Cellular senescence and its effector programs

被引:660
作者
Salama, Rafik [1 ]
Sadaie, Mahito [2 ]
Hoare, Matthew [1 ]
Narita, Masashi [1 ]
机构
[1] Univ Cambridge, Canc Res UK Cambridge Inst, Cambridge CB2 0RE, England
[2] Kyoto Univ, Grad Sch Biostudies, Dept Gene Mech, Sakyo Ku, Kyoto 6068501, Japan
关键词
senescence; aging; DNA damage; oncogenes; tumor suppressors; inflammation; metabolism; DNA-DAMAGE-RESPONSE; ONCOGENE-INDUCED SENESCENCE; DEMETHYLASE JMJD3 CONTRIBUTES; NF-KAPPA-B; TUMOR-SUPPRESSOR; GENE-EXPRESSION; HUMAN-CELLS; REPLICATIVE SENESCENCE; FIBROBLAST SENESCENCE; TRIGGERS SENESCENCE;
D O I
10.1101/gad.235184.113
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cellular senescence is a stress response that accompanies stable exit from the cell cycle. Classically, senescence, particularly in human cells, involves the p53 and p16/Rb pathways, and often both of these tumor suppressor pathways need to be abrogated to bypass senescence. In parallel, a number of effector mechanisms of senescence have been identified and characterized. These studies suggest that senescence is a collective phenotype of these multiple effectors, and their intensity and combination can be different depending on triggers and cell types, conferring a complex and diverse nature to senescence. Series of studies on senescence-associated secretory phenotype (SASP) in particular have revealed various layers of functionality of senescent cells in vivo. Here we discuss some key features of senescence effectors and attempt to functionally link them when it is possible.
引用
收藏
页码:99 / 114
页数:16
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