescence: effect of long-term adherent continuous positive airway pressure.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31552414
-|keywords=* CPAP
-* OSA
-* aging
-* cardiovascular
-* endothelium
-* exosomes
-* extracellular vesicles
-* intermittent hypoxia
-* oxidative stress
-* senescence
-|full-text-url=https://sci-hub.do/10.1093/sleep/zsz217
-}}
-{{medline-entry
-|title=Hydrogen Sulfide Inhibits High Glucose-Induced Neuronal Senescence by Improving Autophagic Flux [i]via[/i] Up-regulation of [[SIRT1]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31481873
-|keywords=* SIRT1
-* autophagic flux
-* high glucose
-* hydrogen sulfide
-* neuronal senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6710442
-}}
-{{medline-entry
-|title=Activation of the miR-34a-Mediated [[SIRT1]]/mTOR Signaling Pathway by Urolithin A Attenuates D-Galactose-Induced Brain Aging in Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31420820
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Coumarins
-* Galactose
-* Male
-* Mice
-* Mice, Inbred ICR
-* MicroRNAs
-* PC12 Cells
-* Random Allocation
-* Rats
-* Signal Transduction
-* Sirtuin 1
-* TOR Serine-Threonine Kinases
-|keywords=* D-Gal
-* SIRT1/mTOR signal pathway
-* Urolithin A
-* aging
-* autophagy
-* miR-34a
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6985387
-}}
-==SIRT2==
-{{medline-entry
-|title=Melatonin ameliorates the advanced maternal age-associated meiotic defects in oocytes through the [[SIRT2]]-dependent H4K16 deacetylation pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31980591
-|keywords=* aging
-* histone acetylation
-* meiosis
-* melatonin
-* oocyte quality
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053624
-}}
-==SIRT3==
-{{medline-entry
-|title=[[SIRT3]] protects endothelial cells from high glucose-induced senescence and dysfunction via the p53 pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33160987
-|keywords=* Endothelial senescence
-* High glucose
-* SIRT3
-* p53
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2020.118724
-}}
-{{medline-entry
-|title=Melatonin and Sirtuins in Buccal Epithelium: Potential Biomarkers of Aging and Age-Related Pathologies.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33143333
-|keywords=* aging
-* arterial hypertension
-* buccal epithelium
-* melatonin
-* sirtuins
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7662974
-}}
-{{medline-entry
-|title=[i][[SIRT3]][/i] Transfection of Aged Human Bone Marrow-Derived Mesenchymal Stem Cells Improves Cell Therapy-Mediated Myocardial Repair.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32228121
-|keywords=* O-hMSC transplantation
-* SIRT3
-* aging
-* gene modification
-* myocardial infarction
-* myocardial repair
-|full-text-url=https://sci-hub.do/10.1089/rej.2019.2260
-}}
-{{medline-entry
-|title=17β-estradiol inhibits H O -induced senescence in HUVEC cells through upregulating [[SIRT3]] expression and promoting autophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32172411
-|keywords=* 17β-estradiol
-* Autophagy
-* SIRT3
-* Senescence
-|full-text-url=https://sci-hub.do/10.1007/s10522-020-09868-w
-}}
-{{medline-entry
-|title=CR6 interacting factor 1 deficiency induces premature senescence via [[SIRT3]] inhibition in endothelial cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109515
-|keywords=* Antioxidant system
-* Mitochondria
-* Oxidative stress
-* Senescence
-* Vascular endothelial cell
-|full-text-url=https://sci-hub.do/10.1016/j.freeradbiomed.2020.02.017
-}}
-{{medline-entry
-|title=Mitochondrial function in skeletal myofibers is controlled by a TRF2-[[SIRT3]] axis over lifetime.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31991048
-|keywords=* aging
-* mitochondria
-* postmitotic cells
-* skeletal muscle
-* telomeres
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059141
-}}
-{{medline-entry
-|title=Context-Dependent Roles for SIRT2 and [[SIRT3]] in Tumor Development Upon Calorie Restriction or High Fat Diet.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31970087
-|keywords=* SIRT2
-* SIRT3
-* aging
-* calorie restriction
-* cancer
-* high fat diet
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6960403
-}}
-{{medline-entry
-|title=The yin and yang faces of the mitochondrial deacetylase sirtuin 3 in age-related disorders.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31740222
-|mesh-terms=* Aging
-* Animals
-* Cardiovascular Diseases
-* Humans
-* Metabolic Diseases
-* Mitochondria
-* Neurodegenerative Diseases
-* Protein Isoforms
-* Sirtuin 3
-|keywords=* Age-related diseases
-* Deacetylation
-* Genetic manipulations
-* Mitochondria
-* Pharmacological modulators
-* Sirtuins
-|full-text-url=https://sci-hub.do/10.1016/j.arr.2019.100983
-}}
-==SIRT5==
-{{medline-entry
-|title=Lysine malonylation and propionylation are prevalent in human lens proteins.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31678036
-|mesh-terms=* Aging
-* Animals
-* Blotting, Western
-* Chromatography, Liquid
-* Crystallins
-* Cytoskeletal Proteins
-* Cytosol
-* Epithelial Cells
-* Humans
-* Immunohistochemistry
-* Lens, Crystalline
-* Lysine
-* Malonates
-* Membrane Proteins
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Middle Aged
-* Mitochondrial Proteins
-* Organ Culture Techniques
-* Paraffin Embedding
-* Propionates
-* Sirtuin 3
-* Sirtuins
-* Tandem Mass Spectrometry
-|keywords=* Lens proteins
-* Malonylation
-* Mass spectrometry
-* Propionylation
-* Sirtuins
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6957740
-}}
-==SIRT6==
-{{medline-entry
-|title=Association between [[SIRT6]] Methylation and Human Longevity in a Chinese Population.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33238266
-|keywords=* DNA Methylation
-* Longevity
-* Messenger RNA
-* SIRT6
-|full-text-url=https://sci-hub.do/10.1159/000508832
-}}
-{{medline-entry
-|title=The [[SIRT6]] activator MDL-800 improves genomic stability and pluripotency of old murine-derived iPS cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33089974
-|keywords=* DNA repair
-* MDL-800
-* SIRT6
-* aging
-* genome integrity
-* pluripotency
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7431819
-}}
-{{medline-entry
-|title=Sirtuins as Possible Predictors of Aging and Alzheimer's Disease Development: Verification in the Hippocampus and Saliva.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33098511
-|keywords=* Alzheimer’s disease
-* aging
-* intravital diagnosis
-* saliva
-* sirtuins
-|full-text-url=https://sci-hub.do/10.1007/s10517-020-04986-4
-}}
-{{medline-entry
-|title=Age-related epigenetic drift deregulates [i][[SIRT6]][/i] expression and affects its downstream genes in human peripheral blood mononuclear cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32573339
-|keywords=* SIRT6
-* aging
-* interaction network
-* longevity
-* methylation
-* miRNA
-* peripheral blood mononuclear cells (PBMCs)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7678931
-}}
-{{medline-entry
-|title=Biological and catalytic functions of sirtuin 6 as targets for small-molecule modulators.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32518153
-|keywords=* SIRT6
-* activator
-* aging
-* cancer
-* cell metabolism
-* chromatin
-* gene expression
-* histone deacetylase (HDAC)
-* longevity
-* metabolic disorder
-* sirtuin
-* small molecule
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7415977
-}}
-{{medline-entry
-|title=Age-dependent role of [[SIRT6]] in jawbone via regulating senescence and autophagy of bone marrow stromal cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32002721
-|mesh-terms=* Adult
-* Aged
-* Aging
-* Animals
-* Bone Marrow Cells
-* Humans
-* Jaw
-* Male
-* Mesenchymal Stem Cells
-* Mice
-* Mice, Knockout
-* Middle Aged
-* Osteogenesis
-* Sirtuins
-|keywords=* Autophagy
-* Bone marrow stromal cells
-* Jawbone
-* Osteoporosis
-* SIRT6
-* Senescence
-|full-text-url=https://sci-hub.do/10.1007/s10735-020-09857-w
-}}
-{{medline-entry
-|title=Mechanism of activation for the sirtuin 6 protein deacylase.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31822559
-|mesh-terms=* Allosteric Regulation
-* Biocatalysis
-* Fatty Acids
-* HEK293 Cells
-* Histones
-* Humans
-* Hydrophobic and Hydrophilic Interactions
-* Kinetics
-* Lipids
-* Mutagenesis
-* Mutation
-* NAD
-* Peptides
-* Protein Binding
-* Protein Conformation
-* Sirtuins
-* Small Molecule Libraries
-|keywords=* SIRT6
-* activator
-* cancer
-* chromatin
-* deacetylation
-* epigenetics
-* histone
-* histone deacetylase (HDAC)
-* lifespan
-* long chain acyl substrate
-* longevity
-* sirtuin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996886
-}}
-{{medline-entry
-|title=Proteomics of Long-Lived Mammals.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31737995
-|keywords=* SIRT6
-* aging
-* long-lived mammals
-* naked mole rats
-* proteomics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7117992
-}}
-{{medline-entry
-|title=Sirtuins and [[SIRT6]] in Carcinogenesis and in Diet.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31591350
-|mesh-terms=* Aging
-* Animals
-* Carcinogenesis
-* Diet
-* Gene Expression Regulation, Neoplastic
-* Humans
-* Nanomedicine
-* Organ Specificity
-* Sirtuins
-|keywords=* SIRT6
-* cancer
-* chemotherapy
-* diet
-* modulator
-* sirtuins
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6801518
-}}
-{{medline-entry
-|title=[[SIRT6]]-mediated transcriptional suppression of MALAT1 is a key mechanism for endothelial to mesenchymal transition.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31399301
-|mesh-terms=* Aging
-* Animals
-* Cells, Cultured
-* Disease Models, Animal
-* Endothelium, Vascular
-* Epithelial-Mesenchymal Transition
-* Gene Expression Regulation
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* RNA, Long Noncoding
-* Signal Transduction
-* Sirtuins
-* Vascular Diseases
-|full-text-url=https://sci-hub.do/10.1016/j.ijcard.2019.07.082
-}}
-==SIRT7==
-{{medline-entry
-|title=[[SIRT7]] antagonizes human stem cell aging as a heterochromatin stabilizer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32504224
-|keywords=* LINE1
-* SIRT7
-* STING
-* aging
-* cGAS
-* stem cell
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305295
-}}
-==SLA==
-{{medline-entry
-|title=Vaccination of aged mice with adjuvanted recombinant influenza nucleoprotein enhances protective immunity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32540272
-|keywords=* Adjuvant
-* Aging
-* Influenza
-* Mouse
-* Nucleoprotein
-* Vaccination
-|full-text-url=https://sci-hub.do/10.1016/j.vaccine.2020.05.085
-}}
-{{medline-entry
-|title=Mechanical Anisotropy and Surface Roughness in Additively Manufactured Parts Fabricated by Stereolithography ([[SLA]]) Using Statistical Analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32486137
-|keywords=* Taguchi methods
-* additive manufacturing
-* aging effect
-* analysis of variance
-* anisotropy
-* design of experiments
-* stereolithography
-* surface roughness
-* tensile testing
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7321476
-}}
-{{medline-entry
-|title=The Effect of Age of Titanium Dental Implants on Implant Survival and Marginal Bone Resorption: A 5-Year Retrospective Follow-Up Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32369581
-|keywords=*
-            aged implant
-*
-            biological aging
-*
-            implant survival
-*
-            marginal bone resorption
-*
-            titanium dental implant
-|full-text-url=https://sci-hub.do/10.1563/aaid-joi-D-19-00316
-}}
-==SLC16A7==
-{{medline-entry
-|title=Genetics of facial telangiectasia in the Rotterdam Study: a genome-wide association study and candidate gene approach.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33095951
-|keywords=* GWAS
-* KIAA0930
-* MC1R
-* SLCA45A2
-* SNP
-* Telangiectasia
-* candidate gene approach
-* epidemiology
-* genetics
-* pigmentation genes
-* red veins
-* skin aging
-|full-text-url=https://sci-hub.do/10.1111/jdv.17014
-}}
-==SLC26A2==
-{{medline-entry
-|title=Phenotypic characterization of Slc26a2 mutant mice reveals a multifactorial etiology of spondylolysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31914611
-|mesh-terms=* Aging
-* Animals
-* Lumbar Vertebrae
-* Male
-* Mice
-* Osteogenesis
-* Phenotype
-* Spondylolysis
-* Sulfate Transporters
-|keywords=* SLC26A2
-* bone loss
-* isthmic defect
-* spondylolysis
-* vertebral development
-|full-text-url=https://sci-hub.do/10.1096/fj.201901040RR
-}}
-==SLC6A4==
-{{medline-entry
-|title=The Psilocybin-Telomere Hypothesis: An empirically falsifiable prediction concerning the beneficial neuropsychopharmacological effects of psilocybin on genetic aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31634774
-|mesh-terms=* Aging
-* Aging, Premature
-* Animals
-* Anxiety
-* Brain-Derived Neurotrophic Factor
-* Consciousness
-* DNA Methylation
-* Depression
-* Disease Models, Animal
-* Endocrine System
-* Humans
-* Models, Genetic
-* Models, Psychological
-* Neurotransmitter Agents
-* Oxidative Stress
-* Personality
-* Psilocybin
-* Psychotropic Drugs
-* Research Design
-* Serotonin Plasma Membrane Transport Proteins
-* Stress, Psychological
-* Telomere Shortening
-|keywords=* Cellular senescence
-* Depression
-* Epigenetic clock
-* Genetic aging
-* Life extension
-* Neurophenomenology
-* Psilocybin
-* Rejuvenation
-* Rumination
-* Senotherapy
-* Telomeres
-|full-text-url=https://sci-hub.do/10.1016/j.mehy.2019.109406
-}}
-==SMAD1==
-{{medline-entry
-|title=TGFB1-Mediated Gliosis in Multiple Sclerosis Spinal Cords Is Favored by the Regionalized Expression of HOXA5 and the Age-Dependent Decline in Androgen Receptor Ligands.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31779094
-|mesh-terms=* Age Factors
-* Aged
-* Aging
-* Brain
-* Data Mining
-* Databases, Genetic
-* Disease Progression
-* Female
-* Gene Expression Profiling
-* Gliosis
-* Homeodomain Proteins
-* Humans
-* Ligands
-* Male
-* Middle Aged
-* Multiple Sclerosis
-* Proteomics
-* Receptors, Androgen
-* Sequence Analysis, RNA
-* Signal Transduction
-* Smad1 Protein
-* Spinal Cord
-* Transforming Growth Factor beta1
-* Up-Regulation
-|keywords=* androgen receptor
-* astrocytes
-* homeobox A5
-* multiple sclerosis
-* spinal cord
-* transforming growth factor beta 1
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6928867
-}}
-==SMAD2==
-{{medline-entry
-|title=Prostate epithelial-specific expression of activated PI3K drives stromal collagen production and accumulation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31674011
-|mesh-terms=* Aging
-* Animals
-* Class I Phosphatidylinositol 3-Kinases
-* Collagen
-* Disease Models, Animal
-* Disease Progression
-* Epithelium
-* Male
-* Mice, Mutant Strains
-* Phosphorylation
-* Prostate
-* Prostatic Hyperplasia
-* Prostatic Intraepithelial Neoplasia
-* Prostatic Neoplasms
-* Signal Transduction
-* Smad2 Protein
-* Stromal Cells
-* Transforming Growth Factor beta
-|keywords=* PIK3CA
-* cancer
-* collagen
-* fibrosis
-* mouse model
-* prostate
-* stroma
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7071816
-}}
-==SMAD3==
-{{medline-entry
-|title=Sirtuin 6 deficiency transcriptionally up-regulates TGF-β signaling and induces fibrosis in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31744885
-|mesh-terms=* Aging
-* Animals
-* Fibroblasts
-* Fibrosis
-* Gene Deletion
-* Male
-* Mice
-* Myocardium
-* Myofibroblasts
-* Signal Transduction
-* Sirtuins
-* Smad3 Protein
-* Transcriptional Activation
-* Transforming Growth Factor beta
-|keywords=* SIRT6 deacetylase
-* SMAD transcription factor
-* SMAD3
-* TGF-beta signaling
-* aging
-* aging-associated fibrosis
-* caloric restriction
-* cardiac disease
-* extracellular matrix (ECM)
-* fibrosis
-* sirtuin
-* transforming growth factor beta (TGF-beta)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6956532
-}}
-==SMN2==
-{{medline-entry
-|title=Age-dependent SMN expression in disease-relevant tissue and implications for SMA treatment.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31589162
-|mesh-terms=* Aging
-* Autopsy
-* Cell Survival
-* Female
-* Humans
-* Male
-* Motor Neurons
-* Muscular Atrophy, Spinal
-* Oligodeoxyribonucleotides, Antisense
-* Spinal Cord
-* Survival of Motor Neuron 2 Protein
-|keywords=* Development
-* Neurodegeneration
-* Neurodevelopment
-* Neuromuscular disease
-* Neuroscience
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6819103
-}}
-==SMS==
-{{medline-entry
-|title=Does a Live Performance Impact Synchronization to Musical Rhythm in Cognitively Impaired Elderly?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33104027
-|keywords=* Aging
-* Alzheimer’s disease
-* cognitive impairment
-* dementia
-* motor activity
-* music therapy
-* social interaction
-|full-text-url=https://sci-hub.do/10.3233/JAD-200521
-}}
-{{medline-entry
-|title=Testing the effectiveness of physical activity advice delivered via text messaging vs. human phone advisors in a Latino population: The On The Move randomized controlled trial design and methods.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32659437
-|keywords=* Aging
-* Digital health
-* Latino
-* Physical activity
-* Text-messaging
-* mHealth
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7351675
-}}
-==SNAP25==
-{{medline-entry
-|title=The Biological Foundations of Sarcopenia: Established and Promising Markers.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31457015
-|keywords=* SNAP25
-* aging
-* biomarkers
-* neuromuscular junction
-* sarcopenia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6700259
-}}
-==SNCA==
-{{medline-entry
-|title=Behavioural and dopaminergic changes in double mutated human A30P*A53T alpha-synuclein transgenic mouse model of Parkinson´s disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31758049
-|mesh-terms=* Aging
-* Alanine
-* Amino Acid Substitution
-* Animals
-* Behavior, Animal
-* Disease Models, Animal
-* Dopaminergic Neurons
-* Humans
-* Locomotion
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Mice, Transgenic
-* Mutation, Missense
-* Parkinson Disease
-* Proline
-* Threonine
-* alpha-Synuclein
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6874660
-}}
-==SND1==
-{{medline-entry
-|title=[Downregulation of [[SND1]] Expression Accelerates Cell Senescence of Human Diploid Fibroblasts 2BS via Modulating the SASP].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32543144
-|mesh-terms=* Cellular Senescence
-* Diploidy
-* Down-Regulation
-* Endonucleases
-* Fibroblasts
-* Humans
-* Nuclear Proteins
-|keywords=* Aging
-* Cellular senescent
-* SND1
-* Senescence-associated-secretory-phenotype
-|full-text-url=https://sci-hub.do/10.12182/20200560504
-}}
-==SOD1==
-{{medline-entry
-|title=[[SOD1]], more than just an antioxidant.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33259795
-|keywords=* Aging
-* Cancer
-* Neurodegenerative diseases
-* Post-translational modifications
-* Superoxide dismutase 1
-|full-text-url=https://sci-hub.do/10.1016/j.abb.2020.108701
-}}
-{{medline-entry
-|title=The Exacerbation of Aging and Oxidative Stress in the Epididymis of [i]Sod1[/i] Null Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32054065
-|keywords=* 4-hydroxynonenal
-* 8-hydroxyguanosine
-* aging
-* epididymis
-* oxidative stress
-* reactive oxygen species
-* spermatozoa
-* superoxide dismutase
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7071042
-}}
-{{medline-entry
-|title=Alterations in lipid metabolism of spinal cord linked to amyotrophic lateral sclerosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31406145
-|mesh-terms=* Aging
-* Amyotrophic Lateral Sclerosis
-* Animals
-* Cardiolipins
-* Cholesterol Esters
-* Disease Models, Animal
-* Disease Progression
-* Fatty Acids, Unsaturated
-* Female
-* Humans
-* Lipid Droplets
-* Lipid Metabolism
-* Lipidomics
-* Male
-* Mass Spectrometry
-* Motor Cortex
-* Motor Neurons
-* Mutation
-* Oxidative Stress
-* Rats
-* Rats, Transgenic
-* Spinal Cord
-* Superoxide Dismutase-1
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691112
-}}
-==SOD2==
-{{medline-entry
-|title=Astaxanthin Counteracts Vascular Calcification In Vitro Through an Early Up-Regulation of [[SOD2]] Based on a Transcriptomic Approach.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33198315
-|keywords=* aortic calcification
-* astaxanthin
-* chronic kidney disease
-* chronic kidney disease-mineral bone disorder
-* oxidative stress
-* reactive oxygen species
-* senescence
-* vascular calcification
-* vascular smooth muscle cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7698184
-}}
-{{medline-entry
-|title=Alginate Oligosaccharide Prevents against D-galactose-mediated Cataract in C57BL/6J Mice via Regulating Oxidative Stress and Antioxidant System.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33153341
-|keywords=* Cataract
-* D-galactose
-* aging
-* alginate oligosaccharide
-* oxidative stress
-|full-text-url=https://sci-hub.do/10.1080/02713683.2020.1842456
-}}
-{{medline-entry
-|title=Protoflavones in melanoma therapy: Prooxidant and pro-senescence effect of protoapigenone and its synthetic alkyl derivative in A375 cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32931795
-|mesh-terms=* Antineoplastic Agents, Phytogenic
-* Autophagy
-* Biomarkers
-* Cell Cycle
-* Cell Line, Tumor
-* Cellular Senescence
-* Cyclohexanones
-* Flavones
-* Humans
-* Melanoma
-* Reactive Oxygen Species
-* Superoxide Dismutase
-* beta-Galactosidase
-|keywords=* Alkyl protoflavone
-* Flavonoid
-* Melanoma
-* Protoapigenone
-* Semi-synthesis
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2020.118419
-}}
-{{medline-entry
-|title=Ginsenoside Rg1 protects against Sca-1  HSC/HPC cell aging by regulating the SIRT1-FOXO3 and SIRT3-[[SOD2]] signaling pathways in a γ-ray irradiation-induced aging mice model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32765665
-|keywords=* SIRT1
-* SIRT3
-* aging
-* ginsenoside Rg1
-* hematopoietic progenitor cells
-* hematopoietic stem cells
-* senescence
-* γ-ray irradiation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388550
-}}
-{{medline-entry
-|title=Almond Skin Extracts and Chlorogenic Acid Delay Chronological Aging and Enhanced Oxidative Stress Response in Yeast.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32481725
-|keywords=* 8-Oxo-guanine
-* aging
-* almond
-* chlorogenic acid
-* lipid peroxidation
-* mitochondria
-* oxidative stress
-* protein carbonylation
-* sirtuin
-* superoxide dismutase
-* yeast
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7345664
-}}
-{{medline-entry
-|title=Opposing p53 and mTOR/AKT promote an in vivo switch from apoptosis to senescence upon telomere shortening in zebrafish.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32427102
-|keywords=* AKT
-* aging
-* apoptosis
-* cell biology
-* p53
-* regenerative medicine
-* senescence
-* stem cells
-* telomeres
-* zebrafish
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7237213
-}}
-{{medline-entry
-|title=Bioactive peptides derived from crimson snapper and in vivo anti-aging effects on fat diet-induced high fat Drosophila melanogaster.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31844865
-|mesh-terms=* Aging
-* Animal Scales
-* Animals
-* Catalase
-* Diet, High-Fat
-* Disease Models, Animal
-* Drosophila Proteins
-* Drosophila melanogaster
-* Female
-* Fish Proteins
-* Fishes
-* Humans
-* Longevity
-* Male
-* Malondialdehyde
-* Oxidative Stress
-* Peptides
-* Superoxide Dismutase
-|full-text-url=https://sci-hub.do/10.1039/c9fo01414d
-}}
-{{medline-entry
-|title=Ellagic acid prolongs the lifespan of Drosophila melanogaster.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31786733
-|keywords=* Drosophila melanogaster
-* Ellagic acid
-* Gene expression
-* Longevity
-* Stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7031466
-}}
-{{medline-entry
-|title=Chlorella vulgaris modulates the expression of senescence-associated genes in replicative senescence of human diploid fibroblasts.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31642042
-|mesh-terms=* Antioxidants
-* Catalase
-* Cell Differentiation
-* Cell Proliferation
-* Cells, Cultured
-* Cellular Senescence
-* Chlorella vulgaris
-* DNA Damage
-* Diploidy
-* Fibroblasts
-* Gene Expression
-* Genes, p53
-* Humans
-* Male
-* Mitogen-Activated Protein Kinase 14
-* Molecular Chaperones
-* Primary Cell Culture
-* Signal Transduction
-* Superoxide Dismutase
-* Superoxide Dismutase-1
-|keywords=* Chlorella vulgaris
-* Fibroblasts
-* Replicative senescence
-* Senescence-associated genes
-|full-text-url=https://sci-hub.do/10.1007/s11033-019-05140-8
-}}
-{{medline-entry
-|title=Age-Associated Changes in Antioxidants and Redox Proteins of Rat Heart.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31647296
-|mesh-terms=* Aging
-* Animals
-* Antioxidants
-* Glutathione Peroxidase
-* Male
-* Myocardium
-* Oxidation-Reduction
-* Rats
-* Rats, Wistar
-* Superoxide Dismutase
-|full-text-url=https://sci-hub.do/10.33549/physiolres.934170
-}}
-{{medline-entry
-|title=Impact of curcumin on replicative and chronological aging in the Saccharomyces cerevisiae yeast.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31659616
-|keywords=* Aging
-* Curcumin
-* Hypertrophy
-* Oxidative stress
-* Yeast
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6942599
-}}
-==SOX13==
-{{medline-entry
-|title=In silico analysis of human renin gene-gene interactions and neighborhood topologically associated domains suggests breakdown of insulators contribute to ageing-associated diseases.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31520345
-|mesh-terms=* Aging
-* Computer Simulation
-* Epistasis, Genetic
-* Humans
-* Promoter Regions, Genetic
-* Renin
-|keywords=* Aging
-* Diseases of aging
-* Gene expression
-* Gene–gene interaction
-* Genomics
-* Longevity
-* Renin-angiotensin system
-* Topologically associated domains
-|full-text-url=https://sci-hub.do/10.1007/s10522-019-09834-1
-}}
-==SOX2==
-{{medline-entry
-|title=Multiple nanosecond pulsed electric fields stimulation with conductive poly(l-lactic acid)/carbon nanotubes films maintains the multipotency of mesenchymal stem cells during prolonged in vitro culture.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32592324
-|keywords=* cell physical stimulus
-* differentiation
-* mesenchymal stem cells
-* multipotency
-* nanosecond pulsed electric fields
-* senescence
-|full-text-url=https://sci-hub.do/10.1002/term.3088
-}}
-{{medline-entry
-|title=Subpopulations of miniature pig mesenchymal stromal cells with different differentiation potentials differ in the expression of octamer-binding transcription factor 4 and sex determining region Y-box 2.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32054231
-|keywords=* Aging
-* Mesenchymal Stromal Cell (MSC) Subpopulations
-* Miniature Pig
-* Octamerbinding Transcription Factor 4 (OCT4)
-* Sex Determining Region Y-box 2 (SOX2)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7054621
-}}
-{{medline-entry
-|title=Increased Type I and Decreased Type II Hair Cells after Deletion of Sox2 in the Developing Mouse Utricle.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31678344
-|mesh-terms=* Aging
-* Animals
-* Cell Count
-* Cell Differentiation
-* Cell Lineage
-* Hair Cells, Vestibular
-* Mice
-* Mice, Knockout
-* Mice, Transgenic
-* SOXB1 Transcription Factors
-* Saccule and Utricle
-|keywords=* SOX2
-* balance disorder
-* hair cell
-* utricle
-* vestibule
-|full-text-url=https://sci-hub.do/10.1016/j.neuroscience.2019.09.027
-}}
-==SOX4==
-{{medline-entry
-|title=Age-induced accumulation of methylmalonic acid promotes tumour progression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32814897
-|mesh-terms=* Adult
-* Aged
-* Aging
-* Animals
-* Cell Line, Tumor
-* Disease Progression
-* Female
-* Gene Expression Regulation, Neoplastic
-* Humans
-* Male
-* Methylmalonic Acid
-* Mice
-* Middle Aged
-* Neoplasm Invasiveness
-* Neoplasm Metastasis
-* Neoplasms
-* SOXC Transcription Factors
-* Signal Transduction
-* Transcriptome
-* Transforming Growth Factor beta
-|full-text-url=https://sci-hub.do/10.1038/s41586-020-2630-0
-}}
-==SOX9==
-{{medline-entry
-|title=Positive Effects of a Young Systemic Environment and High Growth Differentiation Factor 11 Levels on Chondrocyte Proliferation and Cartilage Matrix Synthesis in Old Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32067417
-|mesh-terms=* Adolescent
-* Aged
-* Aging
-* Animals
-* Arthroplasty, Replacement, Knee
-* Bone Morphogenetic Proteins
-* Cartilage, Articular
-* Cell Proliferation
-* Chondrocytes
-* Collagen Type II
-* Collagen Type X
-* Core Binding Factor Alpha 1 Subunit
-* Extracellular Matrix
-* Female
-* Growth Differentiation Factors
-* Humans
-* In Vitro Techniques
-* Knee Joint
-* Male
-* Matrix Metalloproteinase 13
-* Mice
-* Osteoarthritis, Knee
-* Parabiosis
-* Phosphorylation
-* RNA, Messenger
-* Reverse Transcriptase Polymerase Chain Reaction
-* SOX9 Transcription Factor
-* Smad2 Protein
-* Smad3 Protein
-* Stifle
-* Young Adult
-|full-text-url=https://sci-hub.do/10.1002/art.41230
-}}
-==SPARC==
-{{medline-entry
-|title=[[SPARC]] Metrics Provide Mobility Smoothness Assessment in Oldest-Old With and Without a History of Falls: A Case Control Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32587523
-|keywords=* aging
-* falls
-* functional mobility
-* movement smoothness
-* oldest-old
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7298141
-}}
-{{medline-entry
-|title=Reduced fibrillar collagen accumulation in skeletal muscle of secreted protein acidic and rich in cysteine ([[SPARC]])-null mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31582603
-|mesh-terms=* Aging
-* Animals
-* Fibrillar Collagens
-* Gene Expression
-* Male
-* Mice
-* Mice, Knockout
-* Muscle, Skeletal
-* Myofibrils
-* Osteonectin
-|keywords=* Secreted protein acidic and rich in cysteine
-* collagen
-* fibrosis
-* myofiber
-* skeletal muscle
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6895640
-}}
-==SPR==
-{{medline-entry
-|title=Regulation of lifespan by neural excitation and REST.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31619788
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* DNA-Binding Proteins
-* Forkhead Transcription Factors
-* Humans
-* Longevity
-* Mice
-* Mice, 129 Strain
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Mice, Transgenic
-* Neurons
-* RNA Interference
-* RNA-Binding Proteins
-* Repressor Proteins
-* Transcription Factors
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6893853
-}}
-==SPRTN==
-{{medline-entry
-|title=Tandem Deubiquitination and Acetylation of [[SPRTN]] Promotes DNA-Protein Crosslink Repair and Protects against Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32649882
-|mesh-terms=* Acetylation
-* Aging
-* Animals
-* Cell Line
-* DNA Damage
-* DNA Repair
-* DNA-Binding Proteins
-* Deubiquitinating Enzymes
-* Endopeptidases
-* Female
-* Genomic Instability
-* HEK293 Cells
-* Humans
-* Male
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Phosphorylation
-* Protein Domains
-* Protein Processing, Post-Translational
-* Ubiquitination
-|keywords=* DNA repair
-* DNA-protein crosslink
-* SPRTN
-* Top1cc
-* VCPIP1/VCIP135
-* acetylation
-* aging
-* genomic instability
-* metalloprotease
-* ubiquitination
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7484104
-}}
-==SPRY1==
-{{medline-entry
-|title=Sprouty1 Prevents Cellular Senescence Maintaining Proliferation and Differentiation Capacity of Human Adipose Stem/Progenitor Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32304210
-|keywords=* Adipogenesis
-* Adipose stem cell
-* Obesity
-* Senescence
-* Sprouty1
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7662188
-}}
-{{medline-entry
-|title=Mechanism of [[SPRY1]] methylation regulating natural aging of skin epidermal cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31483543
-|keywords=* SPRY1
-* methylation
-* natural aging
-* skin epidermal aging
-|full-text-url=https://sci-hub.do/10.1111/jocd.13126
-}}
-==SQSTM1==
-{{medline-entry
-|title=The selective autophagy receptor [[SQSTM1]]/p62 improves lifespan and proteostasis in an evolutionarily conserved manner.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32041473
-|keywords=* Aging
-* C. elegans
-* Drosophila
-* SQST-1
-* SQSTM1
-* aggrephagy
-* heat shock
-* mitophagy
-* p62
-* proteostasis
-* ref(2)P
-* selective autophagy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7138197
-}}
-==SRC==
-{{medline-entry
-|title=Metabolic characteristics of CD8  T cell subsets in young and aged individuals are not predictive of functionality.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32504069
-|mesh-terms=* Adult
-* Aged
-* Aging
-* Animals
-* CD8-Positive T-Lymphocytes
-* Cell Differentiation
-* Cell Proliferation
-* Disease Models, Animal
-* Female
-* Humans
-* Immunologic Memory
-* Influenza A virus
-* Influenza, Human
-* Male
-* Mice
-* Microscopy, Electron, Transmission
-* Mitochondria
-* T-Lymphocyte Subsets
-* Young Adult
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7275080
-}}
-==SRD5A2==
-{{medline-entry
-|title=Extract of Plumbago zeylanica enhances the growth of hair follicle dermal papilla cells with down-regulation of 5α-reductase type II.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32125089
-|keywords=*
-P zeylanica
-* 5α-reductase
-* dermal papilla
-* hair
-* plumbagin
-* senescence
-|full-text-url=https://sci-hub.do/10.1111/jocd.13355
-}}
-==SRF==
-{{medline-entry
-|title=Changes in snail and [[SRF]] expression in the kidneys of diabetic rats during ageing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31668740
-|mesh-terms=* Aging
-* Animals
-* Diabetes Mellitus, Experimental
-* Diabetic Nephropathies
-* Gene Expression Regulation
-* Kidney
-* Male
-* Rats
-* Rats, Sprague-Dawley
-* Snail Family Transcription Factors
-* Transcription Factors
-|keywords=* Diabetic nephropathy
-* Renal fibrosis
-* SRF
-* Snail
-|full-text-url=https://sci-hub.do/10.1016/j.acthis.2019.151460
-}}
-{{medline-entry
-|title=Mechanosensitive transcriptional coactivators MRTF-A and YAP/TAZ regulate nucleus pulposus cell phenotype through cell shape.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31638828
-|mesh-terms=* Actins
-* Adaptor Proteins, Signal Transducing
-* Aging
-* Biomechanical Phenomena
-* Cells, Cultured
-* Cytoskeleton
-* Gene Expression Regulation
-* Humans
-* Hydrogels
-* Intervertebral Disc Degeneration
-* Nucleus Pulposus
-* RNA Interference
-* Trans-Activators
-* Transcription Factors
-* rho-Associated Kinases
-|keywords=* F-actin
-* SRF
-* TEAD
-* intervertebral disc
-* mechanotransduction
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6894097
-}}
-==SRL==
-{{medline-entry
-|title=Income dividends and subjective survival in a Cherokee Indian cohort: a quasi-experiment.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32432936
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* Cohort Studies
-* Female
-* Humans
-* Income
-* Indians, South American
-* Longevity
-* Male
-* Middle Aged
-* North Carolina
-* Social Class
-* Surveys and Questionnaires
-* Survival Analysis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7250001
-}}
-==SRM==
-{{medline-entry
-|title=[Geriatric specificities of localized renal cell carcinoma].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31771769
-|mesh-terms=* Age Factors
-* Aged
-* Carcinoma, Renal Cell
-* Geriatric Assessment
-* Humans
-* Kidney Neoplasms
-|keywords=* Cancer du rein
-* Diagnosis
-* Diagnostic
-* Elderly
-* Geriatrics
-* Gériatrie
-* Personne âgée
-* Petite masse rénale
-* Renal cell carcinoma
-* Small renal mass
-* Traitement
-* Treatment
-|full-text-url=https://sci-hub.do/10.1016/j.purol.2019.08.281
-}}
-==SSB==
-{{medline-entry
-|title=Modelling the Effects of Beverage Substitution during Adolescence on Later Obesity Outcomes in Early Adulthood: Results from the Raine Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31816850
-|mesh-terms=* Adolescent
-* Adolescent Nutritional Physiological Phenomena
-* Aging
-* Humans
-* Models, Biological
-* Obesity
-* Odds Ratio
-* Risk Factors
-* Sugar-Sweetened Beverages
-* Young Adult
-|keywords=* obesity
-* substitution modelling
-* sugar-sweetened beverages
-* waist circumference
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6950484
-}}
-==SST==
-{{medline-entry
-|title=The distance to death perceptions of older adults explain why they age in place: A theoretical examination.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32972627
-|keywords=* Agency- or belonging-related
-* Distance to death, aging in place
-* Emotions
-* Residential mobility
-* Socioemotional selectivity theory
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7489887
-}}
-{{medline-entry
-|title=Population Segmentation Based on Healthcare Needs: Validation of a Brief Clinician-Administered Tool.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32607929
-|keywords=* aging
-* health services research
-* psychometrics
-|full-text-url=https://sci-hub.do/10.1007/s11606-020-05962-4
-}}
-{{medline-entry
-|title=Examination on how emotion regulation mediates the relationship between future time perspective and well-being: a counter-evidence to the socioemotional selectivity theory.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32158369
-|keywords=* Aging
-* Emotion regulation
-* Future time perspective
-* Socioemotional selectivity theory
-* Time left in life
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7040126
-}}
-==STAT1==
-{{medline-entry
-|title=[[STAT1]]-p53-p21axis-dependent stress-induced progression of chronic nephrosis in adriamycin-induced mouse model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32953802
-|keywords=* Adriamycin
-* STAT1
-* chronic nephrosis (CN)
-* mitogen-activated protein kinase
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7475511
-}}
-{{medline-entry
-|title=Age-Dependent and -Independent Effects of Perivascular Adipose Tissue and Its Paracrine Activities during Neointima Formation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31906225
-|mesh-terms=* Adipose Tissue
-* Aging
-* Animals
-* Carotid Arteries
-* Carotid Artery Diseases
-* Carotid Artery Injuries
-* Humans
-* Mice
-* Mice, Mutant Strains
-* Neointima
-* Paracrine Communication
-* STAT1 Transcription Factor
-|keywords=* aging
-* atherosclerosis
-* neointima formation
-* perivascular adipose tissue
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6981748
-}}
-{{medline-entry
-|title=Legumain-deficient macrophages promote senescence of tumor cells by sustaining JAK1/[[STAT1]] activation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31857155
-|mesh-terms=* Animals
-* Bone Marrow Transplantation
-* Breast Neoplasms
-* Cell Cycle Proteins
-* Cell Line, Tumor
-* Cellular Senescence
-* Disease Models, Animal
-* Female
-* Gene Expression Regulation, Neoplastic
-* Humans
-* Integrin alphaVbeta3
-* Interleukin-1beta
-* Janus Kinase 1
-* Macrophage Activation
-* Macrophages
-* Mice
-* Mice, Knockout
-* STAT1 Transcription Factor
-* Signal Transduction
-|keywords=* Cellular senescence
-* Legumain
-* M1 polarization
-* Tumor-associated macrophage
-|full-text-url=https://sci-hub.do/10.1016/j.canlet.2019.12.013
-}}
-==STAT3==
-{{medline-entry
-|title=Dietary Restriction Suppresses Steatosis-Associated Hepatic Tumorigenesis in Hepatitis C Virus Core Gene Transgenic Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33083279
-|keywords=* Cyclin D1
-* NF-κB
-* STAT3
-* Senescence
-* p62/SQSTM1
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7548900
-}}
-{{medline-entry
-|title=Skeletal glucocorticoid signalling determines leptin resistance and obesity in aging mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33045434
-|keywords=* Aging
-* Appetite
-* Glucocorticoid
-* Leptin
-* Obesity
-* Osteoblast
-* Osteocyte
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7596342
-}}
-{{medline-entry
-|title=AMPK alleviates oxidative stress‑induced premature senescence via inhibition of NF-κB/[[STAT3]] axis-mediated positive feedback loop.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32882228
-|keywords=* AMPK
-* NF-κB/STAT3 signalling
-* Oxidative stress
-* SASP
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2020.111347
-}}
-{{medline-entry
-|title=Age-related loss of neural stem cell O-GlcNAc promotes a glial fate switch through [[STAT3]] activation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32848054
-|mesh-terms=* Aging
-* Animals
-* Cell Differentiation
-* Cell Proliferation
-* Computational Biology
-* Gene Expression Regulation
-* Glucosamine
-* Hippocampus
-* Mice
-* Neural Stem Cells
-* Neurogenesis
-* Neuroglia
-* STAT3 Transcription Factor
-* Sequence Analysis, RNA
-|keywords=* O-GlcNAcylation
-* aging
-* gliogenesis
-* neural stem cells
-* neurogenesis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7486730
-}}
-{{medline-entry
-|title=Cell Death by Gallotannin Is Associated with Inhibition of the JAK/STAT Pathway in Human Colon Cancer Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32714471
-|keywords=* Apoptosis
-* JAK/STAT
-* caspase
-* colon cancer
-* gallotannin
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7378856
-}}
-{{medline-entry
-|title=The effect of interleukin 6 deficiency on myocardial signal transduction pathways activation induced by bacterial lipopolysaccharide in young and old mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32693349
-|keywords=* Aging
-* For review: bacterial lipolisacharide (LPS)
-* Heart
-* Inflammation
-* Interleukin-6
-* Signal transduction
-|full-text-url=https://sci-hub.do/10.1016/j.advms.2020.06.006
-}}
-{{medline-entry
-|title=Silibinin and SARS-CoV-2: Dual Targeting of Host Cytokine Storm and Virus Replication Machinery for Clinical Management of COVID-19 Patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32517353
-|keywords=* IL-6
-* JAK
-* coronavirus
-* cytokine storm
-* remdesivir
-* senescence
-* stat3
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7356916
-}}
-{{medline-entry
-|title=Implication of JAK1/[[STAT3]]/SOCS3 Pathway in Aging of Cerebellum of Male Rat: Histological and Molecular study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32483368
-|mesh-terms=* Aging
-* Animals
-* Caspase 3
-* Cerebellum
-* Glial Fibrillary Acidic Protein
-* Glutathione
-* Immunohistochemistry
-* Janus Kinase 1
-* Male
-* Malondialdehyde
-* Microscopy, Electron
-* Rats
-* Rats, Wistar
-* STAT3 Transcription Factor
-* Signal Transduction
-* Suppressor of Cytokine Signaling 3 Protein
-* Tumor Necrosis Factor-alpha
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7264275
-}}
-{{medline-entry
-|title=Atorvastatin-induced senescence of hepatocellular carcinoma is mediated by downregulation of hTERT through the suppression of the IL-6/[[STAT3]] pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32257389
-|keywords=* Cancer therapy
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7105491
-}}
-{{medline-entry
-|title=Deciphering the Molecular Mechanism of Spontaneous Senescence in Primary Epithelial Ovarian Cancer Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32012719
-|keywords=* aging biomarkers
-* cancer biology
-* cellular senescence
-* epithelial ovarian cancer
-* oxidative stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072138
-}}
-{{medline-entry
-|title=Persistent Activation of [[STAT3]] Pathway in the Retina Induced Vision Impairment and Retinal Degenerative Changes in Ageing Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31884637
-|mesh-terms=* Aging
-* Animals
-* Mice
-* Mice, Inbred C57BL
-* Retina
-* Retinal Degeneration
-* STAT3 Transcription Factor
-* Suppressor of Cytokine Signaling 3 Protein
-* Suppressor of Cytokine Signaling Proteins
-* Uveitis
-|keywords=* EAU
-* Experimental autoimmune uveitis
-* Retinal dystrophies
-* SOCS3
-* STAT3
-* Transgenic mouse
-* Uveitis
-|full-text-url=https://sci-hub.do/10.1007/978-3-030-27378-1_58
-}}
-{{medline-entry
-|title=Interleukin-10 induces senescence of activated hepatic stellate cells via [[STAT3]]-p53 pathway to attenuate liver fibrosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31730896
-|keywords=* Hepatic stellate cells
-* Interleukin-10
-* Liver fibrosis
-* Senescence
-* Signal pathway
-|full-text-url=https://sci-hub.do/10.1016/j.cellsig.2019.109445
-}}
-==STC2==
-{{medline-entry
-|title=Genome-wide Associations Reveal Human-Mouse Genetic Convergence and Modifiers of Myogenesis, CPNE1 and [[STC2]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31761296
-|mesh-terms=* Adult
-* Aged
-* Aging
-* Animals
-* Body Composition
-* Body Weight
-* Calcium-Binding Proteins
-* Case-Control Studies
-* Female
-* Follow-Up Studies
-* Genome-Wide Association Study
-* Glycoproteins
-* Humans
-* Intercellular Signaling Peptides and Proteins
-* Male
-* Mice
-* Middle Aged
-* Muscle Development
-* Muscle, Skeletal
-* Quantitative Trait Loci
-* Thinness
-|keywords=* UK Biobank
-* human and mouse GWAS
-* sarcopenia
-* skeletal muscle
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6904802
-}}
-==STIM1==
-{{medline-entry
-|title=Progerin in muscle leads to thermogenic and metabolic defects via impaired calcium homeostasis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31833196
-|mesh-terms=* Animals
-* Calcium
-* Calnexin
-* Cell Nucleus
-* Disease Models, Animal
-* Endoplasmic Reticulum
-* Endoplasmic Reticulum Stress
-* Lamin Type A
-* Mice
-* Mice, Knockout
-* Microscopy, Electron, Transmission
-* Muscle Proteins
-* Muscle, Skeletal
-* Muscular Dystrophies
-* Mutation
-* Myoblasts
-* ORAI1 Protein
-* Progeria
-* Proteolipids
-* Stromal Interaction Molecule 1
-* Thermogenesis
-* Up-Regulation
-|keywords=* aging
-* calcium homeostasis
-* lamin A
-* muscular dystrophy
-* progeria
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996945
-}}
-==STS==
-{{medline-entry
-|title=Delayed Impairment of Postural, Physical, and Muscular Functions Following Downhill Compared to Level Walking in Older People.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33192547
-|keywords=* aging
-* balance
-* falls
-* fatigue
-* functional performance
-* muscle damage
-* walking
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7609421
-}}
-{{medline-entry
-|title=Autophagy displays divergent roles during intermittent amino acid starvation and toxic stress-induced senescence in cultured skeletal muscle cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33022071
-|keywords=* autophagy
-* caspase
-* cell death
-* remodeling
-* senescence
-|full-text-url=https://sci-hub.do/10.1002/jcp.30079
-}}
-{{medline-entry
-|title=The WRKY53 transcription factor enhances stilbene synthesis and disease resistance by interacting with MYB14 and MYB15 in Chinese wild grape.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32080737
-|keywords=* Chinese wild grape (Vitis quinquangularis)
-* WRKY transcription factor
-* disease resistance
-* leaf senescence
-* stilbene
-* transcriptional regulation
-|full-text-url=https://sci-hub.do/10.1093/jxb/eraa097
-}}
-{{medline-entry
-|title=On the role of ageing and musculoskeletal pain on dynamic balance in manual workers.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31733466
-|mesh-terms=* Aged
-* Aging
-* Female
-* Humans
-* Male
-* Middle Aged
-* Muscle, Skeletal
-* Musculoskeletal Pain
-* Occupational Diseases
-* Postural Balance
-|keywords=* Discomfort
-* Lower extremity function
-* Posturography
-* Sit-to-stand
-|full-text-url=https://sci-hub.do/10.1016/j.jelekin.2019.102374
-}}
-==SUCNR1==
-{{medline-entry
-|title=[The effect of Mexidol on cerebral mitochondriogenesis at a young age and during aging].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32105271
-|mesh-terms=* Age Factors
-* Aging
-* Animals
-* Male
-* Mitochondria
-* Neurodegenerative Diseases
-* Picolines
-* Rats
-* Receptors, G-Protein-Coupled
-* Transcription Factors
-|keywords=* Western blot analysis
-* aging
-* cerebral mitochondriogenesis
-* mexidol
-* mitochondrial dysfunction
-* rats
-* respiratory enzyme subunits
-* succinate receptor
-* transcriptional coactivator PGC-1α
-|full-text-url=https://sci-hub.do/10.17116/jnevro202012001162
-}}
-==SUGCT==
-{{medline-entry
-|title=Knockout of the non-essential gene [[SUGCT]] creates diet-linked, age-related microbiome disbalance with a diabetes-like metabolic syndrome phenotype.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31722069
-|mesh-terms=* Aging
-* Animals
-* Anti-Bacterial Agents
-* Bacteria
-* Carnitine
-* Coenzyme A-Transferases
-* Dietary Supplements
-* Feces
-* Gastrointestinal Microbiome
-* Humans
-* Kidney
-* Lipid Metabolism
-* Liver
-* Lysine
-* Metabolic Syndrome
-* Metabolome
-* Mice
-* Mice, Knockout
-* Obesity
-* Tryptophan
-|keywords=* C7orf10
-* Glutaric aciduria type 3 (GA3)
-* Gut microflora
-* Lipids
-* Metabolomics
-* Obesity
-* Sugct
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7426296
-}}
-==SUV39H1==
-{{medline-entry
-|title=Increase in hippocampal histone H3K9me3 is negatively correlated with memory in old male mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31760560
-|keywords=* Aging
-* H3K9me3
-* Hippocampus
-* IEGs
-* Memory
-* SUV39H1
-|full-text-url=https://sci-hub.do/10.1007/s10522-019-09850-1
-}}
-==SYK==
-{{medline-entry
-|title=miR-25-3p promotes endothelial cell angiogenesis in aging mice via TULA-2/[[SYK]]/VEGFR-2 downregulation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33201836
-|keywords=* TULA-2
-* aging
-* angiogenesis
-* endothelial cell
-* miR-25-3p
-|full-text-url=https://sci-hub.do/10.18632/aging.103834
-}}
-{{medline-entry
-|title=Identification of [[SYK]] inhibitor, R406 as a novel senolytic agent.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32379705
-|keywords=* FAK
-* apoptosis
-* cellular senescence
-* p38
-* senolytics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244031
-}}
-==SYNE1==
-{{medline-entry
-|title=Nesprin-1 impact on tumorigenic cell phenotypes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31741263
-|mesh-terms=* Actins
-* Carcinogenesis
-* Cell Line, Tumor
-* Cell Nucleus
-* Cytoskeletal Proteins
-* Gene Expression
-* Gene Expression Regulation, Neoplastic
-* Humans
-* Microfilament Proteins
-* Nerve Tissue Proteins
-* Nuclear Envelope
-* Phenotype
-|keywords=* Cancer
-* Cellular senescence
-* Genome stability
-* Nesprin-1
-* Nuclear envelope
-|full-text-url=https://sci-hub.do/10.1007/s11033-019-05184-w
-}}
-==TAAR1==
-{{medline-entry
-|title=Minimal Age-Related Alterations in Behavioral and Hematological Parameters in Trace Amine-Associated Receptor 1 ([[TAAR1]]) Knockout Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31399838
-|mesh-terms=* Age Factors
-* Animals
-* Anxiety
-* Dose-Response Relationship, Drug
-* Male
-* Mice
-* Mice, 129 Strain
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Receptors, G-Protein-Coupled
-* Sodium Chloride
-|keywords=* Aging
-* Anxiety
-* Hematology
-* Leukocytes
-* Neutrophils
-* TAAR1
-* Thyroid
-* Trace amines
-|full-text-url=https://sci-hub.do/10.1007/s10571-019-00721-4
-}}
-==TAS2R16==
-{{medline-entry
-|title=Taste receptor polymorphisms and longevity: a systematic review and meta-analysis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33170488
-|keywords=* Immune-inflammatory responses
-* Longevity
-* Meta-analysis
-* Taste receptors
-|full-text-url=https://sci-hub.do/10.1007/s40520-020-01745-3
-}}
-==TAS2R38==
-{{medline-entry
-|title=[[TAS2R38]] bitter taste receptor and attainment of exceptional longevity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31792278
-|mesh-terms=* Adolescent
-* Adult
-* Aged
-* Aged, 80 and over
-* Case-Control Studies
-* Female
-* Food Preferences
-* Gene Frequency
-* Genetic Variation
-* Haplotypes
-* Humans
-* Longevity
-* Male
-* Middle Aged
-* Receptors, G-Protein-Coupled
-* Taste
-* Taste Perception
-* Young Adult
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6889489
-}}
-==TAZ==
-{{medline-entry
-|title=Transcriptional Coactivator [[TAZ]] Negatively Regulates Tumor Suppressor p53 Activity and Cellular Senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31936650
-|keywords=* TAZ
-* cellular senescence
-* oncogene
-* p300
-* p53
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7016652
-}}
-==TBC1D5==
-{{medline-entry
-|title=[[TBC1D5]]-Catalyzed Cycling of Rab7 Is Required for Retromer-Mediated Human Papillomavirus Trafficking during Virus Entry.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32521275
-|keywords=* HPV
-* Rab7B
-* TBC1D5
-* functional genetics screen
-* proximity ligation assay
-* retrograde
-* retromer
-* senescence
-* traptamer
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7339955
-}}
-{{medline-entry
-|title=Retromer and [[TBC1D5]] maintain late endosomal RAB7 domains to enable amino acid-induced mTORC1 signaling.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31431476
-|mesh-terms=* Animals
-* Caenorhabditis elegans
-* Caenorhabditis elegans Proteins
-* Longevity
-* Mechanistic Target of Rapamycin Complex 1
-* Membrane Microdomains
-* Signal Transduction
-* rab GTP-Binding Proteins
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6719456
-}}
-==TBK1==
-{{medline-entry
-|title=Parkin overexpression alleviates cardiac aging through facilitating K63-polyubiquitination of [[TBK1]] to facilitate mitophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33164878
-|keywords=* Aging
-* K63-linked polyubiquitination
-* Mitophagy
-* Parkin
-* TBK1
-|full-text-url=https://sci-hub.do/10.1016/j.bbadis.2020.165997
-}}
-==TCF7L2==
-{{medline-entry
-|title=A myelin-related transcriptomic profile is shared by Pitt-Hopkins syndrome models and human autism spectrum disorder.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32015540
-|mesh-terms=* Aging
-* Animals
-* Autism Spectrum Disorder
-* Cell Count
-* DNA Fingerprinting
-* Facies
-* Gene Expression Regulation
-* Humans
-* Hyperventilation
-* Intellectual Disability
-* Methyl-CpG-Binding Protein 2
-* Mice
-* Mice, Knockout
-* Myelin Sheath
-* Oligodendroglia
-* PTEN Phosphohydrolase
-* Primary Cell Culture
-* Signal Transduction
-* Transcription Factor 4
-* Transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7065955
-}}
-==TEC==
-{{medline-entry
-|title=Vestibular function and cortical and sub-cortical alterations in an aging population.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32904672
-|keywords=* Aging
-* Cognition
-* Diffeomorphometry
-* Epidemiology
-* Eye-ear-nose-throat
-* MRI
-* Medical imaging
-* Shape
-* Vestibular
-* Volume
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7457317
-}}
-{{medline-entry
-|title=Metabolic Flexibility and Innate Immunity in Renal Ischemia Reperfusion Injury: The Fine Balance Between Adaptive Repair and Tissue Degeneration.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32733450
-|keywords=* cell death
-* innate immunity
-* kidney transplantation
-* mitochondria
-* senescence
-* tubular repair
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7358591
-}}
-{{medline-entry
-|title=Postnatal Involution and Counter-Involution of the Thymus.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32477366
-|keywords=* Myc
-* aging
-* cyclin D1
-* growth
-* involution
-* thymus
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7235445
-}}
-{{medline-entry
-|title=Gender Disparity Impacts on Thymus Aging and LHRH Receptor Antagonist-Induced Thymic Reconstitution Following Chemotherapeutic Damage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32194555
-|keywords=* aging
-* chemotherapy
-* gender
-* luteinizing hormone-releasing hormone
-* regeneration
-* sex hormone deprivation
-* thymic epithelial cell
-* thymus
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7062683
-}}
-{{medline-entry
-|title=Clonogenic Culture of Mouse Thymic Epithelial Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31396938
-|mesh-terms=* Aging
-* Animals
-* Cell Differentiation
-* Cell Line
-* Coculture Techniques
-* Colony-Forming Units Assay
-* DNA-Binding Proteins
-* Epithelial Cells
-* Flow Cytometry
-* Fluorescent Antibody Technique, Direct
-* Fluorescent Dyes
-* Immunomagnetic Separation
-* Mice
-* Mice, Knockout
-* Primary Cell Culture
-* Rhodamines
-* Self Tolerance
-* Staining and Labeling
-* Stem Cells
-* Thymus Gland
-|keywords=* Clonogenic assay
-* Thymic epithelial cells
-* Thymic epithelial stem cells
-* Thymus
-|full-text-url=https://sci-hub.do/10.1007/978-1-4939-9728-2_15
-}}
-==TEF==
-{{medline-entry
-|title=Expression of human HSP27 in yeast extends replicative lifespan and uncovers a hormetic response.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32189112
-|keywords=* Aging
-* Cancer
-* HSP27
-* Hormesis
-* Neurodegeneratve diseases
-* Proteasome
-|full-text-url=https://sci-hub.do/10.1007/s10522-020-09869-9
-}}
-==TERT==
-{{medline-entry
-|title=Telomeres and telomerase in risk assessment of cardiovascular diseases.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33171154
-|keywords=* Cardiovascular diseases
-* Senescence
-* Telomerase
-* Telomeres
-|full-text-url=https://sci-hub.do/10.1016/j.yexcr.2020.112361
-}}
-{{medline-entry
-|title=A 4-Base-Pair Core-Enclosing Helix in Telomerase RNA Is Essential for Activity and for Binding to the Telomerase Reverse Transcriptase Catalytic Protein Subunit.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33046533
-|keywords=* RNA
-* RNP
-* TERT
-* TLC1
-* senescence
-* telomerase
-* telomerase RNA
-* telomere
-* two-hybrid screening
-* yeast
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7685517
-}}
-{{medline-entry
-|title=Angiotensin inhibition and cellular senescence in the developing rat kidney.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33010296
-|keywords=* Apoptosis
-* Cellular senescence
-* Fetal development
-* Kidney
-* Renin-angiotensin system
-|full-text-url=https://sci-hub.do/10.1016/j.yexmp.2020.104551
-}}
-{{medline-entry
-|title=Decreased expression of [[TERT]] and telomeric proteins as human ovaries age may cause telomere shortening.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32856217
-|keywords=* Ovarian aging
-* TERT
-* Telomere
-* Telomere-binding proteins
-|full-text-url=https://sci-hub.do/10.1007/s10815-020-01932-1
-}}
-{{medline-entry
-|title=The secrets of telomerase: Retrospective analysis and future prospects.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32698073
-|mesh-terms=* Aging
-* Animals
-* Diabetes Mellitus
-* Humans
-* Neoplasms
-* Telomerase
-* Telomere Shortening
-|keywords=* Cancers
-* G-quadruplex formation
-* Metabolic disorders
-* TERT gene
-* Telomere-telomerase system
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2020.118115
-}}
-{{medline-entry
-|title=Gene expression in human mesenchymal stem cell aging cultures: modulation by short peptides.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32399807
-|keywords=* Cell aging
-* Genes
-* Human mesenchymal stem cells
-* Short peptides
-|full-text-url=https://sci-hub.do/10.1007/s11033-020-05506-3
-}}
-{{medline-entry
-|title=Unravelling Cellular Mechanisms of Stem Cell Senescence: An Aid from Natural Bioactive Molecules.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32244882
-|keywords=* cellular mechanisms
-* gene expression
-* nutraceuticals
-* oxidative stress
-* senescence
-* stem cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7150900
-}}
-{{medline-entry
-|title=Expression of telomerase reverse transcriptase positively correlates with duration of lithium treatment in bipolar disorder.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32114208
-|mesh-terms=* Adult
-* Aging
-* Antimanic Agents
-* Bipolar Disorder
-* Cellular Senescence
-* Female
-* Humans
-* Lithium
-* Lithium Compounds
-* Male
-* Middle Aged
-* Mitochondria
-* Oxidative Stress
-* Polymorphism, Single Nucleotide
-* Real-Time Polymerase Chain Reaction
-* Telomerase
-* Telomere
-* Telomere Homeostasis
-* Telomere Shortening
-|keywords=* Affective disorder
-* Aging
-* Mitochondria
-* Oxidative stress
-* TERT
-* Telomere
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7334059
-}}
-{{medline-entry
-|title=FAM96B inhibits the senescence of dental pulp stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32039527
-|keywords=* FAM96B
-* aging
-* dental pulp stem cells (DPSCs)
-* proteomic analysis
-|full-text-url=https://sci-hub.do/10.1002/cbin.11319
-}}
-{{medline-entry
-|title=Aging and biomarkers: Transcriptional levels evaluation of Osteopontin/miRNA-181a axis in hepatic tissue of rats in different age ranges.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32061643
-|keywords=* Aging
-* Long non-coding RNA
-* Osteopontin
-* Telomeres
-* miRNA
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110879
-}}
-{{medline-entry
-|title=Resveratrol inhibits adipocyte differentiation and cellular senescence of human bone marrow stromal stem cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31978617
-|keywords=* Adipogenesis
-* Antioxidant
-* Bone marrow adiposity
-* Bone marrow skeletal stromal cells
-* Cellular senescence
-* Osteogenesis
-|full-text-url=https://sci-hub.do/10.1016/j.bone.2020.115252
-}}
-{{medline-entry
-|title=Characterization of human telomerase reverse transcriptase immortalized anterior cruciate ligament cell lines.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31948601
-|mesh-terms=* Adolescent
-* Aged
-* Anterior Cruciate Ligament
-* Cell Differentiation
-* Cell Separation
-* Cells, Cultured
-* Humans
-* Mesenchymal Stem Cells
-* Telomerase
-|keywords=* Anterior cruciate ligament
-* Immortalization
-* Mesenchymal stem cells
-* Multilineage differentiation
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6962762
-}}
-{{medline-entry
-|title=Mitochondria, Telomeres and Telomerase Subunits.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31781563
-|keywords=* TERC
-* TERT
-* aging
-* mitochondria
-* telomerase
-* telomere
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6851022
-}}
-{{medline-entry
-|title=Towards Therapeutic Alternatives for Mercury Neurotoxicity in the Amazon: Unraveling the Pre-Clinical Effects of the Superfruit Açaí ([i]Euterpe oleracea[/i], Mart.) as Juice for Human Consumption.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31717801
-|mesh-terms=* Animals
-* Antioxidants
-* Behavior, Animal
-* Brain Chemistry
-* Euterpe
-* Fruit and Vegetable Juices
-* Lipid Peroxidation
-* Male
-* Mercury
-* Mice
-* Motor Skills
-* Neurotoxins
-* Plant Extracts
-* Telomere
-|keywords=* Euterpe
-* acai
-* aging
-* antioxidant
-* açaí
-* extract
-* intoxication
-* methylmercury
-* telomere
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6893510
-}}
-{{medline-entry
-|title=Replication Stress at Telomeric and Mitochondrial DNA: Common Origins and Consequences on Ageing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31597307
-|mesh-terms=* Aging
-* Animals
-* Cellular Senescence
-* DNA Damage
-* DNA Replication
-* DNA, Mitochondrial
-* Epigenesis, Genetic
-* Humans
-* Mitochondria
-* Oxidative Stress
-* Stress, Physiological
-* Telomere
-* Telomere Homeostasis
-* Telomere Shortening
-|keywords=* G-quadruplex
-* R-loop
-* ageing
-* helicase
-* mitochondria
-* replication stress
-* senescence
-* telomere
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6801922
-}}
-{{medline-entry
-|title=Telomerase Biology Associations Offer Keys to Cancer and Aging Therapeutics.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31544708
-|keywords=* Aging
-* TERT
-* associates
-* cancer
-* cell cycle
-* diseases
-* oncogenes
-* viral infection.
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7403649
-}}
-{{medline-entry
-|title=Transient induction of telomerase expression mediates senescence and reduces tumorigenesis in primary fibroblasts.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31481614
-|mesh-terms=* Animals
-* Cell Cycle
-* Cell Transformation, Neoplastic
-* Cells, Cultured
-* Cellular Senescence
-* Fibroblasts
-* Gene Expression
-* Gene Expression Regulation
-* Gene Knockdown Techniques
-* Humans
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Phenotype
-* Telomerase
-* Telomere
-|keywords=* ATM
-* senescence
-* telomerase
-* tumorigenesis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6754593
-}}
-==TET2==
-{{medline-entry
-|title=Non-coding and Loss-of-Function Coding Variants in [[TET2]] are Associated with Multiple Neurodegenerative Diseases.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32330418
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Alzheimer Disease
-* Animals
-* Cognition
-* DNA-Binding Proteins
-* Female
-* Frontotemporal Dementia
-* Humans
-* Loss of Function Mutation
-* Male
-* Mice
-* Neurodegenerative Diseases
-* Proto-Oncogene Proteins
-|keywords=* AD
-* ALS
-* Alzheimer
-* FTD
-* TET2
-* aging
-* amyotrophic lateral sclerosis
-* frontotemporal dementia
-* genome sequencing
-* non-coding
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7212268
-}}
-{{medline-entry
-|title=60 Years of clonal hematopoiesis research: From X-chromosome inactivation studies to the identification of driver mutations.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32001340
-|mesh-terms=* Adult
-* Aging
-* Biomedical Research
-* Chromosomes, Human, X
-* DNA-Binding Proteins
-* Female
-* Hematopoiesis
-* Hematopoietic Stem Cells
-* History, 20th Century
-* History, 21st Century
-* Humans
-* Male
-* Mutation
-* Proto-Oncogene Proteins
-* Receptors, Androgen
-* Repressor Proteins
-* X Chromosome Inactivation
-|full-text-url=https://sci-hub.do/10.1016/j.exphem.2020.01.008
-}}
-{{medline-entry
-|title=DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31842975
-|mesh-terms=* Animals
-* Caco-2 Cells
-* Cell Line, Tumor
-* Colonic Neoplasms
-* DNA Methylation
-* DNA-Binding Proteins
-* Down-Regulation
-* Epigenesis, Genetic
-* Female
-* Gene Regulatory Networks
-* HT29 Cells
-* Humans
-* Male
-* Mice
-* Mixed Function Oxygenases
-* Mutation
-* Neoplasms, Experimental
-* Proto-Oncogene Proteins
-* Proto-Oncogene Proteins B-raf
-|keywords=* Aging
-* BRAF V600E
-* CIMP
-* Colon cancer
-* DNA methylation
-* TET
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6916434
-}}
-{{medline-entry
-|title=Clonal haematopoiesis: connecting ageing and inflammation in cardiovascular disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31406340
-|mesh-terms=* Adult
-* Age Factors
-* Aged
-* Aged, 80 and over
-* Aging
-* Animals
-* Cardiovascular Diseases
-* DNA (Cytosine-5-)-Methyltransferases
-* DNA-Binding Proteins
-* Genetic Predisposition to Disease
-* Hematopoiesis
-* Hematopoietic Stem Cells
-* Humans
-* Inflammation
-* Middle Aged
-* Mutation
-* Phenotype
-* Proto-Oncogene Proteins
-* Repressor Proteins
-* Risk Assessment
-* Risk Factors
-|full-text-url=https://sci-hub.do/10.1038/s41569-019-0247-5
-}}
-==TF==
-{{medline-entry
-|title=A preliminary investigation of the contribution of different tenderness factors to beef loin, tri-tip and heel tenderness.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32736289
-|keywords=* Aging
-* Beef
-* Collagen
-* Tenderness
-* Trained panel
-|full-text-url=https://sci-hub.do/10.1016/j.meatsci.2020.108247
-}}
-{{medline-entry
-|title=The transcription factor ZmNAC126 accelerates leaf senescence downstream of the ethylene signalling pathway in maize.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32430911
-|keywords=* ZmNAC
-* chlorophyll catabolic genes
-* ethylene
-* leaf senescence
-* maize
-|full-text-url=https://sci-hub.do/10.1111/pce.13803
-}}
-{{medline-entry
-|title=Extensive transcriptome changes during seasonal leaf senescence in field-grown black cottonwood (Populus trichocarpa Nisqually-1).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32313054
-|mesh-terms=* Aging
-* Gene Expression Profiling
-* Gene Expression Regulation, Plant
-* Genome, Plant
-* Photosynthesis
-* Plant Leaves
-* Populus
-* Seasons
-* Transcription Factors
-* Transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7170949
-}}
-{{medline-entry
-|title=Expression of Transferrin and Albumin in the Sperm-Storage Tubules of Japanese Quail and their Possible Involvement in Long-Term Sperm Storage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32174770
-|keywords=* Japanese quail
-* albumin
-* sperm longevity
-* sperm storage tubules
-* transferrin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7063080
-}}
-{{medline-entry
-|title=OsWRKY5 Promotes Rice Leaf Senescence via Senescence-Associated NAC and Abscisic Acid Biosynthesis Pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31505875
-|mesh-terms=* Abscisic Acid
-* Chlorophyll
-* Gene Expression Regulation, Plant
-* Gene Knockdown Techniques
-* Oryza
-* Plant Leaves
-* Plant Proteins
-* Transcription Factors
-|keywords=* NAC
-* OsWRKY
-* abscisic acid (ABA)
-* leaf senescence
-* rice
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6770167
-}}
-{{medline-entry
-|title=BrTCP7 Transcription Factor Is Associated with MeJA-Promoted Leaf Senescence by Activating the Expression of [i]BrOPR3[/i] and [i]BrRCCR[/i].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31416297
-|mesh-terms=* Amino Acid Sequence
-* Brassica
-* Cellular Senescence
-* Cyclopentanes
-* Gene Expression Regulation, Plant
-* Oxylipins
-* Phenotype
-* Phylogeny
-* Plant Growth Regulators
-* Plant Leaves
-* Plant Proteins
-* Promoter Regions, Genetic
-* Protein Binding
-* Transcription Factors
-|keywords=* Chinese flowering cabbage
-* JA
-* leaf senescence
-* transcriptional activation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6719003
-}}
-{{medline-entry
-|title=Activation of the Transcription of [i]BrGA20ox3[/i] by a BrTCP21 Transcription Factor Is Associated with Gibberellin-Delayed Leaf Senescence in Chinese Flowering Cabbage during Storage.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31398806
-|mesh-terms=* Aging
-* Base Sequence
-* Brassica
-* Food Preservation
-* Gene Expression Regulation, Plant
-* Gibberellins
-* Phenotype
-* Phylogeny
-* Plant Leaves
-* Plant Proteins
-* Promoter Regions, Genetic
-* Protein Binding
-* Transcription Factors
-|keywords=* Chinese flowering cabbage
-* GA
-* leaf senescence
-* transcriptional activation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6720506
-}}
-==TFEB==
-{{medline-entry
-|title=A Novel Lipofuscin-detecting Marker of Senescence Relates With Hypoxia, Dysregulated Autophagy and With Poor Prognosis in Non-small-cell-lung Cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33144423
-|keywords=* Senescence
-* autophagy
-* glycolysis
-* hypoxia
-* lipofuscin
-* lung cancer
-|full-text-url=https://sci-hub.do/10.21873/invivo.12154
-}}
-{{medline-entry
-|title=ESC-sEVs Rejuvenate Senescent Hippocampal NSCs by Activating Lysosomes to Improve Cognitive Dysfunction in Vascular Dementia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32440476
-|keywords=* embryonic stem cells derived small extracellular vesicles (ESC‐sEVs)
-* hippocampal neural stem cells (HNSCs)
-* lysosomes
-* senescence
-* vascular dementia
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7237844
-}}
-{{medline-entry
-|title=Nitrative Stress-Related Autophagic Insufficiency Participates in Hyperhomocysteinemia-Induced Renal Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32047576
-|mesh-terms=* Aging
-* Animals
-* Autophagy
-* Cells, Cultured
-* Homocysteine
-* Humans
-* Hyperhomocysteinemia
-* Kidney
-* Kidney Diseases
-* Male
-* Metalloporphyrins
-* Peroxynitrous Acid
-* Rats
-* Rats, Sprague-Dawley
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7007752
-}}
-{{medline-entry
-|title=Polyamines reverse immune senescence via the translational control of autophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31679458
-|mesh-terms=* Aging
-* Animals
-* Autophagy
-* Humans
-* Lysosomes
-* Polyamines
-* Protein Processing, Post-Translational
-* Spermidine
-|keywords=* Aging
-* B cells
-* EIF5A
-* TFEB
-* autophagy
-* hypusine
-* spermidine
-* translation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6984486
-}}
-{{medline-entry
-|title=Polyamines Control eIF5A Hypusination, [[TFEB]] Translation, and Autophagy to Reverse B Cell Senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31474573
-|mesh-terms=* Adaptive Immunity
-* Age Factors
-* Aging
-* Animals
-* Autophagy
-* B-Lymphocytes
-* Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
-* Cellular Senescence
-* HEK293 Cells
-* Humans
-* Immunologic Memory
-* Immunosenescence
-* Jurkat Cells
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* NIH 3T3 Cells
-* Peptide Initiation Factors
-* Protein Processing, Post-Translational
-* RNA-Binding Proteins
-* Signal Transduction
-* Spermidine
-|keywords=* B cell
-* TFEB
-* aging
-* autophagy
-* eIF5A
-* spermidine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6863385
-}}
-==TFPI==
-{{medline-entry
-|title=Identification of cardiovascular health gene variants related to longevity in a Chinese population.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32897244
-|keywords=* Chinese
-* factor related to cardiovascular health (FCH)
-* genetic variation
-* lipid metabolism
-* longevity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7521493
-}}
-==TG==
-{{medline-entry
-|title=Inhibition of the alternative lengthening of telomeres pathway by subtelomeric sequences in Saccharomyces cerevisiae.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33126043
-|keywords=* Budding yeast
-* Rad52
-* Replicative senescence
-* Subtelomeric Y’ elements
-* Telomerase-independent telomere maintenance
-* Telomere recombination
-|full-text-url=https://sci-hub.do/10.1016/j.dnarep.2020.102996
-}}
-{{medline-entry
-|title=E4orf1, an Adeno-viral protein, attenuates renal lipid accumulation in high fat fed mice: A novel approach to reduce a key risk factor for chronic kidney disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33102865
-|keywords=* Aging
-* CKD
-* Diabetes
-* Diet
-* E4orf1
-* FA synthesis
-* Hyperinsulinemia
-* Insulin
-* Lipid metabolism
-* Obesity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7575883
-}}
-{{medline-entry
-|title=Resistance exercise attenuates postprandial metabolic responses to a high-fat meal similarly in younger and older men.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33032071
-|keywords=* Aging
-* Cardiometabolic
-* Lipemia
-* Metabolism
-* Nutrition
-|full-text-url=https://sci-hub.do/10.1016/j.nutres.2020.08.012
-}}
-{{medline-entry
-|title=Aging-induced aberrant RAGE/PPARα axis promotes hepatic steatosis via dysfunctional mitochondrial β oxidation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32936538
-|keywords=* PPARα
-* RAGE
-* aging
-* hepatic steatosis
-* mitochondria
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7576254
-}}
-{{medline-entry
-|title=Fenofibrate impairs liver function and structure more pronounced in old than young rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32927318
-|keywords=* Aging
-* Fenofibrate
-* Lipids
-* Liver function and morphology
-* Rat
-* serum
-|full-text-url=https://sci-hub.do/10.1016/j.archger.2020.104244
-}}
-{{medline-entry
-|title=Awareness of major cardiovascular risk factors and its relationship with markers of vascular aging: Data from the Brisighella Heart Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32249143
-|mesh-terms=* Adolescent
-* Adult
-* Age Factors
-* Aged
-* Aged, 80 and over
-* Aging
-* Biomarkers
-* Blood Glucose
-* Blood Pressure
-* Cardiovascular Diseases
-* Cholesterol
-* Cross-Sectional Studies
-* Diabetes Mellitus
-* Female
-* Humans
-* Hypercholesterolemia
-* Hypertension
-* Hypertriglyceridemia
-* Italy
-* Male
-* Middle Aged
-* Risk Assessment
-* Risk Factors
-* Triglycerides
-* Vascular Stiffness
-* Young Adult
-|keywords=* Arterial aging
-* Awareness
-* Epidemiology
-* Pulse wave velocity
-* Risk factors
-|full-text-url=https://sci-hub.do/10.1016/j.numecd.2020.03.005
-}}
-{{medline-entry
-|title=Characterisation of the dynamic nature of lipids throughout the lifespan of genetically identical female and male Daphnia magna.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32221338
-|mesh-terms=* Aging
-* Animals
-* Daphnia
-* Diglycerides
-* Female
-* Lipid Metabolism
-* Longevity
-* Male
-* Phosphatidylcholines
-* Sphingomyelins
-* Triglycerides
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7101400
-}}
-{{medline-entry
-|title=Effects of laboratory biotic aging on the characteristics of biochar and its water-soluble organic products.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31472466
-|mesh-terms=* Benzopyrans
-* Charcoal
-* Humic Substances
-* Microbiota
-* Soil Microbiology
-* Solubility
-* Triticum
-* Water
-|keywords=* Biochar
-* Biotic incubation aging
-* Dissolved organic matter (DOM)
-* Excitation-emission matrix
-* Humification
-|full-text-url=https://sci-hub.do/10.1016/j.jhazmat.2019.121071
-}}
-{{medline-entry
-|title=Using Caenorhabditis elegans for Studying Trans- and Multi-Generational Effects of Toxicants.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31403614
-|mesh-terms=* Animals
-* Caenorhabditis elegans
-* Hazardous Substances
-* Humans
-* Longevity
-* Reproduction
-* Toxicity Tests
-|full-text-url=https://sci-hub.do/10.3791/59367
-}}
-==TH==
-{{medline-entry
-|title=Thyroid hormone signaling is associated with physical performance, muscle mass, and strength in a cohort of oldest-old: results from the Mugello study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33219914
-|keywords=* Aging
-* Muscle mass
-* Muscle strength
-* Oldest-old
-* Physical performance
-* Rehabilitation
-* Thyroid hormone signaling
-|full-text-url=https://sci-hub.do/10.1007/s11357-020-00302-0
-}}
-{{medline-entry
-|title=Social Environment Ameliorates Behavioral and Immune Impairments in Tyrosine Hydroxylase Haploinsufficient Female Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32772235
-|keywords=* Behavioral responses
-* Immunosenescence
-* Oxidative-inflammatory stress
-* Social environmental strategy
-* Tyrosine hydroxylase haploinsufficient mice
-|full-text-url=https://sci-hub.do/10.1007/s11481-020-09947-2
-}}
-{{medline-entry
-|title=Mechanism of thyroid hormone signaling in skeletal muscle of aging mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32720201
-|keywords=* Aging
-* Mice
-* Skeletal muscle
-* Thyroid hormone signaling
-|full-text-url=https://sci-hub.do/10.1007/s12020-020-02428-9
-}}
-{{medline-entry
-|title=Longitudinal changes in bone mineral density and trabecular bone score in Korean adults: a community-based prospective study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32621253
-|mesh-terms=* Absorptiometry, Photon
-* Adult
-* Bone Density
-* Cancellous Bone
-* Cohort Studies
-* Female
-* Humans
-* Lumbar Vertebrae
-* Male
-* Prospective Studies
-* Republic of Korea
-|keywords=* Aging
-* Bone mineral density
-* Natural history
-* Osteoporosis
-|full-text-url=https://sci-hub.do/10.1007/s11657-020-00731-6
-}}
-{{medline-entry
-|title=Quantitative proteomic profiling of the rat substantia nigra places glial fibrillary acidic protein at the hub of proteins dysregulated during aging: Implications for idiopathic Parkinson's disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32270889
-|keywords=* RRID:AB_11145309
-* RRID:AB_2109791
-* RRID:AB_228307
-* RRID:AB_228341
-* RRID:AB_2336820
-* RRID:AB_2631098
-* RRID:AB_390204
-* RRID:MGI:5651135
-* RRID:SCR_001881
-* RRID:SCR_002798
-* RRID:SCR_003070
-* RRID:SCR_004946
-* RRID:SCR_005223
-* aging
-* dopaminergic neuron
-* glial fibrillary acidic protein
-* proteome
-* proteomics
-* substantia nigra
-|full-text-url=https://sci-hub.do/10.1002/jnr.24622
-}}
-{{medline-entry
-|title=Withaferin-A Protects the Nigral Dopamine Neuron and Recovers Motor Activity in Aged Rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31982873
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Corpus Striatum
-* Dopaminergic Neurons
-* Male
-* Motor Activity
-* Neuroprotective Agents
-* Rats
-* Rats, Wistar
-* Substantia Nigra
-* Tyrosine 3-Monooxygenase
-* Withanolides
-|keywords=* Ageing
-* Dopamine
-* Striatum
-* Substantia nigra
-* Withaferin-A
-|full-text-url=https://sci-hub.do/10.1159/000505183
-}}
-{{medline-entry
-|title=Effects of physical activity on bone mineral density in older adults: Korea National Health and Nutrition Examination Survey, 2008-2011.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31655946
-|mesh-terms=* Absorptiometry, Photon
-* Aged
-* Bone Density
-* Cross-Sectional Studies
-* Exercise
-* Female
-* Femur Neck
-* Humans
-* Lumbar Vertebrae
-* Male
-* Middle Aged
-* Nutrition Surveys
-* Osteoporosis
-* Republic of Korea
-* Surveys and Questionnaires
-|keywords=* Aging
-* Bone mineral density
-* Exercise
-* Gender
-* Osteoporosis
-* Physical activity
-|full-text-url=https://sci-hub.do/10.1007/s11657-019-0655-5
-}}
-{{medline-entry
-|title=Age-Related Resistance to Thyroid Hormone Action.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31512083
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Animals
-* Humans
-* Hyperthyroidism
-* Hypothyroidism
-* Iodide Peroxidase
-* Male
-* Receptors, Thyroid Hormone
-* Thyroid Hormones
-* Thyroxine
-* Triiodothyronine
-|full-text-url=https://sci-hub.do/10.1007/s40266-019-00711-7
-}}
-{{medline-entry
-|title=Age-Dependent Changes in Glucose Homeostasis in Male Deiodinase Type 2 Knockout Zebrafish.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31504428
-|mesh-terms=* Aging
-* Animals
-* Animals, Genetically Modified
-* Glucose
-* Glucose Transport Proteins, Facilitative
-* Homeostasis
-* Hyperglycemia
-* Iodide Peroxidase
-* Islets of Langerhans
-* Male
-* Proglucagon
-* Proinsulin
-* Receptor, Insulin
-* Receptors, Glucagon
-* Zebrafish
-|full-text-url=https://sci-hub.do/10.1210/en.2019-00445
-}}
-{{medline-entry
-|title=Age effect on thyroid hormone brain response in male mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31494803
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Gene Expression
-* Hyperthyroidism
-* Hypothyroidism
-* Male
-* Maze Learning
-* Mice, Inbred C57BL
-* Monocarboxylic Acid Transporters
-* Organic Cation Transport Proteins
-* Rotarod Performance Test
-* Symporters
-* Thyroid Hormones
-* Thyrotropin
-* Thyrotropin-Releasing Hormone
-|keywords=* Ageing
-* Hyperthyroidism
-* Hypothyroidism
-* Male mice
-* Thyroid hormones
-|full-text-url=https://sci-hub.do/10.1007/s12020-019-02078-6
-}}
-{{medline-entry
-|title=Aging Is Associated with Low Thyroid State and Organ-Specific Sensitivity to Thyroxine.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31441387
-|mesh-terms=* Aging
-* Animals
-* DNA-Binding Proteins
-* Hypothalamo-Hypophyseal System
-* Liver
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Myocardium
-* Pituitary Gland
-* Thyroid Gland
-* Thyroid Hormones
-* Thyrotropin
-* Thyroxine
-* Transcription Factors
-|keywords=* HPT-axis
-* aging
-* mice
-* thyroid gland
-* thyroid hormones
-|full-text-url=https://sci-hub.do/10.1089/thy.2018.0377
-}}
-==TLR1==
-{{medline-entry
-|title=Effects of aging and lifelong aerobic exercise on expression of innate immune components in human skeletal muscle.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32969782
-|keywords=* TLR
-* aging
-* innate immunity
-* lifelong exercise
-* skeletal muscle
-|full-text-url=https://sci-hub.do/10.1152/japplphysiol.00615.2020
-}}
-{{medline-entry
-|title=Association of TLR gene variants in a Czech Red Pied cattle population with reproductive traits.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31901560
-|mesh-terms=* Age Factors
-* Animals
-* Breeding
-* Cattle
-* Czech Republic
-* Female
-* Genotype
-* Longevity
-* Male
-* Phenotype
-* Polymorphism, Single Nucleotide
-* Reproduction
-* Toll-Like Receptor 1
-* Toll-Like Receptor 2
-* Toll-Like Receptor 6
-* Toll-Like Receptors
-|keywords=* Cattle
-* Diversity
-* Effect prediction
-* Health traits
-* Toll-like receptors
-|full-text-url=https://sci-hub.do/10.1016/j.vetimm.2019.109997
-}}
-==TLR2==
-{{medline-entry
-|title=Changes in salivary microbial sensing proteins CD14 and [[TLR2]] with aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32529494
-|mesh-terms=* Adolescent
-* Adult
-* Aging
-* Biomarkers
-* Child
-* Child, Preschool
-* Humans
-* Lipopolysaccharide Receptors
-* Middle Aged
-* Saliva
-* Salivary Proteins and Peptides
-* Toll-Like Receptor 2
-* Young Adult
-|keywords=* Age changes
-* CD14
-* Saliva
-* Toll-like receptor-2
-|full-text-url=https://sci-hub.do/10.1007/s00784-020-03274-9
-}}
-{{medline-entry
-|title=Culture Model for Non-human Primate Choroid Plexus.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31555096
-|keywords=* aging
-* cell culture
-* choroid plexus
-* epithelial cell
-* infectious disease
-* rhesus macaque
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6724611
-}}
-==TLR4==
-{{medline-entry
-|title=Age-Dependent Changes of Adipokine and Cytokine Secretion From Rat Adipose Tissue by Endogenous and Exogenous Toll-Like Receptor Agonists.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32973755
-|keywords=* adipokines
-* aging
-* batokines
-* biglycan
-* cytokines
-* fat explant cultures
-* high mobility group box-1 protein
-* lipopolysaccharide
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7466552
-}}
-{{medline-entry
-|title=Role of Toll Like Receptor 4 in Alzheimer's Disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32983082
-|keywords=* Alzheimer’s disease
-* TLR4
-* aging
-* amyloid beta oligomers
-* calcium
-* hippocampal neurons
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7479089
-}}
-{{medline-entry
-|title=Commentary on Some Recent Theses Relevant to Combating Aging: August 2020.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32718230
-|keywords=* aging
-* dissertations
-* theses
-|full-text-url=https://sci-hub.do/10.1089/rej.2020.2378
-}}
-{{medline-entry
-|title=Sialylation and Galectin-3 in Microglia-Mediated Neuroinflammation and Neurodegeneration.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32581723
-|keywords=* aging
-* desialylation
-* galectin-3
-* microglia
-* neurodegeneration
-* phagocytosis
-* sialic acid
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7296093
-}}
-{{medline-entry
-|title=Chemerin facilitates intervertebral disc degeneration via [[TLR4]] and CMKLR1 and activation of NF-kB signaling pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32526705
-|keywords=* chemerin
-* inflammation
-* intervertebral disc
-* nucleus pulposus
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343479
-}}
-{{medline-entry
-|title=Toll-like receptor 4 differentially regulates adult hippocampal neurogenesis in an age- and sex-dependent manner.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32343455
-|keywords=* TLR4
-* adult hippocampal neurogenesis
-* aging
-* proliferation
-* sex differences
-|full-text-url=https://sci-hub.do/10.1002/hipo.23209
-}}
-{{medline-entry
-|title=Aging-associated immunosenescence via alterations in splenic immune cell populations in rat.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31838133
-|mesh-terms=* Animals
-* B-Lymphocytes
-* Cells, Cultured
-* Immunity, Cellular
-* Immunosenescence
-* Male
-* Malondialdehyde
-* Oxidative Stress
-* Rats
-* Rats, Wistar
-* Spleen
-* Superoxide Dismutase
-* T-Lymphocytes
-|keywords=* Aging
-* Immunohistochemistry
-* Immunosenescence
-* Oxidative stress
-* Spleen
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2019.117168
-}}
-{{medline-entry
-|title=Leptin induces immunosenescence in human B cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31831137
-|mesh-terms=* Adult
-* Aged
-* B-Lymphocytes
-* Humans
-* Immunoglobulin Class Switching
-* Immunosenescence
-* Leptin
-* Middle Aged
-* Obesity
-|keywords=* B cells
-* Immunosenescence
-* Leptin
-* Obesity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7002206
-}}
-{{medline-entry
-|title=Genetic Variation in the Magnitude and Longevity of the IgG Subclass Response to a Diphtheria-Tetanus-Acellular Pertussis (DTaP) Vaccine in Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31547158
-|keywords=* DTaP
-* IgG subclass
-* antibody longevity
-* antibody magnitude
-* genetics
-* vaccine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6963843
-}}
-{{medline-entry
-|title=Rapamycin improves sevoflurane‑induced cognitive dysfunction in aged rats by mediating autophagy through the [[TLR4]]/MyD88/NF‑κB signaling pathway.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31432123
-|mesh-terms=* Aging
-* Animals
-* Autophagic Cell Death
-* Cognitive Dysfunction
-* Male
-* Myeloid Differentiation Factor 88
-* NF-kappa B
-* Rats
-* Rats, Sprague-Dawley
-* Sevoflurane
-* Signal Transduction
-* Sirolimus
-* Toll-Like Receptor 4
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6755174
-}}
-==TLR9==
-{{medline-entry
-|title=Age-Associated B Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31986068
-|keywords=* B lymphocytes
-* aging
-* autoimmunity
-* memory B cells
-|full-text-url=https://sci-hub.do/10.1146/annurev-immunol-092419-031130
-}}
-==TMEM106B==
-{{medline-entry
-|title=Genetics of Gene Expression in the Aging Human Brain Reveal TDP-43 Proteinopathy Pathophysiology.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32526197
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Alzheimer Disease
-* Amyloid beta-Peptides
-* Apolipoproteins E
-* Brain
-* Cohort Studies
-* DNA-Binding Proteins
-* Female
-* Gene Expression Regulation
-* Haplotypes
-* Humans
-* Lysosomes
-* Male
-* Membrane Proteins
-* Myelin Sheath
-* Nerve Tissue Proteins
-* Progranulins
-* Quantitative Trait Loci
-* RNA Splicing Factors
-* TDP-43 Proteinopathies
-|keywords=* Alzheimer's disease
-* Amyloid-β
-* GRN
-* RBFOX1
-* TDP-43
-* TMEM106B
-* co-expression module
-* cognitive resilience
-* eQTL
-* expression quantitative trait loci
-* sQTL
-* splicing quantitative trait loci
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7416464
-}}
-==TMPRSS2==
-{{medline-entry
-|title=Susceptibility to COVID-19 in populations with health disparities: Posited involvement of mitochondrial disorder, socioeconomic stress, and pollutants.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32905655
-|keywords=* SARS-CoV-2
-* dysfunction
-* exposome
-* immunosenescence
-* metabolomics
-* mitochondria
-* pollutant
-* socioeconomic
-* stress
-|full-text-url=https://sci-hub.do/10.1002/jbt.22626
-}}
-{{medline-entry
-|title=Expression of the SARS-CoV-2 Entry Proteins, ACE2 and [[TMPRSS2]], in Cells of the Olfactory Epithelium: Identification of Cell Types and Trends with Age.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32379417
-|mesh-terms=* Age Factors
-* Angiotensin-Converting Enzyme 2
-* Animals
-* Betacoronavirus
-* COVID-19
-* Coronavirus Infections
-* Gene Expression
-* Gene Expression Profiling
-* Immunohistochemistry
-* In Situ Hybridization
-* Mice
-* Olfaction Disorders
-* Olfactory Mucosa
-* Olfactory Receptor Neurons
-* Pandemics
-* Peptidyl-Dipeptidase A
-* Pneumonia, Viral
-* RNA-Seq
-* Reverse Transcriptase Polymerase Chain Reaction
-* SARS-CoV-2
-* Serine Endopeptidases
-* Virus Internalization
-|keywords=* ACE2 expression
-* COVID-19
-* SARS-CoV-2
-* aging
-* anosmia
-* olfactory epithelium
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7241737
-}}
-==TNC==
-{{medline-entry
-|title=Effects of Tenascin C on the Integrity of Extracellular Matrix and Skin Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33217999
-|keywords=* TGF-β
-* aging
-* collagen
-* extracellular matrix
-* fibroblast
-* skin
-* tenascin C
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7698786
-}}
-{{medline-entry
-|title=Tenascin-C expression controls the maturation of articular cartilage in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32066496
-|mesh-terms=* Aging
-* Animals
-* Cartilage, Articular
-* Cell Count
-* Genotype
-* Mice
-* Tenascin
-|keywords=* Adhesion
-* Articular cartilage
-* Cartilage defect
-* Cell density
-* Knock-out mouse
-* Load
-* Tenascin C
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7027060
-}}
-{{medline-entry
-|title=Effects of hydrothermal aging, thermal cycling, and water storage on the mechanical properties of a machinable resin-based composite containing nano-zirconia fillers.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31877525
-|keywords=* Aging
-* Mechanical properties
-* Nano-zirconia
-* Phase transformation
-* Resin nano-ceramic
-* Resin-based composite
-|full-text-url=https://sci-hub.do/10.1016/j.jmbbm.2019.103522
-}}
-==TNF==
-{{medline-entry
-|title=Naringenin alleviates nonalcoholic steatohepatitis in middle-aged Apoe mice: role of SIRT1.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33234364
-|keywords=* AML-12 cells
-* Aging
-* ApoE(−/−) mice
-* Naringenin
-* Nonalcoholic steatohepatitis
-* SIRT1
-|full-text-url=https://sci-hub.do/10.1016/j.phymed.2020.153412
-}}
-{{medline-entry
-|title=Protective role of microglial HO-1 blockade in aging: Implication of iron metabolism.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33212416
-|keywords=* Aging
-* Ferroptosis
-* Heme oxygenase-1
-* Iron metabolism
-* Microglia
-* Neuroinflammation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7680814
-}}
-{{medline-entry
-|title=Anti-aging effect of DL-β-hydroxybutyrate against hepatic cellular senescence induced by D-galactose or γ-irradiation via autophagic flux stimulation in male rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33147533
-|keywords=* Autophagy
-* D-galacose
-* Ionizing radiation
-* Senescence
-* β-hydroxybutyric acid
-|full-text-url=https://sci-hub.do/10.1016/j.archger.2020.104288
-}}
-{{medline-entry
-|title=Exploring the extensive crosstalk between the antagonistic cytokines- TGF-β and [[TNF]]-α in regulating cancer pathogenesis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33153895
-|keywords=* Apoptosis
-* Autophagy
-* EMT
-* Fibrogenesis
-* Senescence
-* TGF-β and TNF-α
-|full-text-url=https://sci-hub.do/10.1016/j.cyto.2020.155348
-}}
-{{medline-entry
-|title=Long non-coding RNA SNHG29 regulates cell senescence via p53/p21 signaling in spontaneous preterm birth.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33080448
-|keywords=* Cellular senescence
-* Oxidative stress
-* SASP
-* SNHG29
-* Spontaneous preterm birth
-* p53/p21
-|full-text-url=https://sci-hub.do/10.1016/j.placenta.2020.10.009
-}}
-{{medline-entry
-|title=Cognition Is Associated With Peripheral Immune Molecules in Healthy Older Adults: A Cross-Sectional Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32983153
-|keywords=* chemokines
-* cognition
-* cytokines
-* healthy aging
-* immune molecules
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7493640
-}}
-{{medline-entry
-|title=Anti-aging effects of [i]Ribes meyeri[/i] anthocyanins on neural stem cells and aging mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32920547
-|keywords=* Ribes meyeri anthocyanin
-* aging
-* cognition
-* naringenin
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7521483
-}}
-{{medline-entry
-|title=Effects of a four week detraining period on physical, metabolic, and inflammatory profiles of elderly women who regularly participate in a program of strength training.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32863968
-|keywords=* Aging
-* Inflammation
-* Physical exercise
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7450596
-}}
-{{medline-entry
-|title=Contribution of Porphyromonas gingivalis lipopolysaccharide to experimental periodontitis in relation to aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32851571
-|keywords=* Aging
-* Bone loss
-* Osteoclastogenesis
-* Periodontitis
-* Porphyromonas gingivalis lipopolysaccharide
-|full-text-url=https://sci-hub.do/10.1007/s11357-020-00258-1
-}}
-{{medline-entry
-|title=New MoDC-Targeting [[TNF]] Fusion Proteins Enhance Cyclic Di-GMP Vaccine Adjuvanticity in Middle-Aged and Aged Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32849581
-|keywords=* 3′
-* 5′-cyclic diguanylic acid (cyclic di-GMP)
-* aging
-* monocyte-derived dendritic cells (moDCs)
-* tumor necrosis factor (TNF)
-* vaccine
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7427090
-}}
-{{medline-entry
-|title=Cognitive impairment in elderly patients with rheumatic disease and the effect of disease-modifying anti-rheumatic drugs.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32862311
-|keywords=* Aging
-* Biologics
-* Cognition
-* Rheumatic diseases
-|full-text-url=https://sci-hub.do/10.1007/s10067-020-05372-1
-}}
-{{medline-entry
-|title=Cotinine ameliorates memory and learning impairment in senescent mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32818583
-|keywords=* Aging
-* Cognitive impairment
-* Cotinine
-* Improvement
-* α(7)nAChRs
-|full-text-url=https://sci-hub.do/10.1016/j.brainresbull.2020.08.010
-}}
-{{medline-entry
-|title=Kynurenines link chronic inflammation to functional decline and physical frailty.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32814718
-|keywords=* Aging
-* Cytokines
-* Inflammation
-* Neurodegeneration
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7455140
-}}
-{{medline-entry
-|title=Voluntary exercise training attenuated the middle-aged maturity-induced cardiac apoptosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32781061
-|mesh-terms=* Aging
-* Animals
-* Apoptosis
-* Heart
-* In Situ Nick-End Labeling
-* Male
-* Mice
-* Mice, Inbred C57BL
-* Mitochondria, Heart
-* Muscle, Skeletal
-* Physical Conditioning, Animal
-* Running
-* Sedentary Behavior
-|keywords=* Caspase-independent
-* Cell death
-* Fas dependent
-* IGF-related
-* Mitochondrial
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2020.118187
-}}
-{{medline-entry
-|title=Preclinical Evaluation of a Food-Derived Functional Ingredient to Address Skeletal Muscle Atrophy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32751276
-|keywords=* aging
-* bioactive
-* functional ingredient
-* immobilization
-* inflammation
-* muscle atrophy
-* peptide
-* protein synthesis
-* skeletal muscle
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7469066
-}}
-{{medline-entry
-|title=Childhood survivors of high-risk neuroblastoma show signs of immune recovery and not immunosenescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32744364
-|keywords=* adverse late effects
-* childhood
-* immune recovery
-* immunosenescence
-* neuroblastoma
-|full-text-url=https://sci-hub.do/10.1002/eji.202048541
-}}
-{{medline-entry
-|title=FK506 induces lung lymphatic endothelial cell senescence and downregulates LYVE-1 expression, with associated decreased hyaluronan uptake.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32736525
-|keywords=* Endothelial cells
-* Fk506
-* Hyaluronan
-* LYVE-1
-* Lung lymphatic
-* Senescence
-* TERT
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7395348
-}}
-{{medline-entry
-|title=Late-onset hypogonadism: Reductio ad absurdum of the cardiovascular risk-benefit of testosterone replacement therapy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32737921
-|keywords=* aging
-* androgen
-* heart failure
-* myocardial infarction
-* testosterone
-* thromboembolism
-|full-text-url=https://sci-hub.do/10.1111/andr.12876
-}}
-{{medline-entry
-|title=Doxorubicin generates senescent microglia that exhibit altered proteomes, higher levels of cytokine secretion, and a decreased ability to internalize amyloid β.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32738344
-|keywords=* Aging
-* Alzheimer's disease
-* Inflammation
-* Microglia
-* Proteomics
-* Senescence
-|full-text-url=https://sci-hub.do/10.1016/j.yexcr.2020.112203
-}}
-{{medline-entry
-|title=Time restricted feeding provides a viable alternative to alternate day fasting when evaluated in terms of redox homeostasis in rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32717588
-|keywords=* Aging
-* Alternate day fasting (ADF)
-* Intermittent fasting (IF)
-* Oxidative stress
-* Time-Restricted feeding (TRF)
-|full-text-url=https://sci-hub.do/10.1016/j.archger.2020.104188
-}}
-{{medline-entry
-|title=Associations Between Plasma Immunomodulatory and Inflammatory Mediators With VACS Index Scores Among Older HIV-Infected Adults on Antiretroviral Therapy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32695109
-|keywords=* HIV
-* aging
-* anti-retroviral therapy
-* inflammation
-* morbidity
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7338430
-}}
-{{medline-entry
-|title=Chrysin Impact on Oxidative and Inflammation Damages in the Liver of Aged Male Rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32679027
-|keywords=* Aging
-* chrysin
-* inflammation
-* liver
-* oxidative stress
-* rat.
-|full-text-url=https://sci-hub.do/10.2174/1871530320666200717162304
-}}
-{{medline-entry
-|title=Correction of immunosuppression in aged septic rats by human ghrelin and growth hormone through the vagus nerve-dependent inhibition of TGF-β production.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32677895
-|keywords=* Aging
-* Ghrelin
-* Immunosuppression
-* Sepsis
-* Vagus nerve
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7364485
-}}
-{{medline-entry
-|title=Epigenetics of neuroinflammation: Immune response, inflammatory response and cholinergic synaptic involvement evidenced by genome-wide DNA methylation analysis of delirious inpatients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32590150
-|keywords=* Aging
-* Delirium
-* Genome-wide DNA methylation
-* Immune response
-* Inflammatory response
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7486988
-}}
-{{medline-entry
-|title=[i]Andrographis paniculata[/i] and Its Bioactive Diterpenoids Against Inflammation and Oxidative Stress in Keratinocytes.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32560449
-|keywords=* Andrographis paniculata
-* andrographolide
-* inflammation
-* keratinocytes
-* oxidative stress
-* skin aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7346124
-}}
-{{medline-entry
-|title=Etanercept improves aging-induced cognitive deficits by reducing inflammation and vascular dysfunction in rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32569601
-|keywords=* Aging
-* Etanercept
-* Inflammation
-* Learning
-* Memory
-* TNFα
-* Vascular dementia
-|full-text-url=https://sci-hub.do/10.1016/j.physbeh.2020.113019
-}}
-{{medline-entry
-|title=Bacterial antigen translocation and age as BMI-independent contributing factors on systemic inflammation in NAFLD patients.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32559006
-|keywords=* NAFLD
-* aging
-* bacterial translocation
-* cytokines
-* insulin resistance
-|full-text-url=https://sci-hub.do/10.1111/liv.14571
-}}
-{{medline-entry
-|title=Bone marrow mesenchymal stem cells improve thymus and spleen function of aging rats through affecting P21/PCNA and suppressing oxidative stress.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32561691
-|keywords=* BMSCs
-* P21/PCNA
-* aging
-* immune system
-* oxidative stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343510
-}}
-{{medline-entry
-|title=Glycolic acid adjusted to pH 4 stimulates collagen production and epidermal renewal without affecting levels of proinflammatory [[TNF]]-alpha in human skin explants.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32583600
-|keywords=* cosmetics
-* glycolic acid
-* keratolytic agents
-* rejuvenation
-* skin aging
-|full-text-url=https://sci-hub.do/10.1111/jocd.13570
-}}
-{{medline-entry
-|title=A20 of nucleus pulposus cells plays a self-protection role via the nuclear factor-kappa B pathway in the inflammatory microenvironment.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32566144
-|keywords=* A20
-* Nuclear factor-kappa B
-* Nucleus pulposus
-* Senescence
-* Tumour necrosis factor alpha
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7284293
-}}
-{{medline-entry
-|title=Age-associated decline in neural, endocrine, and immune responses in men and women: Involvement of intracellular signaling pathways.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32563124
-|mesh-terms=* Adult
-* Aging
-* Estradiol
-* Female
-* Humans
-* Hydrocortisone
-* Immunity, Cellular
-* Intracellular Fluid
-* Male
-* Middle Aged
-* Signal Transduction
-* Testosterone
-* Young Adult
-|keywords=* 17β-estradiol
-* Cortisol
-* Cytokines
-* Testosterone
-* Tyrosine hydroxylase
-|full-text-url=https://sci-hub.do/10.1016/j.jneuroim.2020.577290
-}}
-{{medline-entry
-|title=Classical and lectin complement pathways and markers of inflammation for investigation of susceptibility to infections among healthy older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32536956
-|keywords=* Aging
-* Complement system
-* Elderly
-* Immune
-* Inflammation
-* Lectin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7285792
-}}
-{{medline-entry
-|title=Activation of FoxO1/SIRT1/RANKL/OPG pathway may underlie the therapeutic effects of resveratrol on aging-dependent male osteoporosis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32532246
-|keywords=* Aging
-* FoxO1
-* Male osteoporosois
-* OPG
-* RANKL
-* Resveratrol
-* SIRT1
-* Type II osteoporosis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7293127
-}}
-{{medline-entry
-|title=The senescence-associated secretome as an indicator of age and medical risk.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32554926
-|keywords=* Aging
-* Cellular senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7406245
-}}
-{{medline-entry
-|title=Exercise Partially Rejuvenates Muscle Stem Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32484032
-|keywords=* TGF-beta
-* aging
-* cyclin D1
-* longevity
-* regeneration
-* stem cells
-|full-text-url=https://sci-hub.do/10.1089/rej.2020.2359
-}}
-{{medline-entry
-|title=Brazilian berry extract (Myrciaria jaboticaba): A promising therapy to minimize prostatic inflammation and oxidative stress.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32460430
-|mesh-terms=* Age Factors
-* Animals
-* Anti-Inflammatory Agents
-* Antioxidants
-* Cyclooxygenase 2
-* Diet, High-Fat
-* Dose-Response Relationship, Drug
-* Fruit
-* Interleukin-1beta
-* Interleukin-6
-* Lipid Peroxidation
-* Male
-* Mice
-* Myrtaceae
-* Oxidative Stress
-* Plant Extracts
-* Prostatitis
-* T-Lymphocytes
-|keywords=* aging
-* bioactive compounds
-* obesity
-* overweight
-* polyphenols
-|full-text-url=https://sci-hub.do/10.1002/pros.24017
-}}
-{{medline-entry
-|title=Potential therapeutic effects of endothelial cells trans-differentiated from Wharton's Jelly-derived mesenchymal stem cells on altered vascular functions in aged diabetic rat model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32426041
-|keywords=* Aging
-* Diabetes mellitus
-* Endothelial cells
-* Hypertension
-* Mesenchymal stem cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7216374
-}}
-{{medline-entry
-|title=[Effect of fragmented sleep on postoperative cognitive function and central neuroinflammation].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32375444
-|mesh-terms=* Aging
-* Animals
-* Cognition
-* Cognition Disorders
-* Fear
-* Hippocampus
-* Mice
-* Mice, Inbred ICR
-|keywords=* Central nervous system
-* Cognition disorders
-* Inflammation
-* Postoperative period
-* Sleep deprivation
-|full-text-url=https://sci-hub.do/10.3760/cma.j.cn112137-20191215-02734
-}}
-{{medline-entry
-|title=Can blocking inflammation enhance immunity during aging?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32386656
-|keywords=* Inflammaging
-* p38-MAP Kinase
-* senescence
-* senolytics
-|full-text-url=https://sci-hub.do/10.1016/j.jaci.2020.03.016
-}}
-{{medline-entry
-|title=[FAS- and [[TNF]]-dependent ways participation in apoptosis mechanisms in hypotalumus in physiological and pathological aging.]
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32362081
-|mesh-terms=* Aging
-* Animals
-* Apoptosis
-* Female
-* Hypothalamus
-* Mice
-* Mice, Transgenic
-* Signal Transduction
-* Tumor Necrosis Factor-alpha
-* fas Receptor
-|keywords=* FAS-, TNF-dependent pathways
-* aging
-* apoptosis
-* hypothalamus
-* neurons
-}}
-{{medline-entry
-|title=Ultrasound-guided continuous thoracic paravertebral block alleviates postoperative delirium in elderly patients undergoing esophagectomy: A randomized controlled trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32332664
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Analgesia, Patient-Controlled
-* Delirium
-* Esophagectomy
-* Female
-* Geriatrics
-* Humans
-* Male
-* Middle Aged
-* Nerve Block
-* Postoperative Complications
-* Prospective Studies
-* Ultrasonography
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7440095
-}}
-{{medline-entry
-|title=17β-Estradiol improves insulin signalling and insulin resistance in the aged female hearts: Role of inflammatory and anti-inflammatory cytokines.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32311377
-|mesh-terms=* Aging
-* Animals
-* Anti-Inflammatory Agents
-* Blood Glucose
-* Cytokines
-* Estradiol
-* Female
-* Heart
-* Insulin
-* Insulin Resistance
-* Lipid Metabolism
-* Menopause
-* Ovariectomy
-* Rats
-* Rats, Wistar
-* Signal Transduction
-|keywords=* 17β-estradiol
-* Aging
-* Cytokines
-* Heart
-* Insulin signalling
-|full-text-url=https://sci-hub.do/10.1016/j.lfs.2020.117673
-}}
-{{medline-entry
-|title=Synergistic Antitumor Efficacy of Magnetohyperthermia and Poly(lactic-co-glycolic acid)-Encapsulated Selol in Ehrlich Breast Adenocarcinoma Treatment in Elderly Swiss Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32252879
-|mesh-terms=* Adenocarcinoma
-* Aging
-* Animals
-* Cell Line, Tumor
-* Glycols
-* Humans
-* Mice
-* Nanoparticles
-* Polylactic Acid-Polyglycolic Acid Copolymer
-* Selenium Compounds
-|full-text-url=https://sci-hub.do/10.1166/jbn.2020.2890
-}}
-{{medline-entry
-|title=Pinitol suppresses [[TNF]]-α-induced chondrocyte senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32200264
-|keywords=* Cellular senescence
-* Nrf2
-* Osteoarthritis
-* Pinitol
-* TNF-α
-|full-text-url=https://sci-hub.do/10.1016/j.cyto.2020.155047
-}}
-{{medline-entry
-|title=[Aging of skin fibroblasts: genetic and epigenetic factors.]
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32160428
-|mesh-terms=* Cells, Cultured
-* Epigenesis, Genetic
-* Fibroblasts
-* Humans
-* Skin Aging
-|keywords=* aging
-* melatonin
-* signal molecules
-* skin fibroblasts
-}}
-{{medline-entry
-|title=Functional and traditional training improve muscle power and reduce proinflammatory cytokines in older women: A randomized controlled trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32151735
-|keywords=* Aging
-* Cytokines.
-* Dynapenia
-* Inflamm-aging
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110920
-}}
-{{medline-entry
-|title=Associations of [[TNF]]-α -308 G>A and [[TNF]]-β 252 A>G with Physical Function and BNP-Rugao Longevity and Ageing Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32115620
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Female
-* Humans
-* Longevity
-* Male
-* Natriuretic Peptide, Brain
-* Tumor Necrosis Factor-alpha
-|keywords=* Physical function
-* TNF-α -308 G>A polymorphism
-* TNF-β 252 A>G polymorphism
-* plasma BNP
-* population study.
-|full-text-url=https://sci-hub.do/10.1007/s12603-020-1336-1
-}}
-{{medline-entry
-|title=3D TECA hydrogel reduces cellular senescence and enhances fibroblasts migration in wound healing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32104405
-|keywords=* 3D TECA
-* Cellular senescence
-* Fibroblast migration
-* SA-β-gal
-* TNF-α
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7032142
-}}
-{{medline-entry
-|title=Regulatory Effect of Anwulignan on the Immune Function Through Its Antioxidation and Anti-Apoptosis in D-Galactose-Induced Aging Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32099340
-|mesh-terms=* Animals
-* Antioxidants
-* Apoptosis
-* Cytokines
-* Immunologic Factors
-* Immunosenescence
-* Male
-* Medicine, Chinese Traditional
-* Mice
-* Models, Animal
-* NF-E2-Related Factor 2
-* Oxidative Stress
-* Phytochemicals
-* Schisandra
-* Spleen
-|keywords=* Anwulignan
-* anti-apoptosis
-* antioxidation
-* immunosenescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996228
-}}
-{{medline-entry
-|title=Pretreatment Frailty Is Independently Associated With Increased Risk of Infections After Immunosuppression in Patients With Inflammatory Bowel Diseases.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32105728
-|keywords=* Aging
-* Immunosuppression
-* Side Effect
-* Thiopurine
-|full-text-url=https://sci-hub.do/10.1053/j.gastro.2020.02.032
-}}
-{{medline-entry
-|title=The Citrus Flavonoid Naringenin Protects the Myocardium from Ageing-Dependent Dysfunction: Potential Role of SIRT1.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32047577
-|mesh-terms=* Aging
-* Animals
-* Antioxidants
-* Cell Line
-* Cellular Senescence
-* Citrus
-* Cytoprotection
-* Disease Models, Animal
-* Flavanones
-* Humans
-* Interleukin-6
-* Mice
-* Myocardium
-* Protein Binding
-* Rats
-* Reactive Oxygen Species
-* Sirtuin 1
-* Tumor Necrosis Factor-alpha
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7003265
-}}
-{{medline-entry
-|title=In the Absence of a TCR Signal IL-2/IL-12/18-Stimulated γδ T Cells Demonstrate Potent Anti-Tumoral Function Through Direct Killing and Senescence Induction in Cancer Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31947966
-|keywords=* IL-12
-* IL-18
-* TCR bypass stimulation
-* senescence
-* γδ T cells
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7017313
-}}
-{{medline-entry
-|title=Aging is associated with loss of beneficial effects of estrogen on leptin responsiveness in mice fed high fat diet: Role of estrogen receptor α and cytokines.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31904410
-|keywords=* Aging
-* Cytokines
-* ERα
-* Estrogen
-* Leptin sensitivity
-|full-text-url=https://sci-hub.do/10.1016/j.mad.2019.111198
-}}
-{{medline-entry
-|title=Mitochondrial Dysfunction and Alpha-Lipoic Acid: Beneficial or Harmful in Alzheimer's Disease?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31885820
-|mesh-terms=* Aging
-* Alzheimer Disease
-* Amyloid beta-Peptides
-* Animals
-* Cytokines
-* Humans
-* Inflammation Mediators
-* Mitochondria
-* Neurofibrillary Tangles
-* Neurons
-* Neuroprotective Agents
-* Thioctic Acid
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6914903
-}}
-{{medline-entry
-|title=Design, synthesis and evaluation of diosgenin carbamate derivatives as multitarget anti-Alzheimer's disease agents.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31837501
-|mesh-terms=* Aging
-* Alzheimer Disease
-* Amyloid beta-Peptides
-* Animals
-* Anti-Inflammatory Agents, Non-Steroidal
-* Astrocytes
-* Carbamates
-* Cell Line, Tumor
-* Cell Survival
-* Diosgenin
-* Dose-Response Relationship, Drug
-* Drug Design
-* Galactose
-* Humans
-* Inflammation
-* Male
-* Mice
-* Mice, Inbred ICR
-* Molecular Structure
-* Neuroprotective Agents
-* Oxidative Stress
-* Protein Aggregates
-* Structure-Activity Relationship
-|keywords=* Alzheimer’s disease
-* Anti-Aβ activity
-* Anti-inflammatory
-* Antioxidant
-* Diosgenin
-* Multi-target-directed ligands
-|full-text-url=https://sci-hub.do/10.1016/j.ejmech.2019.111913
-}}
-{{medline-entry
-|title=Oral Administration of Okara Soybean By-Product Attenuates Cognitive Impairment in a Mouse Model of Accelerated Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31816987
-|mesh-terms=* Aging
-* Animal Feed
-* Animals
-* Brain-Derived Neurotrophic Factor
-* Cognitive Dysfunction
-* Diet
-* Gastrointestinal Microbiome
-* Gene Expression Regulation
-* Hippocampus
-* Male
-* Mice
-* Soybeans
-* Tumor Necrosis Factor-alpha
-|keywords=* BDNF
-* SAMP8
-* cognitive impairment
-* neuroprotection
-* okara
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6950093
-}}
-{{medline-entry
-|title=Electric vagal nerve stimulation inhibits inflammation and improves early postoperation cognitive dysfunction in aged rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31759387
-|mesh-terms=* Aging
-* Anesthesia, General
-* Animals
-* Behavior, Animal
-* Hippocampus
-* Inflammation
-* Male
-* Maze Learning
-* NF-kappa B
-* Postoperative Cognitive Complications
-* Rats
-* Rats, Sprague-Dawley
-* Splenectomy
-* Tumor Necrosis Factor-alpha
-* Vagus Nerve Stimulation
-|keywords=* Cognitive dysfunction
-* General anesthesia
-* Inflammation
-* Vagus nerve stimulation
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6875068
-}}
-{{medline-entry
-|title=Metformin decreases LPS-induced inflammatory response in rabbit annulus fibrosus stem/progenitor cells by blocking HMGB1 release.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31772144
-|mesh-terms=* Animals
-* Annulus Fibrosus
-* Anti-Inflammatory Agents
-* Cellular Senescence
-* HMGB1 Protein
-* Inflammation
-* Intervertebral Disc Degeneration
-* Lipopolysaccharides
-* Metformin
-* Rabbits
-* Stem Cells
-|keywords=* HMGB1
-* annulus fibrosis stem cells
-* cell senescence
-* intervertebral disc degeneration
-* metformin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6914423
-}}
-{{medline-entry
-|title=The effects of blueberry and strawberry serum metabolites on age-related oxidative and inflammatory signaling in vitro.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31746877
-|mesh-terms=* Aged
-* Aging
-* Animals
-* Blueberry Plants
-* Double-Blind Method
-* Female
-* Fragaria
-* Fruit
-* Humans
-* Male
-* Microglia
-* Middle Aged
-* Nitric Oxide
-* Nitric Oxide Synthase Type II
-* Oxidative Stress
-* Postprandial Period
-* Rats
-* Tumor Necrosis Factor-alpha
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6906224
-}}
-{{medline-entry
-|title=Arsenic induces human chondrocyte senescence and accelerates rat articular cartilage aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31734849
-|keywords=* Aging
-* Arsenic
-* Articular cartilage
-* Human chondrocyte
-* Senescence
-* Senescence-associated secretory phenotype
-|full-text-url=https://sci-hub.do/10.1007/s00204-019-02607-2
-}}
-{{medline-entry
-|title=Bone Benefits of Fish Oil Supplementation Depend on its EPA and DHA Content.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31717258
-|mesh-terms=* Age Factors
-* Animals
-* Bone Density
-* Bone Density Conservation Agents
-* Bone Marrow Cells
-* Bone Remodeling
-* Bone and Bones
-* Cells, Cultured
-* Cytokines
-* Dietary Supplements
-* Disease Models, Animal
-* Docosahexaenoic Acids
-* Eicosapentaenoic Acid
-* Female
-* JNK Mitogen-Activated Protein Kinases
-* Mice, Inbred C57BL
-* Osteoporosis
-* Signal Transduction
-* p38 Mitogen-Activated Protein Kinases
-|keywords=* aging
-* bone mineral density
-* bone resorption
-* concentrated fish oil
-* cytokines
-* inflammation
-* omega-3 fatty acids
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6893665
-}}
-{{medline-entry
-|title=Inflammaging phenotype in rhesus macaques is associated with a decline in epithelial barrier-protective functions and increased pro-inflammatory function in CD161-expressing cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31713098
-|mesh-terms=* Aging
-* Animals
-* Chronic Disease
-* Cytokines
-* Disease Models, Animal
-* Epithelium
-* Flow Cytometry
-* Immunity, Innate
-* Inflammation
-* Macaca mulatta
-* NK Cell Lectin-Like Receptor Subfamily B
-* Phenotype
-* Th17 Cells
-|keywords=* CD161+ cells
-* I-FABP
-* Inflammaging
-* LBP
-* Leaky gut
-* sCD14
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6925095
-}}
-{{medline-entry
-|title=Single-cell transcriptomics reveals expansion of cytotoxic CD4 T cells in supercentenarians.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31719197
-|mesh-terms=* Adult
-* Aged
-* Aged, 80 and over
-* B-Lymphocytes
-* CD4-Positive T-Lymphocytes
-* Case-Control Studies
-* Cell Differentiation
-* Cells, Cultured
-* Clonal Evolution
-* Gene Expression Profiling
-* Humans
-* Interferon-gamma
-* Leukocytes, Mononuclear
-* Middle Aged
-* Single-Cell Analysis
-* Tumor Necrosis Factor-alpha
-|keywords=* CD4 CTL
-* aging
-* centenarian
-* single-cell transcriptome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6883788
-}}
-{{medline-entry
-|title=Gut microbiota combined with metabolomics reveals the metabolic profile of the normal aging process and the anti-aging effect of FuFang Zhenshu TiaoZhi(FTZ) in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31704617
-|mesh-terms=* Aging
-* Animals
-* Bacteria
-* Biomarkers
-* Drugs, Chinese Herbal
-* Gastrointestinal Microbiome
-* Hyperlipidemias
-* Lipid Metabolism
-* Male
-* Metabolome
-* Metabolomics
-* Mice
-* Mice, Inbred C57BL
-|keywords=* Aging
-* FTZ
-* Gut microbiota
-* Metabolomics
-|full-text-url=https://sci-hub.do/10.1016/j.biopha.2019.109550
-}}
-{{medline-entry
-|title=Intervertebral disc ageing and degeneration: The antiapoptotic effect of oestrogen.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31669486
-|mesh-terms=* Aging
-* Animals
-* Apoptosis
-* Cytokines
-* Estrogens
-* Female
-* Humans
-* Inflammation
-* Intervertebral Disc
-* Intervertebral Disc Degeneration
-* Intervertebral Disc Displacement
-* Male
-* Phosphatidylinositol 3-Kinases
-* Signal Transduction
-|keywords=* Ageing
-* Apoptosis
-* Intervertebral disc degeneration
-* Oestrogen
-* Spine
-|full-text-url=https://sci-hub.do/10.1016/j.arr.2019.100978
-}}
-{{medline-entry
-|title=MicroRNA 16-5p is upregulated in calorie-restricted mice and modulates inflammatory cytokines of macrophages.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31654705
-|mesh-terms=* Aging
-* Animals
-* Caloric Restriction
-* Cytokines
-* Diet Therapy
-* Inflammation
-* Interleukin-1beta
-* Macrophages
-* Male
-* Mice
-* Mice, Inbred C57BL
-* MicroRNAs
-* Models, Animal
-* RAW 264.7 Cells
-* Transcriptional Activation
-* Tumor Necrosis Factor-alpha
-* Up-Regulation
-|keywords=* Caloric restriction
-* Cellular immunology
-* Cytokines
-* Macrophages
-* microRNA
-|full-text-url=https://sci-hub.do/10.1016/j.gene.2019.144191
-}}
-{{medline-entry
-|title=Aerobic exercise modulates cytokine profile and sleep quality in elderly.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31656505
-|mesh-terms=* Aged
-* Cytokines
-* Exercise
-* Female
-* Humans
-* Male
-* Middle Aged
-* Sedentary Behavior
-* Sleep Wake Disorders
-|keywords=* Sleep quality
-* aerobic exercise
-* aging
-* inflammatory cytokines
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6794533
-}}
-{{medline-entry
-|title=Trehalose targets Nrf2 signal to alleviate d-galactose induced aging and improve behavioral ability.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31630800
-|mesh-terms=* Aging
-* Animals
-* Disease Models, Animal
-* Dose-Response Relationship, Drug
-* Galactose
-* Male
-* Memory Disorders
-* Mice
-* Mice, Inbred ICR
-* NF-E2-Related Factor 2
-* Signal Transduction
-* Trehalose
-|keywords=* Antioxidant stress
-* Cognitive impairment
-* Inflammation
-* Nrf2
-* Trehalose
-* d-galactose
-|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2019.10.088
-}}
-{{medline-entry
-|title=Anti-Inflammatory and Anti-Aging Evaluation of Pigment-Protein Complex Extracted from [i]Chlorella Pyrenoidosa[/i].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31623220
-|mesh-terms=* Aging
-* Animals
-* Anti-Inflammatory Agents
-* Antioxidants
-* Biological Products
-* Chlorella
-* Cytokines
-* Disease Models, Animal
-* Galactose
-* Inflammation
-* Interleukin-6
-* Lipopolysaccharides
-* Macrophages
-* Male
-* Mice
-* Mice, Inbred C57BL
-* NF-kappa B
-* Nitric Oxide
-* Oxidative Stress
-* RAW 264.7 Cells
-* Superoxide Dismutase
-* Tumor Necrosis Factor-alpha
-|keywords=* Chlorella pyrenoidosa
-* NF-κB
-* PPARs
-* anti-aging
-* anti-inflammation
-* pigment–protein complex
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6836285
-}}
-{{medline-entry
-|title=Inflammatory mediators and the risk of falls among older women with acute low back pain: data from Back Complaints in the Elders (BACE)-Brazil.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31606818
-|keywords=* Aging
-* BACE
-* Cytokines
-* Disability
-* Fall risk
-* Low back pain
-|full-text-url=https://sci-hub.do/10.1007/s00586-019-06168-x
-}}
-{{medline-entry
-|title=Acetylcholinesterase inhibitors targeting the cholinergic anti-inflammatory pathway: a new therapeutic perspective in aging-related disorders.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31583530
-|keywords=* Acetylcholinesterase inhibitor
-* Aging
-* CHRFAM7A
-* CHRNA7
-* Cholinergic anti-inflammatory pathway
-* Neuroinflammation
-|full-text-url=https://sci-hub.do/10.1007/s40520-019-01359-4
-}}
-{{medline-entry
-|title=Study on Metabolic Trajectory of Liver Aging and the Effect of Fufang Zhenzhu Tiaozhi on Aging Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31555127
-|keywords=* Fufang Zhenzhu Tiaozhi
-* liver aging
-* mass spectrometry
-* metabolomics
-* ultra-performance liquid chromatography
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6722462
-}}
-{{medline-entry
-|title=Systemic Tumor Necrosis Factor-Alpha Trajectories Relate to Brain Health in Typically Aging Older Adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31549145
-|keywords=* Brain aging
-* Cognition
-* Gray matter volume
-* Inflammation
-* Neuroimaging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7457183
-}}
-{{medline-entry
-|title=Targeting senescence improves angiogenic potential of adipose-derived mesenchymal stem cells in patients with preeclampsia.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31521202
-|mesh-terms=* Adipose Tissue
-* Adult
-* Cell Movement
-* Cell Proliferation
-* Cell Survival
-* Cellular Senescence
-* Dasatinib
-* Female
-* Humans
-* Mesenchymal Stem Cells
-* Pre-Eclampsia
-* Pregnancy
-* Protein Kinase Inhibitors
-|keywords=* Angiogenesis, Senolytics, Dasatinib
-* Mesenchymal stem cells
-* Preeclampsia
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6744626
-}}
-{{medline-entry
-|title=Suppression of gut dysbiosis by Bifidobacterium longum alleviates cognitive decline in 5XFAD transgenic and aged mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31413350
-|mesh-terms=* Aging
-* Animals
-* Bifidobacterium longum
-* Cognitive Dysfunction
-* Dysbiosis
-* Feces
-* Gastrointestinal Microbiome
-* Humans
-* Lipopolysaccharides
-* Mice
-* Mice, Transgenic
-* Probiotics
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6694197
-}}
-{{medline-entry
-|title=Moderate hyperoxia induces senescence in developing human lung fibroblasts.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31411059
-|mesh-terms=* Autophagy
-* CCAAT-Enhancer-Binding Protein-beta
-* Cell Proliferation
-* Cellular Senescence
-* Cyclin-Dependent Kinase Inhibitor p21
-* DNA Damage
-* Endoplasmic Reticulum Stress
-* Etoposide
-* Extracellular Matrix
-* Fetus
-* Fibroblasts
-* G2 Phase Cell Cycle Checkpoints
-* Gene Expression Regulation
-* Humans
-* Hyperoxia
-* Interleukin-1
-* Interleukin-8
-* Lung
-* Matrix Metalloproteinase 3
-* Oxygen
-* Plasminogen Activator Inhibitor 1
-* Primary Cell Culture
-* Tumor Necrosis Factor-alpha
-* Tumor Suppressor Protein p53
-|keywords=* autophagy
-* endoplasmic reticulum stress
-* lung development
-* oxygen
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6879905
-}}
-{{medline-entry
-|title=Aging-related carcinoembryonic antigen-related cell adhesion molecule 1 signaling promotes vascular dysfunction.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31389127
-|mesh-terms=* Aged
-* Aging
-* Animals
-* Antigens, CD
-* Cell Adhesion Molecules
-* Cells, Cultured
-* Endothelium, Vascular
-* Humans
-* Mice
-* Mice, Inbred C57BL
-* Mice, Knockout
-* Middle Aged
-* Signal Transduction
-|keywords=* aging
-* anti-aging
-* cytokines
-* inflammation
-* mouse
-* reactive oxygen species
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826129
-}}
-{{medline-entry
-|title=Microglia Express Insulin-Like Growth Factor-1 in the Hippocampus of Aged APP /PS1  Transgenic Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31417357
-|keywords=* aging
-* cerebral amyloidosis
-* insulin-like growth factor
-* neurogenesis
-* neuroinflammation
-* tumor necrosis factor
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6682662
-}}
-{{medline-entry
-|title=Age- and diet-specific effects of chronic exposure to chlorpyrifos on hormones, inflammation and gut microbiota in rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31400786
-|mesh-terms=* Aging
-* Animals
-* Chlorpyrifos
-* Diet, High-Fat
-* Gastrointestinal Microbiome
-* Hypothalamo-Hypophyseal System
-* Inflammation
-* Male
-* Pituitary-Adrenal System
-* RNA, Ribosomal, 16S
-* Rats
-|keywords=* 16S rRNA gene sequencing
-* Gut endocrine
-* Gut-brain axis
-* Hormone
-* Hypothalamic-pituitary-adrenal axis
-* Inflammation
-|full-text-url=https://sci-hub.do/10.1016/j.pestbp.2019.05.018
-}}
-==TOMM20==
-{{medline-entry
-|title=Effect of aging on mitochondria and metabolism of bovine granulosa cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32921645
-|keywords=* Aging
-* Cow
-* Granulosa cells
-* Mitochondria
-|full-text-url=https://sci-hub.do/10.1262/jrd.2020-071
-}}
-==TP53==
-{{medline-entry
-|title=p53 inhibits the osteogenic differentiation but does not induce senescence in human dental follicle cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32473528
-|keywords=* Cellular senescence
-* Dental follicle cells
-* E2F-1
-* Osteogenic differentiation
-* p53
-|full-text-url=https://sci-hub.do/10.1016/j.diff.2020.05.003
-}}
-{{medline-entry
-|title=Mutational spectrum and dynamics of clonal hematopoiesis in anemia of older individuals.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32243522
-|mesh-terms=* Age Factors
-* Aged
-* Aging
-* Anemia
-* Female
-* Hematopoiesis
-* Humans
-* Kaplan-Meier Estimate
-* Male
-* Middle Aged
-* Mutation
-* Prospective Studies
-|full-text-url=https://sci-hub.do/10.1182/blood.2019004362
-}}
-{{medline-entry
-|title=[[TP53]]/miR-34a-associated signaling targets [i]SERPINE1[/i] expression in human pancreatic cancer.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31986125
-|keywords=* Aging
-* PDAC
-* SERPINE1
-* TP53
-* cancer
-* miR-34a
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7041729
-}}
-{{medline-entry
-|title=Expression of p16 in nodular fasciitis: an implication for self-limited and inflammatory nature of the lesion.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31933915
-|keywords=* CDK4
-* MDM2
-* TP53
-* nodular fasciitis
-* p16
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6945175
-}}
-==TPH1==
-{{medline-entry
-|title=[i]Lactobacillus plantarum[/i] DR7 improved brain health in aging rats via the serotonin, inflammatory and apoptosis pathways.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33245015
-|keywords=* Lactobacillus spp.
-* aging
-* brain
-|full-text-url=https://sci-hub.do/10.3920/BM2019.0200
-}}
-==TPO==
-{{medline-entry
-|title=Megakaryocytes promote osteoclastogenesis in aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32634116
-|keywords=* aging
-* bone marrow macrophage
-* megakaryocyte
-* osteoclast
-* thrombopoietin
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7425434
-}}
-==TPP1==
-{{medline-entry
-|title=FBW7 Mediates Senescence and Pulmonary Fibrosis through Telomere Uncapping.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33086033
-|keywords=* DNA damage response
-* FBXW7
-* TPP1
-* cellular senescence
-* chronic stress
-* idiopathic pulmonary fibrosis
-* premature aging
-* proteostasis
-* stem cells
-* telomere
-* telomere uncapping
-|full-text-url=https://sci-hub.do/10.1016/j.cmet.2020.10.004
-}}
-==TPR==
-{{medline-entry
-|title=Catalytic Performances of Cu/MCM-22 Zeolites with Different Cu Loadings in NH -SCR.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33143192
-|keywords=* Cu loading
-* Cu/MCM-22
-* NH3-SCR
-* hydrothermal aging
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7694057
-}}
-{{medline-entry
-|title=Do traits of plant species predict the efficacy of species distribution models for finding new occurrences?
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32551077
-|keywords=* dispersal
-* generalist
-* lifespan
-* niche models
-* range size
-* specialist
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7297770
-}}
-{{medline-entry
-|title=In-situ modified the surface of Pt-doped perovskite catalyst for soot oxidation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31541957
-|keywords=* Aging resistance
-* Amorphization
-* Surface modification
-* Symmetrical structure
-|full-text-url=https://sci-hub.do/10.1016/j.jhazmat.2019.121210
-}}
-==TRAF3==
-{{medline-entry
-|title=[[TRAF3]], a Target of MicroRNA-363-3p, Suppresses Senescence and Regulates the Balance Between Osteoblastic and Adipocytic Differentiation of Rat Bone Marrow-Derived Mesenchymal Stem Cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32111144
-|keywords=* TRAF3
-* adipogenic differentiation
-* bone marrow-derived mesenchymal stem cells
-* miR-363-3p
-* osteogenic differentiation
-* senescence
-|full-text-url=https://sci-hub.do/10.1089/scd.2019.0276
-}}
-==TREM2==
-{{medline-entry
-|title=Loss of [[TREM2]] Confers Resilience to Synaptic and Cognitive Impairment in Aged Mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33139402
-|keywords=* TREM2
-* aging
-* dendritic spine density
-* learning and memory
-* long-term potentiation
-* synaptic plasticity
-|full-text-url=https://sci-hub.do/10.1523/JNEUROSCI.2193-20.2020
-}}
-{{medline-entry
-|title=Triggering Receptor Expressed on Myeloid Cell 2 R47H Exacerbates Immune Response in Alzheimer's Disease Brain.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33101276
-|keywords=* NKG2D ligands
-* aging
-* inflammation
-* interferon type I response
-* microglia
-* neurodegeneration
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7546799
-}}
-{{medline-entry
-|title=Knockdown of astrocytic [[TREM2]] in the hippocampus relieves cognitive decline in elderly male mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32991925
-|keywords=* Aging
-* Long-term potentiation
-* TREM2
-* astrocytes
-* learning and memory
-|full-text-url=https://sci-hub.do/10.1016/j.bbr.2020.112939
-}}
-==TRIM21==
-{{medline-entry
-|title=[[TRIM21]] overexpression promotes tumor progression by regulating cell proliferation, cell migration and cell senescence in human glioma.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32064156
-|keywords=* Glioma
-* TRIM21
-* cell senescence
-* drug resistance
-* p53-p21 pathway
-* prognosis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7017742
-}}
-==TRIM27==
-{{medline-entry
-|title=[[TRIM27]] Functions as a Novel Oncogene in Non-Triple-Negative Breast Cancer by Blocking Cellular Senescence through p21 Ubiquitination.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33251042
-|keywords=* EP300
-* TRIM27
-* breast cancer
-* cell apoptosis
-* cell senescence
-* chemoresistance
-* p21
-* prognosis
-* transcription
-* ubiquitination
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7666371
-}}
-==TRIP13==
-{{medline-entry
-|title=BubR1 allelic effects drive phenotypic heterogeneity in mosaic-variegated aneuploidy progeria syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31738183
-|mesh-terms=* Aging
-* Alleles
-* Animals
-* Cell Cycle Proteins
-* Chromosome Disorders
-* Lung Neoplasms
-* Mice
-* Mice, Inbred C57BL
-* Mitosis
-* Mosaicism
-* Mutation
-* Phenotype
-* Progeria
-* Protein-Serine-Threonine Kinases
-|keywords=* Aging
-* Cancer
-* Cellular senescence
-* Genetic diseases
-* Oncology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6934189
-}}
-==TRPC6==
-{{medline-entry
-|title=Redox and mTOR-dependent regulation of plasma lamellar calcium influx controls the senescence-associated secretory phenotype.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32686475
-|keywords=* SASP
-* Senescence
-* TRPC6
-* calcium
-* hydrogen peroxide
-* mTOR
-|full-text-url=https://sci-hub.do/10.1177/1535370220943122
-}}
-==TRPC7==
-{{medline-entry
-|title=Nociceptive transient receptor potential canonical 7 ([[TRPC7]]) mediates aging-associated tumorigenesis induced by ultraviolet B.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31755176
-|keywords=* TRPC7
-* aging
-* p53
-* tumor initiator gene
-* tumorigenesis
-* ultraviolet pathology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6974716
-}}
-==TRPV4==
-{{medline-entry
-|title=[[TRPV4]] receptor as a functional sensory molecule in bladder urothelium: Stretch-independent, tissue-specific actions and pathological implications.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31914645
-|mesh-terms=* Animals
-* Calcium
-* Guinea Pigs
-* Humans
-* Muscle Contraction
-* Muscle, Smooth
-* TRPV Cation Channels
-* Urinary Bladder
-* Urothelium
-|keywords=* ATP release
-* TRPV4 receptor
-* aging
-* overactive bladders
-* urothelium
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6973053
-}}
-{{medline-entry
-|title=Exercise restores impaired endothelium-derived hyperpolarizing factor-mediated vasodilation in aged rat aortic arteries via the [[TRPV4]]-K 2.3 signaling complex.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31564840
-|mesh-terms=* Animals
-* Biological Factors
-* Cardiovascular Diseases
-* Endothelial Cells
-* Endothelium, Vascular
-* Male
-* Potassium Channels, Calcium-Activated
-* Rats
-* Rats, Sprague-Dawley
-* TRPV Cation Channels
-* Vasodilation
-|keywords=* EDHF
-* KCa2.3
-* TRPV4
-* aging
-* endothelium
-* exercise
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6731547
-}}
-==TSPO==
-{{medline-entry
-|title=Age and Sex Influence the Neuro-inflammatory Response to a Peripheral Acute LPS Challenge.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31749696
-|keywords=* 18 kDa translocator protein
-* aging
-* astrocytes
-* microglia
-* neuroinflammation
-* triggering receptor expressed on myeloid cells 2
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6848890
-}}
-{{medline-entry
-|title=Upregulation of cannabinoid receptor type 2, but not [[TSPO]], in senescence-accelerated neuroinflammation in mice: a positron emission tomography study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31707986
-|mesh-terms=* Aging
-* Animals
-* Brain
-* Inflammation
-* Mice
-* Microglia
-* Positron-Emission Tomography
-* Radiopharmaceuticals
-* Receptor, Cannabinoid, CB2
-* Receptors, GABA
-* Up-Regulation
-|keywords=* Cannabinoid receptor type 2
-* Immunostaining
-* Microglial activation
-* Positron emission tomography
-* Senescence-accelerated prone mouse
-* Translocator protein
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6842455
-}}
-==TST==
-{{medline-entry
-|title=H S Donors Reverse Age-Related Gastric Malfunction Impaired Due to Fructose-Induced Injury [i]via[/i] CBS, CSE, and [[TST]] Expression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32848752
-|keywords=* aging
-* donor
-* fructose
-* gastric mucosa
-* hydrogen sulfide
-* oxidative stress
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7396573
-}}
-{{medline-entry
-|title=Adaptations in mechanical muscle function, muscle morphology, and aerobic power to high-intensity endurance training combined with either traditional or power strength training in older adults: a randomized clinical trial.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32239311
-|keywords=* Aging
-* Concurrent training
-* Explosive force
-* Functional capacity
-* HIIT
-|full-text-url=https://sci-hub.do/10.1007/s00421-020-04355-z
-}}
-{{medline-entry
-|title=Digital phenotyping by consumer wearables identifies sleep-associated markers of cardiovascular disease risk and biological aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31602410
-|mesh-terms=* Adult
-* Aged
-* Aging
-* Body Mass Index
-* Cardiovascular Diseases
-* Cohort Studies
-* Female
-* Humans
-* Male
-* Middle Aged
-* Risk Factors
-* Self Report
-* Sleep
-* Telomere
-* Waist Circumference
-* Wearable Electronic Devices
-* Young Adult
-|keywords=* Data integration
-* Predictive markers
-* Risk factors
-* Senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6778117
-}}
-{{medline-entry
-|title=Objective Sleep Duration in Older Adults: Results From The Irish Longitudinal Study on Ageing.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31579942
-|mesh-terms=* Accelerometry
-* Aged
-* Aging
-* Cross-Sectional Studies
-* Exercise
-* Female
-* Health Status
-* Humans
-* Independent Living
-* Ireland
-* Longitudinal Studies
-* Male
-* Polysomnography
-* Self Report
-* Sleep
-* Time Factors
-|keywords=* GENEActiv
-* accelerometer
-* actigraphy
-* older population
-* sleep duration
-|full-text-url=https://sci-hub.do/10.1111/jgs.16177
-}}
-==TTL==
-{{medline-entry
-|title=Longitudinal Associations of Body Mass Index, Waist Circumference, and Waist-to-Hip Ratio with Biomarkers of Oxidative Stress in Older Adults: Results of a Large Cohort Study.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31986512
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Biomarkers
-* Body Mass Index
-* Cohort Studies
-* Female
-* Germany
-* Humans
-* Longitudinal Studies
-* Male
-* Middle Aged
-* Oxidative Stress
-* Waist Circumference
-* Waist-Hip Ratio
-|keywords=* Body mass index
-* Free radicals
-* Oxidative stress
-* Reactive oxygen metabolites
-* Total thiol levels
-* Waist circumference
-* Waist-to-hip ratio
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7098284
-}}
-==TTN==
-{{medline-entry
-|title=LncRNA [[TTN]]-AS1 regulates osteosarcoma cell apoptosis and drug resistance via the miR-134-5p/MBTD1 axis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31600142
-|mesh-terms=* Aging
-* Apoptosis
-* Brain Neoplasms
-* Cell Line, Tumor
-* Cell Proliferation
-* Chromosomal Proteins, Non-Histone
-* Computational Biology
-* Drug Resistance
-* Gene Expression Regulation, Neoplastic
-* Humans
-* MicroRNAs
-* Osteosarcoma
-* RNA, Long Noncoding
-|keywords=* aging and age-related diseases
-* lncRNA TTN-AS1
-* malignant brain tumour domain containing protein 1
-* miR-134-5p
-* osteosarcoma
-* resistance
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6814585
-}}
-==TTR==
-{{medline-entry
-|title=Cellular secretion and cytotoxicity of transthyretin mutant proteins underlie late-onset amyloidosis and neurodegeneration.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31728576
-|mesh-terms=* Amyloid Neuropathies, Familial
-* Animals
-* Cell Death
-* Cell Line, Tumor
-* Disease Models, Animal
-* Drosophila
-* HEK293 Cells
-* Humans
-* Locomotion
-* Longevity
-* Mutant Proteins
-* Mutation
-* Nerve Degeneration
-* Prealbumin
-|keywords=* Amyloidosis
-* Drosophila melanogaster
-* ERQC
-* Endoplasmic reticulum quality control
-* Proteostasis
-* TTR
-* Transthyretin
-|full-text-url=https://sci-hub.do/10.1007/s00018-019-03357-1
-}}
-==TXNIP==
-{{medline-entry
-|title=Panax notoginseng saponins attenuate neuroinflammation through [[TXNIP]]-mediated NLRP3 inflammasome activation in aging rats.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33176641
-|keywords=* Aging
-* Microglia
-* NLRP3 inflammasome
-* Saponins from Panax notoginseng.
-* TXNIP
-* neuroinflammation
-|full-text-url=https://sci-hub.do/10.2174/1389201021999201110204735
-}}
-{{medline-entry
-|title=Redox homeostasis and cell cycle activation mediate beta-cell mass expansion in aged, diabetes-prone mice under metabolic stress conditions: Role of thioredoxin-interacting protein ([[TXNIP]]).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33128997
-|keywords=* Aging
-* Beta-cells
-* Cell cycle
-* Metabolic stress
-* Redox homeostasis
-* Thioredoxin-interacting protein
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7589534
-}}
-{{medline-entry
-|title=[Effect of diabetic induced thioredoxin interacting protein ([[TXNIP]]) on islet cell senescence].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32744003
-|mesh-terms=* Animals
-* Carrier Proteins
-* Cellular Senescence
-* Diabetes Mellitus, Experimental
-* Islets of Langerhans
-* Mice
-* Thioredoxins
-|keywords=* INS-1 cell
-* cell senescence
-* diabetes
-* thioredoxin interacting protein
-|full-text-url=https://sci-hub.do/10.12047/j.cjap.5878.2020.027
-}}
-{{medline-entry
-|title=PRMT5-TRIM21 interaction regulates the senescence of osteosarcoma cells by targeting the [[TXNIP]]/p21 axis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32023548
-|keywords=* PRMT5
-* TRIM21
-* TXNIP
-* p21
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7041745
-}}
-==TXNRD2==
-{{medline-entry
-|title=Wogonin induces cellular senescence in breast cancer via suppressing [[TXNRD2]] expression.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32671444
-|keywords=* Breast cancer
-* Immune surveillance
-* ROS
-* Senescence
-* TXNRD2
-* Wogonin
-|full-text-url=https://sci-hub.do/10.1007/s00204-020-02842-y
-}}
-==U2AF1==
-{{medline-entry
-|title=Isobaric tags for relative and absolute quantitation (iTRAQ)-based proteomic analysis of mRNA splicing relevant proteins in aging HSPCs.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32141009
-|keywords=* Aging
-* DEPs
-* HSPC
-* iTRAQ
-* mRNA splicing
-|full-text-url=https://sci-hub.do/10.1007/s40520-020-01509-z
-}}
-==UACA==
-{{medline-entry
-|title=Knockdown of [i][[UACA]][/i] inhibitsproliferation and invasion and promotes senescence of hepatocellular carcinoma cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31949867
-|keywords=* HIF1α
-* UACA
-* hepatocellular carcinoma
-* invasion
-* knockdown
-* proliferation
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6962967
-}}
-==UCHL1==
-{{medline-entry
-|title=Abolishing [[UCHL1]]'s hydrolase activity exacerbates TBI-induced axonal injury and neuronal death in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33159930
-|keywords=* Aging
-* Axonal injury
-* Neurodegeneration
-* Traumatic brain injury
-* Ubiquitin carboxy terminal hydrolase L1
-* Ubiquitin proteasome pathway
-|full-text-url=https://sci-hub.do/10.1016/j.expneurol.2020.113524
-}}
-==UCP1==
-{{medline-entry
-|title=Muscle-dependent regulation of adipose tissue function in long-lived growth hormone-mutant mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32464603
-|keywords=* adipose tissue
-* aging
-* growth hormone
-* inflammation
-* uncoupling protein 1 (UCP1)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7288969
-}}
-{{medline-entry
-|title=Lack of [[UCP1]] stimulates fatty liver but mediates [[UCP1]]-independent action of beige fat to improve hyperlipidemia in Apoe knockout mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32179129
-|keywords=* Apoe knockout mice
-* Beige fat
-* Gene expression
-* Hyperlipidemia
-* Longevity
-* Uncoupling protein 1
-|full-text-url=https://sci-hub.do/10.1016/j.bbadis.2020.165762
-}}
-{{medline-entry
-|title=Postnatal leptin surge is critical for the transient induction of the developmental beige adipocytes in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31961706
-|mesh-terms=* Adipocytes, Beige
-* Adipocytes, White
-* Adipose Tissue
-* Aging
-* Animals
-* Dose-Response Relationship, Drug
-* Female
-* Leptin
-* Male
-* Mice
-* Mice, Obese
-* Sympathetic Nervous System
-* Tyrosine 3-Monooxygenase
-* Uncoupling Protein 1
-|keywords=* beige adipocytes
-* leptin
-* sympathetic nerve system
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191411
-}}
-{{medline-entry
-|title=Age-related sex differences in the expression of important disease-linked mitochondrial proteins in mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31806023
-|mesh-terms=* Adipose Tissue, Brown
-* Aging
-* Animals
-* Brain
-* Female
-* Male
-* Mice, Inbred C57BL
-* Mitochondrial Proteins
-* Muscle, Skeletal
-* Sex Characteristics
-* Spleen
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6896328
-}}
-{{medline-entry
-|title=An anti-inflammatory phenotype in visceral adipose tissue of old lean mice, augmented by exercise.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31427677
-|mesh-terms=* Adipocytes
-* Aging
-* Animals
-* Humans
-* Inflammation
-* Intra-Abdominal Fat
-* Macrophages
-* Mice
-* Obesity
-* Phenotype
-* Physical Conditioning, Animal
-* Resistance Training
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6700172
-}}
-==UGT2B28==
-{{medline-entry
-|title=Ages of hepatocellular carcinoma occurrence and life expectancy are associated with a [[UGT2B28]] genomic variation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31805979
-|mesh-terms=* Adult
-* Age of Onset
-* Aged
-* Aged, 80 and over
-* Carcinoma, Hepatocellular
-* Female
-* Genetic Association Studies
-* Genetic Predisposition to Disease
-* Glucuronosyltransferase
-* Humans
-* Life Expectancy
-* Liver Neoplasms
-* Male
-* Middle Aged
-* Neoplasm Metastasis
-* Neoplasm Recurrence, Local
-* Odds Ratio
-* Polymorphism, Single Nucleotide
-* Survival Analysis
-* Young Adult
-|keywords=* Alcoholism
-* Xenobiotic metabolizing enzymes
-* Young hepatocellular carcinoma; age of death
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6896495
-}}
-==USP7==
-{{medline-entry
-|title=Deubiquitinase [[USP7]] regulates [i]Drosophila[/i] aging through ubiquitination and autophagy.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33221768
-|keywords=* DMC
-* Drosophila
-* USP7
-* aging
-* autophagy
-|full-text-url=https://sci-hub.do/10.18632/aging.104067
-}}
-==VCAM1==
-{{medline-entry
-|title=Sunitinib facilitates metastatic breast cancer spreading by inducing endothelial cell senescence.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32993785
-|keywords=* Cell senescence
-* Metastasis
-* Metastatic breast cancer (MBC)
-* Receptor tyrosine kinase (RTK)
-* Sunitinib
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7526390
-}}
-==VDAC1==
-{{medline-entry
-|title=Low abundance of NDUFV2 and NDUFS4 subunits of the hydrophilic complex I domain and [[VDAC1]] predicts mammalian longevity.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32353747
-|keywords=* Complex I
-* Droplet digital PCR
-* Longevity
-* Mammals
-* Mitochondria
-* NDUFS4 subunit
-* NDUFV2 subunit
-* VDAC
-* Western blot
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191849
-}}
-{{medline-entry
-|title=Changes in the expression of oxidative phosphorylation complexes in the aging intestinal mucosa.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32173460
-|keywords=* Aging
-* Colonic crypt
-* Expression
-* Intestine
-* Mitochondria
-* OXPHOS
-|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110924
-}}
-==VDR==
-{{medline-entry
-|title=25-Hydroxyvitamin D  positively regulates periodontal inflammaging via SOCS3/STAT signaling in diabetic mice.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31917967
-|keywords=* 25-Hydroxyvitamin D(3)
-* Diabetic periodontitis
-* Inflammaging
-* SOCS3
-* Senescence
-* Senescence-associated secretory phenotypes
-|full-text-url=https://sci-hub.do/10.1016/j.steroids.2019.108570
-}}
-{{medline-entry
-|title=1,25-Dihydroxyvitamin D protects against age-related osteoporosis by a novel [[VDR]]-Ezh2-p16 signal axis.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31880094
-|mesh-terms=* 25-Hydroxyvitamin D3 1-alpha-Hydroxylase
-* Aging
-* Animals
-* Bone and Bones
-* Cells, Cultured
-* Cyclin-Dependent Kinase Inhibitor p16
-* Cyclin-Dependent Kinase Inhibitor p19
-* DNA Damage
-* Enhancer of Zeste Homolog 2 Protein
-* Female
-* Histones
-* Male
-* Mesenchymal Stem Cells
-* Mice
-* Mice, Knockout
-* Osteocytes
-* Osteogenesis
-* Osteoporosis
-* Oxidative Stress
-* Receptors, Calcitriol
-* Vitamin D
-|keywords=* Ezh2
-* Vitamin D
-* cellular senescence
-* osteogenesis
-* osteoporosis
-* p16
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6996957
-}}
-{{medline-entry
-|title=Active vitamin D impedes the progression of non-alcoholic fatty liver disease by inhibiting cell senescence in a rat model.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31810868
-|keywords=* Active vitamin D
-* Cell senescence
-* Non-alcoholic fatty liver disease
-* Oxidative stress
-* P53-p21 signaling pathway
-* Vitamin D receptor
-|full-text-url=https://sci-hub.do/10.1016/j.clinre.2019.10.007
-}}
-==VEGFA==
-{{medline-entry
-|title=APOE ε4-specific associations of VEGF gene family expression with cognitive aging and Alzheimer's disease.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31791659
-|mesh-terms=* Aged
-* Aged, 80 and over
-* Aging
-* Apolipoprotein E4
-* Cognitive Aging
-* Cognitive Dysfunction
-* Female
-* Gene Expression
-* Genetic Association Studies
-* Genetic Predisposition to Disease
-* Genotype
-* Humans
-* Male
-* Neovascularization, Physiologic
-* Neuropilin-1
-* Vascular Endothelial Growth Factor A
-|keywords=* APOE-ε4
-* Aging
-* Cognition
-* Gene expression
-* Vascular endothelial growth factor (VEGF)
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7064375
-}}
-==VGLL4==
-{{medline-entry
-|title=The lncRNA MEG3/miR-16-5p/[[VGLL4]] regulatory axis is involved in etoposide-induced senescence of tumor cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33141998
-|keywords=* LncRNA MEG3
-* breast cancer
-* cell senescence
-* etoposide
-* lung adenocarcinoma
-|full-text-url=https://sci-hub.do/10.1002/jgm.3291
-}}
-==VHL==
-{{medline-entry
-|title=Hypoxic response regulators RHY-1 and EGL-9/PHD promote longevity through a [[VHL]]-1-independent transcriptional response.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32399915
-|keywords=* Aging
-* C. elegans
-* EGL-9/PHD
-* HIF-1 signaling
-* Hypoxic response
-* Lifespan
-* RHY-1
-|full-text-url=https://sci-hub.do/10.1007/s11357-020-00194-0
-}}
-==VIM==
-{{medline-entry
-|title=Establishment and characterization of a fibroblast cell line from postmortem skin of an adult Chinese muntjac (Muntiacus reevesi).
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31898011
-|mesh-terms=* Aging
-* Animals
-* Cell Culture Techniques
-* Cell Line
-* Cell Proliferation
-* Cell Shape
-* Chromosomes, Mammalian
-* Fibroblasts
-* Male
-* Muntjacs
-* Postmortem Changes
-* Skin
-|keywords=* Characteristics
-* Chinese muntjac
-* Fibroblast cell line
-* Postmortem skin
-|full-text-url=https://sci-hub.do/10.1007/s11626-019-00422-8
-}}
-==VIP==
-{{medline-entry
-|title=Alterations in Intrinsic and Synaptic Properties of Hippocampal CA1 [[VIP]] Interneurons During Aging.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33173468
-|keywords=* VIP
-* action potential
-* aging
-* calretinin
-* circuit disinhibition
-* hippocampus
-* synapse
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7591401
-}}
-{{medline-entry
-|title=Nutrition and exercise interventions could ameliorate age-related cognitive decline: a meta-analysis of randomized controlled trials.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33052590
-|keywords=* Aging
-* Cognitive impairment
-* Exercise
-* Meta-analysis
-* Nutrition
-|full-text-url=https://sci-hub.do/10.1007/s40520-020-01730-w
-}}
-==VSIG4==
-{{medline-entry
-|title=Immune checkpoint protein [[VSIG4]] as a biomarker of aging in murine adipose tissue.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32856419
-|keywords=* VSIG4
-* adipose tissue
-* aging
-* frailty index
-* immune checkpoint
-* inflammation
-* macrophage
-* mouse
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7576241
-}}
-==WASL==
-{{medline-entry
-|title=Loss of Wasl improves pancreatic cancer outcome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32434991
-|keywords=* Cancer
-* Cellular senescence
-* Mouse models
-* Oncology
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7259520
-}}
-==WDR5==
-{{medline-entry
-|title=Inhibition of the H3K4 methyltransferase MLL1/[[WDR5]] complex attenuates renal senescence in ischemia reperfusion mice by reduction of p16 .
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31570196
-|mesh-terms=* Acute Kidney Injury
-* Animals
-* Biphenyl Compounds
-* Cell Line
-* Cyclin-Dependent Kinase Inhibitor p16
-* Dihydropyridines
-* Drug Evaluation, Preclinical
-* Fibroblasts
-* Histone-Lysine N-Methyltransferase
-* Histones
-* Intracellular Signaling Peptides and Proteins
-* Male
-* Mice, Inbred C57BL
-* Myeloid-Lymphoid Leukemia Protein
-* Rats
-* Renal Insufficiency
-* Reperfusion Injury
-|keywords=* H3K4me3
-* MLL1
-* WDR5
-* acute kidney injury
-* p16(INK4a)
-* senescence
-|full-text-url=https://sci-hub.do/10.1016/j.kint.2019.06.021
-}}
-==WFDC2==
-{{medline-entry
-|title=Differences in biomarkers and molecular pathways according to age for patients with HFrEF.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33002110
-|keywords=* aging
-* biological age
-* biomarkers
-* chronological age
-* heart failure with reduced ejection fraction
-|full-text-url=https://sci-hub.do/10.1093/cvr/cvaa279
-}}
-==WIPI2==
-{{medline-entry
-|title=Neuronal autophagy declines substantially with age and is rescued by overexpression of [[WIPI2]].
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31794336
-|mesh-terms=* Aging
-* Animals
-* Autophagy
-* Autophagy-Related Proteins
-* Mice, Transgenic
-* Models, Biological
-* Neurons
-* Phagosomes
-* Phosphate-Binding Proteins
-* RNA, Messenger
-|keywords=* Aging
-* WIPI2
-* autophagosome biogenesis
-* autophagy
-* macroautophagy
-* neurodegeneration
-* neuronal autophagy
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6984449
-}}
-==WNT1==
-{{medline-entry
-|title=Plasma proteomic profile of age, health span, and all-cause mortality in older adults.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33089916
-|keywords=* SomaScan® assay
-* aging
-* proteomics
-* weighted gene co-expression network analysis
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7681045
-}}
-==WNT10A==
-{{medline-entry
-|title=Dysregulation of the Wnt Signaling Pathway and Synovial Stem Cell Dysfunction in Osteoarthritis Development.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31964233
-|keywords=* Wnt signaling pathway
-* cell senescence
-* differentiation
-* osteoarthritis
-* synovial mesenchymal stem cells (SMSCs)
-|full-text-url=https://sci-hub.do/10.1089/scd.2019.0260
 }}
 ==WNT3A==
@@ Строка 37 307: / Строка 4118: @@
 |title=Chronic WNT/β-catenin signaling induces cellular senescence in lung epithelial cells.
 |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32109549
+|abstract=The rapid expansion of the elderly population has led to the recent epidemic of age-related diseases, including increased incidence and mortality of chronic lung diseases, such as Idiopathic Pulmonary Fibrosis (IPF). Cellular senescence is a major hallmark of aging and has a higher occurrence in IPF. The lung epithelium represents a major site of tissue injury, cellular senescence and aberrant activity of developmental pathways such as the WNT/β-catenin pathway in IPF. The potential impact of WNT/β-catenin signaling on alveolar epithelial senescence in general as well as in IPF, however, remains elusive. Here, we characterized alveolar epithelial cells of aged mice and assessed the contribution of chronic WNT/β-catenin signaling on alveolar epithelial type (AT) II cell senescence. Whole lungs from old (16-24 months) versus young (3 months) mice had relatively less epithelial (EpCAM ) but more inflammatory (CD45 ) cells, as assessed by flow cytometry. Compared to young ATII cells, old ATII cells showed decreased expression of the ATII cell marker Surfactant Protein C along with increased expression of the ATI cell marker Hopx, accompanied by increased WNT/β-catenin activity. Notably, when placed in an organoid assay, old ATII cells exhibited decreased progenitor cell potential. Chronic canonical WNT/β-catenin activation for up to 7 days in primary ATII cells as well as alveolar epithelial cell lines induced a robust cellular senescence, whereas the non-canonical ligand WNT5A was not able to induce cellular senescence. Moreover, chronic [[WNT3A]] treatment of precision-cut lung slices (PCLS) further confirmed ATII cell senescence. Simultaneously, chronic but not acute WNT/β-catenin activation induced a profibrotic state with increased expression of the impaired ATII cell marker Keratin 8. These results suggest that chronic WNT/β-catenin activity in the IPF lung contributes to increased ATII cell senescence and reprogramming. In the fibrotic environment, WNT/β-catenin signaling thus might lead to further progenitor cell dysfunction and impaired lung repair.
 |keywords=* ATII cells
@@ Строка 37 315: / Строка 4126: @@
 * WNT signaling
 |full-text-url=https://sci-hub.do/10.1016/j.cellsig.2020.109588
-}}
-==WNT7A==
-{{medline-entry
-|title=Exogenous Expression of [[WNT7A]] in Leukemia-Derived Cell Lines Induces Resistance to Chemotherapeutic Agents.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32436833
-|keywords=* WNT signaling
-* WNT7A
-* cell cycle
-* chemotherapeutic agents
-* leukemias
-* senescence
-|full-text-url=https://sci-hub.do/10.2174/1871520620666200521114100
-}}
-==WRN==
-{{medline-entry
-|title=The Impact of Vitamin C on Different System Models of Werner Syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33202145
-|keywords=* Werner syndrome
-* aging
-* mouse
-* stem cells
-* vitamin C
-* worm
-|full-text-url=https://sci-hub.do/10.1089/ars.2020.8147
-}}
-{{medline-entry
-|title=[[WRN]] modulates translation by influencing nuclear mRNA export in HeLa cancer cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33054770
-|keywords=* Cancer
-* NXF1 export receptor
-* Senescence
-* Translation
-* Werner syndrome protein
-* mRNA export
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7557079
-}}
-{{medline-entry
-|title=MIB1-mediated degradation of [[WRN]] promotes cellular senescence in response to camptothecin treatment.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32652764
-|keywords=* CPT
-* Mind bomb 1
-* Werner syndrome protein
-* aging
-* protein stability
-|full-text-url=https://sci-hub.do/10.1096/fj.202000268RRR
-}}
-{{medline-entry
-|title=A Case Report of Werner's Syndrome With a Novel Mutation From India.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32528764
-|keywords=* aging
-* novel mutation
-* progeria
-* werner syndrome
-* wrn gene
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7282380
-}}
-{{medline-entry
-|title=Evidence for premature aging in a Drosophila model of Werner syndrome.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31518666
-|mesh-terms=* Aging, Premature
-* Animals
-* Behavior, Animal
-* Body Composition
-* Body Weight
-* DNA Repair
-* Drosophila
-* Drosophila Proteins
-* Exonucleases
-* Female
-* Gastrointestinal Neoplasms
-* Male
-* Motor Activity
-* Muscle Weakness
-* Mutation
-* Phenotype
-* Werner Syndrome
-|keywords=* Aging
-* DNA repair
-* Locomotor function
-* Tumor
-* Werner syndrome
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6935377
-}}
-==WT1==
-{{medline-entry
-|title=Age and weight at first mating affects plasma leptin concentration but no effects on reproductive performance of gilts.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31602307
-|keywords=* Backfat
-* Gilts
-* Leptin
-* Litter performance
-* Longevity
-* Mating
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6778857
-}}
-==WWP1==
-{{medline-entry
-|title=The ubiquitin ligase [[WWP1]] contributes to shifts in matrix proteolytic profiles and a myocardial aging phenotype with diastolic heart.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32822210
-|mesh-terms=* Age Factors
-* Animals
-* Cells, Cultured
-* Diastole
-* Disease Models, Animal
-* Extracellular Matrix
-* Female
-* Fibroblasts
-* Heart Failure
-* Hypertrophy, Left Ventricular
-* Male
-* Mice, Inbred C57BL
-* Mice, Transgenic
-* Myocardium
-* Phenotype
-* Proteolysis
-* Stroke Volume
-* Ubiquitin-Protein Ligases
-* Ventricular Dysfunction, Left
-* Ventricular Function, Left
-* Ventricular Remodeling
-|keywords=* aging
-* cardiac hypertrophy
-* diastolic dysfunction
-* heart failure
-* ventricular remodeling
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7717125
-}}
-==XBP1==
-{{medline-entry
-|title=Age-dependent impairment of adipose-derived stem cells isolated from horses.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31900232
-|keywords=* Aging
-* Endoplasmic reticulum stress
-* Equine adipose-derived mesenchymal stem cells
-* Insulin resistance
-* Pro-inflammatory cytokines
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6942290
 }}
 ==XDH==
@@ Строка 37 479: / Строка 4132: @@
 |title=Enhancing xanthine dehydrogenase activity is an effective way to delay leaf senescence and increase rice yield.
 |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32162142
+|abstract=Xanthine dehydrogenase ([[XDH]]) is an important enzyme in purine metabolism. It is involved in regulation of the normal growth and non-biological stress-induced ageing processes in plants. The present study investigated [[XDH]]'s role in regulating rice leaf senescence. We measured physical characteristics, chlorophyll content and fluorescence parameters, active oxygen metabolism, and purine metabolism in wild-type Kitaake rice (Oryza sativa L.), an Os[[XDH]] over-expression transgenic line (OE9), and an Os[[XDH]] RNA interference line (Ri3) during different growth stages. The expression patterns of the Os[[XDH]] gene confirmed that [[XDH]] was involved in the regulation of normal and abiotic stress-induced ageing processes in rice. There was no significant difference between the phenotypes of transgenic lines and wild type at the seedling stage, but differences were observed at the full heading and maturation stages. The OE9 plants were taller, with higher chlorophyll content, and their photosystems had stronger light energy absorption, transmission, dissipation, and distribution capacity, which ultimately improved the seed setting rate and 1000-seed weight. The opposite effect was found in the Ri3 plants. The OE9 line had a strong ability to remove reactive oxygen species, with increased accumulation of allantoin and alantoate. Experimental spraying of allantoin on leaves showed that it could alleviate chlorophyll degradation and decrease the content of H O  and malonaldehyde (MDA) in rice leaves after the full heading stage. The urate oxidase gene (UO) expression levels in the interference line were significantly lower than those in the over-expression line and wild-type lines. The allantoinase (ALN) and allantoate amidinohydrolase (AAH) genes had significantly higher expression in the Ri3 plants than the in OE9 or wild-type plants, with OE9 plants showing the lowest levels. The senescence-related genes ACD1, WRKY23, WRKY53, SGR, XERO1, and GH27 in Ri3 plants had the highest expression levels, followed by those in the wild-type plants, with OE9 plants showing the lowest levels. These results suggest that enhanced activity of [[XDH]] can regulate the synthesis of urea-related substances, improve plant antioxidant capacity, effectively delay the ageing process in rice leaves, and increase rice yield.
 |keywords=* Allantoin
@@ Строка 37 488: / Строка 4141: @@
 * Yield
 |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7065298
-}}
-==ZC3H12A==
-{{medline-entry
-|title=Keratinocyte-specific ablation of Mcpip1 impairs skin integrity and promotes local and systemic inflammation.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31786670
-|mesh-terms=* Aging
-* Animals
-* Calgranulin A
-* Cell Differentiation
-* Cell Proliferation
-* Cells, Cultured
-* Cornified Envelope Proline-Rich Proteins
-* Epidermis
-* Gene Expression Regulation
-* Gene Ontology
-* Inflammation
-* Interleukin-1
-* Keratinocytes
-* Keratins
-* Lymph Nodes
-* Mice
-* Mice, Inbred C57BL
-* Mice, Transgenic
-* Proliferating Cell Nuclear Antigen
-* Ribonucleases
-* Skin
-* Spleen
-* Transcriptome
-|keywords=* MCPIP1
-* Regnase-1
-* Skin inflammation
-* ZC3H12A
-|full-text-url=https://sci-hub.do/10.1007/s00109-019-01853-2
 }}
 ==ZEB2==
@@ Строка 37 529: / Строка 4147: @@
 |title=miR-200b regulates cellular senescence and inflammatory responses by targeting [[ZEB2]] in pulmonary emphysema.
 |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32070140
+|abstract=Smoking is an important factor in the pathogenesis of chronic obstructive pulmonary disease (COPD), which is commonly characterised by cellular senescence and inflammation. Recently, miR-200b has emerged as an important target to cure lung disease; however, the function of miR-200b in reducing cellular senescence and inflammatory responses has not been reported. In this study, we found that miR-200b was downregulated in the lungs of COPD model mice, and its expression is correlated with cellular senescence and inflammatory responses. We hypothesised that miR-200b may be a potential novel therapy for treating COPD. We performed senescence-Associated-β-galactosidase (SA-β-GAL) staining, western blot, qRT-PCR and ELISA; our data suggested that miR-200b is an anti-aging factor in the lungs that is involved in inflammatory responses. We also confirmed that [[ZEB2]] (Zinc finger E-box binding homeobox 2) is a target gene of miR-200b using luciferase reporter assay. In addition, we verified the function of [[ZEB2]] in cellular senescence and inflammatory responses through transfection experiments. Moreover, we found that the protective effects of miR-200b are inhibited when cells overexpress the [[ZEB2]] protein. In conclusion, our results suggest that miR-200b may attenuate cellular senescence and inflammatory responses by targeting [[ZEB2]] in pulmonary emphysema.
 |mesh-terms=* Animals
 * Cell Line
@@ Строка 37 548: / Строка 4166: @@
 * pulmonary emphysema
 |full-text-url=https://sci-hub.do/10.1080/21691401.2020.1725029
-}}
-==ZMPSTE24==
-{{medline-entry
-|title=Bone marrow-derived mesenchymal stem cells in three-dimensional co-culture attenuate degeneration of nucleus pulposus cells.
-|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31666429
-|mesh-terms=* Bone Marrow Cells
-* Cell Cycle
-* Cell Proliferation
-* Cell Survival
-* Cells, Cultured
-* Cellular Senescence
-* Coculture Techniques
-* Collagen Type II
-* Female
-* Humans
-* Intervertebral Disc Degeneration
-* Male
-* Matrix Metalloproteinase 9
-* Membrane Proteins
-* Mesenchymal Stem Cells
-* Metalloendopeptidases
-* Middle Aged
-* Nucleus Pulposus
-* Signal Transduction
-* Transcription Factor RelA
-* Up-Regulation
-* beta-Galactosidase
-|keywords=* 3D co-culture
-* ZMPSTE24
-* bone marrow-derived mesenchymal stem cells
-* nucleus pulposus
-* senescence
-|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834418
 }}