Редактирование: FOXA3 (раздел)

==Publications==

{{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
|abstract=Caloric restriction (CR) is an important means to delay senescence, and glucose restriction is one of the measures to achieve CR. On the basis of our previous work and bioinformatics analysis, we hypothesized that glucose restriction can up-regulate autophagy, inhibit senescence and promote proliferation via the AMPK/[[SIRT1]]-[[FOXA3]]-Beclin1 pathway in human umbilical vein endothelial cells (HUVECs). We found that compared with 5.5 mmol/L and 25 mmol/L glucose, 2.5 mmol/L glucose restriction significantly reduced senescence, enhanced autophagy, increased migration speed, relieved G /G  phase arrest and enhanced proliferation of HUVECs. Furthermore, glucose restriction up-regulated AMPKα1, [[SIRT1]], [[FOXA3]] and Beclin1 expression in HUVECs. Additionally, we demonstrated that AMPKα1 phosphorylated [[FOXA3]] at S170 and S305 in the cytoplasm and promoted [[FOXA3]] nuclear translocation under glucose restriction. [[FOXA3]] in the nucleus was deacetylated by [[SIRT1]] at K214 and K221. Deacetylated [[FOXA3]] specifically bound to  109 C in the Beclin1 transcriptional regulatory region, and significantly enhanced Beclin1 transcription and expression. siRNA knock down of AMPKα1, [[SIRT1]], [[FOXA3]] or Beclin1 expression impaired the glucose restriction-induced inhibition of senescence, enhanced autophagy, increased migration, and induced proliferation of HUVECs. This study confirmed that glucose restriction can enhance autophagy, inhibit senescence, and enhance proliferation of HUVECs through the AMPK/[[SIRT1]]-[[FOXA3]]-Beclin1 pathway.

|keywords=* Beclin1
* Endothelial cells
* FOXA3
* Glucose restriction
* Proliferation
* Senescence
|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.111053
}}