The Mitochondrial Basis of Aging

被引:1024
作者
Sun, Nuo [1 ]
Youle, Richard J. [2 ]
Finkel, Toren [1 ]
机构
[1] NHLBI, Ctr Mol Med, NIH, Bldg 10, Bethesda, MD 20892 USA
[2] NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA
关键词
EXTENDS LIFE-SPAN; SKELETAL-MUSCLE; PYRUVATE-DEHYDROGENASE; DNA MUTATIONS; STEM-CELLS; NLRP3; INFLAMMASOME; PHYSICAL-EXERCISE; OXIDATIVE STRESS; QUALITY-CONTROL; LONGEVITY;
D O I
10.1016/j.molcel.2016.01.028
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
A decline inmitochondrial 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.
引用
收藏
页码:654 / 666
页数:13
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