Connecting autophagy to senescence in pathophysiology
Connecting autophagy to senescence in pathophysiology
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DOI：
10.1016/j.ceb.2009.12.005
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发表时间：
2010-04-01
影响因子：
7.5
通讯作者：
Narita, Masashi
中科院分区：
文献类型：
--
作者：
Young, Andrew R. J.;Narita, Masashi
细胞衰老是响应应激而激活的细胞周期停滞的一种极其稳定的形式。自噬是一种溶酶体依赖性细胞分解代谢过程，也可由细胞应激触发。衰老和自噬都与一系列相似的病理生理学有关，包括癌症、衰老和年龄相关症状。衰老是一种由多种效应机制组成的异质表型，自噬最近被确定为一种新的衰老效应器。自噬似乎通过多种作用对细胞应对应激产生不同的影响：代谢废物的回收、细胞存活和蛋白质表达调节。
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.