衰老的线粒体基础
The Mitochondrial Basis of Aging.
作者信息
Sun Nuo, Youle Richard J, Finkel Toren
机构信息
Center for Molecular Medicine, National Heart, Lung and Blood Institute, NIH, Bethesda, MD 20892, USA.
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20892, USA.
出版信息
Mol Cell. 2016 Mar 3;61(5):654-666. doi: 10.1016/j.molcel.2016.01.028.
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.
线粒体质量和活性的下降与正常衰老相关，并与多种年龄相关疾病的发生有关。在此，我们综述了线粒体功能下降导致衰老的证据。特别地，我们讨论了线粒体如何促成衰老过程的特定方面，包括细胞衰老、慢性炎症以及干细胞活性随年龄增长的下降。还综述了调节线粒体未折叠蛋白反应和线粒体自噬的信号通路，尤其着重于这些通路如何反过来调节寿命。综上所述，这些观察结果表明线粒体影响或调节衰老的一些关键方面，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。
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