Cellular Senescence in Postmitotic Cells: Beyond Growth Arrest

被引：142

作者：

Sapieha, Przemyslaw ^{[1
,2
,3
]}

Mallette, Frederick A. ^{[1
,3
,4
]}

机构：

[1] Dept Biochim & Med Mol, CP 6128 Succ Ctr Ville, Montreal, PQ H3C 3J7, Canada

[2] Univ Montreal, Dept Ophthalmol, CP 6128 Succ Ctr Ville, Montreal, PQ H3C 3J7, Canada

[3] Maisonneuve Rosemont Hosp, Res Ctr, Montreal, PQ H1T 2M4, Canada

[4] Univ Montreal, Dept Med, CP 6128 Succ Ctr Ville, Montreal, PQ H3C 3J7, Canada

来源：

TRENDS IN CELL BIOLOGY | 2018年 / 28卷 / 08期

基金：

加拿大自然科学与工程研究理事会; 加拿大健康研究院;

关键词：

ONCOGENE-INDUCED SENESCENCE; DNA-DAMAGE RESPONSE; LIPOFUSCIN PIGMENT ACCUMULATION; DEMETHYLASE JMJD3 CONTRIBUTES; SECRETORY PHENOTYPE; ER STRESS; TUMOR-SUPPRESSOR; SIGNALING PATHWAY; HUMAN FIBROBLASTS; IMMUNE-RESPONSES;

D O I：

10.1016/j.tcb.2018.03.003

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

In mitotic cells, cellular senescence is a permanent state of G1 arrest, that may have evolved in parallel to apoptosis, to limit proliferation of damaged cells and oncogenesis. Recent studies have suggested that postmitotic cells are also capable of entering a state of senescence, although the repercussions of postmitotic cellular senescence (PoMiCS) on tissue health and function are currently ill-defined. In tissues made largely of post-mitotic cells, it is evolutionary advantageous to preserve cellular integrity and cellular senescence of post-mitotic cells may prevent stressor-induced tissue degeneration and promote tissue repair. Paradoxically, PoMiCS may also contribute to disease progression through the generation of inflammatory mediators, termed the senescence-associated secretory phenotype. Here, we discuss the potential roles of PoMiCS and propose to enlarge the current definition of cellular senescence to postmitotic terminally differentiated cells.

引用

页码：595 / 607

页数：13

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