Mitochondria Initiate and Regulate Sarcopenia

被引：133

作者：

Alway, Stephen E. ^{[1
,2
]}

Mohamed, Junaith S. ^{[1
,2
,3
]}

Myers, Matthew J. ^{[1
,2
]}

机构：

[1] West Virginia Univ, Sch Med, Div Exercise Physiol, 1 Med Ctr Dr,PO 9227, Morgantown, WV 26506 USA

[2] West Virginia Univ, Sch Med, Ctr Cardiovasc & Resp Sci & Mitochondria Metab &, Morgantown, WV 26506 USA

[3] West Virginia Univ, Sch Med, Ctr Neurosci, Morgantown, WV 26506 USA

来源：

EXERCISE AND SPORT SCIENCES REVIEWS | 2017年 / 45卷 / 02期

关键词：

muscle wasting; autophagy; apoptosis; aging; ubiquitin proteasome; lysosome; DNA DELETION MUTATIONS; CHAPERONE-MEDIATED AUTOPHAGY; SKELETAL-MUSCLE FUNCTION; OXIDATIVE STRESS; PERMEABILITY TRANSITION; ENDURANCE EXERCISE; UBIQUITIN-LIGASES; MOTOR-NEURONS; ISOMETRIC CONTRACTIONS; GASTROCNEMIUS-MUSCLES;

D O I：

10.1249/JES.0000000000000101

中图分类号：

Q4 [生理学];

学科分类号：

071003 [生理学];

摘要：

We present the hypothesis that an accumulation of dysfunctional mitochondria initiates a signaling cascade leading to motor neuron and muscle fiber death and culminating in sarcopenia. Interactions between neural and muscle cells that contain dysfunctional mitochondria exacerbate sarcopenia. Preventing sarcopenia will require identifying mitochondrial sources of dysfunction that are reversible.

引用

收藏

页码：58 / 69

页数：12

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