https://transhumanist.ru/index.php?action=history&feed=atom&title=CEACAM1 2026-10-05T04:01:57Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=CEACAM1&diff=6175&oldid=prev 2021-05-12T15:15:27Z

<p>Новая страница: «Carcinoembryonic antigen-related cell adhesion molecule 1 precursor (Biliary glycoprotein 1) (BGP-1) (CD66a antigen) [BGP] [BGP1] ==Publications== {{medline-ent...»</p> <p><b>Новая страница</b></p><div>Carcinoembryonic antigen-related cell adhesion molecule 1 precursor (Biliary glycoprotein 1) (BGP-1) (CD66a antigen) [BGP] [BGP1]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Aging-related carcinoembryonic antigen-related cell adhesion molecule 1 signaling promotes vascular dysfunction.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31389127<br /> |abstract=Aging is an independent risk factor for cardiovascular diseases and therefore of particular interest for the prevention of cardiovascular events. However, the mechanisms underlying vascular aging are not well understood. Since carcinoembryonic antigen-related cell adhesion molecule 1 ([[CEACAM1]]) is crucially involved in vascular homeostasis, we sought to identify the role of [[CEACAM1]] in vascular aging. Using human internal thoracic artery and murine aorta, we show that [[CEACAM1]] is upregulated in the course of vascular aging. Further analyses demonstrated that [[TNF]]-α is [[CEACAM1]]-dependently upregulated in the aging vasculature. Vice versa, [[TNF]]-α induces [[CEACAM1]] expression. This results in a feed-forward loop in the aging vasculature that maintains a chronic pro-inflammatory milieu. Furthermore, we demonstrate that age-associated vascular alterations, that is, increased oxidative stress and vascular fibrosis, due to increased medial collagen deposition crucially depend on the presence of [[CEACAM1]]. Additionally, age-dependent upregulation of vascular [[CEACAM1]] expression contributes to endothelial barrier impairment, putatively via increased VEGF/VEGFR-2 signaling. Consequently, aging-related upregulation of vascular [[CEACAM1]] expression results in endothelial dysfunction that may promote atherosclerotic plaque formation in the presence of additional risk factors. Our data suggest that [[CEACAM1]] might represent an attractive target in order to delay physiological aging and therefore the transition to vascular disorders such as atherosclerosis.<br /> |mesh-terms=* Aged<br /> * Aging<br /> * Animals<br /> * Antigens, CD<br /> * Cell Adhesion Molecules<br /> * Cells, Cultured<br /> * Endothelium, Vascular<br /> * Humans<br /> * Mice<br /> * Mice, Inbred C57BL<br /> * Mice, Knockout<br /> * Middle Aged<br /> * Signal Transduction<br /> |keywords=* aging<br /> * anti-aging<br /> * cytokines<br /> * inflammation<br /> * mouse<br /> * reactive oxygen species<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826129<br /> }}</div>

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