Connecting autophagy to senescence in pathophysiology

被引:69
|
作者
Young, Andrew R. J. [1 ]
Narita, Masashi [1 ]
机构
[1] Canc Res UK, Cambridge Res Inst, Li Ka Shing Ctr, Cambridge CB2 0RE, England
关键词
ONCOGENE-INDUCED SENESCENCE; CELLULAR SENESCENCE; IN-VIVO; PREMATURE SENESCENCE; TUMOR-SUPPRESSOR; LIFE-SPAN; TUMORIGENESIS; CELLS; MICE; DAMAGE;
D O I
10.1016/j.ceb.2009.12.005
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cellular senescence is an extremely stable form of cell cycle arrest activated in response to stress. Autophagy, a lysosome-dependent cellular catabolic process, can also be triggered by cellular stresses. Both senescence and autophagy have been implicated in a similar range of pathophysiologies, including cancer, aging and age-related symptoms. Senescence is a heterogeneous phenotype that is composed of multiple effector mechanisms and autophagy was recently identified as a new effector of senescence. Autophagy seemingly has different impacts on cells responding to stress through a diversity of effects: recycling of metabolic waste, cell survival and protein expression regulation.
引用
收藏
页码:234 / 240
页数:7
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