Epigenetic Regulation of Cellular Senescence

被引：72

作者：

Crouch, Jack ^{[1
]}

Shvedova, Maria ^{[1
]}

Thanapaul, Rex Jeya Rajkumar Samdavid ^{[1
]}

Botchkarev, Vladimir ^{[2
]}

Roh, Daniel ^{[1
]}

机构：

[1] Boston Univ, Div Plast & Reconstruct Surg, Dept Surg, Sch Med, Boston, MA 02118 USA

[2] Boston Univ, Dept Dermatol, Sch Med, Boston, MA 02118 USA

来源：

CELLS | 2022年 / 11卷 / 04期

关键词：

senescence; epigenetics; aging; SASP; histone modification; DNA methylation; ONCOGENE-INDUCED SENESCENCE; DNA-DAMAGE RESPONSE; NUCLEAR ARCHITECTURE; SECRETORY PHENOTYPE; HETEROCHROMATIN FOCI; BMI-1; ONCOPROTEIN; HUMAN FIBROBLASTS; PHASE-II; CELLS; CHROMATIN;

D O I：

10.3390/cells11040672

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Senescence is a complex cellular stress response that abolishes proliferative capacity and generates a unique secretory pattern that is implicated in organismal aging and age-related disease. How a cell transitions to a senescent state is multifactorial and often requires transcriptional regulation of multiple genes. Epigenetic alterations to DNA and chromatin are powerful regulators of genome architecture and gene expression, and they play a crucial role in mediating the induction and maintenance of senescence. This review will highlight the changes in chromatin, DNA methylation, and histone alterations that establish and maintain cellular senescence, alongside the specific epigenetic regulation of the senescence-associated secretory phenotype (SASP).

引用

页数：16

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