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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.


DOI:10.1016/j.molcel.2016.01.028
PMID:26942670
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4779179/
Abstract

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.

摘要

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本文引用的文献

[1]
Mito-Morphosis: Mitochondrial Fusion, Fission, and Cristae Remodeling as Key Mediators of Cellular Function.

Annu Rev Physiol. 2016

[2]
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Sci Rep. 2015-12-2

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Cell Metab. 2015-11-3

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Cell Metab. 2015-7-7

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