The Mitochondrial Basis of Aging.
The Mitochondrial Basis of Aging.
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DOI：
10.1016/j.molcel.2016.01.028
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发表时间：
2016-03-03
期刊：
影响因子：
16
通讯作者：
Finkel T
中科院分区：
文献类型：
--
作者：
Sun N;Youle RJ;Finkel T
线粒体质量和活性的下降与正常衰老有关，并与广泛的年龄相关疾病的发展有关。在这里，我们回顾了线粒体功能下降导致衰老的证据。特别是，我们讨论了线粒体如何促进衰老过程的特定方面，包括细胞衰老，慢性炎症和干细胞活性的年龄依赖性下降。调节线粒体未折叠蛋白反应和线粒体自噬的信号通路也进行了审查，特别强调这些途径可能反过来调节寿命。总之，这些观察结果表明，线粒体影响或调节衰老的许多关键方面，并表明旨在改善线粒体质量和功能的策略可能具有深远的有益影响。
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.