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将自噬与病理生理学中的衰老联系起来。

Connecting autophagy to senescence in pathophysiology.

机构信息

Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Cambridge, CB2 0RE, United Kingdom.

出版信息

Curr Opin Cell Biol. 2010 Apr;22(2):234-40. doi: 10.1016/j.ceb.2009.12.005. Epub 2010 Jan 4.

Abstract

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.

摘要

细胞衰老(Cellular senescence)是一种应对压力时激活的极其稳定的细胞周期停滞形式。自噬(Autophagy)是一种溶酶体依赖性的细胞分解代谢过程,也可以被细胞应激所触发。衰老和自噬都与类似的病理生理学有关,包括癌症、衰老和与年龄相关的症状。衰老(Senescence)是一种异质表型,由多种效应机制组成,自噬最近被确定为衰老的一种新效应机制。自噬(Autophagy)通过多种效应似乎对细胞对压力的反应产生不同的影响:代谢废物的回收、细胞存活和蛋白质表达调节。

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