Journal
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
Volume 76, Issue 7, Pages 1161-1168Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/gerona/glab029
Keywords
Aerobic exercise; Age-related sarcopenia; AMPK alpha 2; Mitochondrial function; Sestrin2
Categories
Funding
- National Natural Science Foundation of China [31871206, 31671237]
- China Postdoctoral Science Foundation [2019M661042]
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Regular exercise can reverse the negative effects of sarcopenia on muscle mass and function, by regulating the Sesn2/AMPK alpha 2 pathway. This study provides new insights into the molecular mechanism by which exercise alleviates the consequences of sarcopenia.
Sarcopenia, the age-related loss of skeletal muscle mass and function, contributes to high morbidity and mortality in the older population. Regular exercise is necessary to avoid the initiation and progression of sarcopenia, in which the underlying molecular mechanism is still not clear. Our data revealed that the outcomes induced by sarcopenia, including muscle mass and strength loss, decreased cross-sectional area of gastrocnemius fiber, chronic inflammation, and increased dysfunctional mitochondria, were reversed by regulation exercise. Knockout or silencing of Sestrin2 (Sesn2) resulted in imbalanced mitochondrial fusion and fission, mitochondrial biogenesis, and mitophagy damage in vivo and in vitro, which was attenuated by aerobic exercise or overexpression of Sesn2. Moreover, we found that the effects of Sesn2 on mitochondrial function are dependent on AMP-activated protein kinase alpha 2 (AMPK alpha 2). This study indicates that aerobic exercise alleviates the negative effects resulting from sarcopenia via the Sesn2/AMPK alpha 2 pathway and provides new insights into the molecular mechanism by which the Sesn2/AMPK alpha 2 signaling axis mediates the beneficial impact of exercise on sarcopenia.
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