粒体自噬
生物
线粒体
衰老
细胞生物学
长寿
功能(生物学)
自噬
遗传学
细胞凋亡
作者
Nuo Sun,Richard J. Youle,Toren Finkel
出处
期刊:Molecular Cell
[Elsevier BV]
日期:2016-03-01
卷期号:61 (5): 654-666
被引量:1232
标识
DOI:10.1016/j.molcel.2016.01.028
摘要
A decline in mitochondrial quality and activity has been associated with normal aging and correlated with the development of a wide range of age-related diseases. Here, we review the evidence that a decline in mitochondria function contributes to aging. In particular, we discuss how mitochondria contribute to specific aspects of the aging process, including cellular senescence, chronic inflammation, and the age-dependent decline in stem cell activity. Signaling pathways regulating the mitochondrial unfolded protein response and mitophagy are also reviewed, with particular emphasis placed on how these pathways might, in turn, regulate longevity. Taken together, these observations suggest that mitochondria influence or regulate a number of key aspects of aging and suggest that strategies directed at improving mitochondrial quality and function might have far-reaching beneficial effects.
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