Aerobic Exercise Improves Mitochondrial Function in Sarcopenia Mice Through Sestrin2 in an AMPKα2-Dependent Manner
Abstract
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 α2 (AMPKα2). This study indicates that aerobic exercise alleviates the negative effects resulting from sarcopenia via the Sesn2/AMPKα2 pathway and provides new insights into the molecular mechanism by which the Sesn2/AMPKα2 signaling axis mediates the beneficial impact of exercise on sarcopenia.
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Mitochondria-related proteins Drp1, Mfn2, PGC-1α, and COX significantly increased in mice through Sestrin2 in an AMPKα2-dependent manner following 8-month treadmill training, suggesting aerobic exercise enhanced mitochondrial fusion and fission in gastrocnemius with age-related sarcopenia.
“The mitochondria-related proteins Drp1, Mfn2, PGC-1α, and COX significantly increased in mice through Sestrin2 in an AMP-activated protein kinase α2 (AMPKα2)-dependent manner following an 8-month treadmill training (60 min/day, 12 m/min) program, suggesting that aerobic exercise enhanced the mitochondrial fusion and fission in gastrocnemius with age-related sarcopenia [62].”
From Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis (2025) · cites this paper as [62]
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“Long-term exercise can enhance the mitochondrial fusion mediated by AMPK/MFN2 in aged mice and has an improving effect on age-related muscle atrophy [86].”
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Yang, X., Zou, Y., Li, X., Rong, Z., Niu, Y., & Fu, L. (2026) · Journal of Cellular Physiology · doi:10.1002/jcp.70241
“Although previous work has established that Sestrin2 is crucial for maintaining mitochondrial homeostasis in skeletal muscle (Liu et al. 2021), whether Sestrin1 could alleviate mitochondrial dysfunction remains incompletely defined.”
Influential
- Authors
- Liu, S., Yu, C., Xie, L., Niu, Y., & Fu, L.
- Affiliations
- Tianjin Medical University (CN)
- Corresponding author
- Fu, Li
- Venue
- The Journals of Gerontology Series A
- Publisher
- Oxford University Press (OUP)
- Published
- 2021-01-29
- Volume
- 76
- Issue
- 7
- Pages
- 1161-1168
- ISSN
- 1079-5006 (ISSN-L)
- 1758-535X
- OpenAlex
- W3121520191
- Cited by
- 51
- References
- 43
- Citations by year
- 2026: 11 · 2025: 15 · 2024: 6 · 2023: 13 · 2022: 5 · 2021: 1
- FWCI
- 1.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- The Journals of Gerontology Series A (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (31871206, 31671237)
- China Postdoctoral Science Foundation (2019M661042)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- sarcopenia, aerobic exercise, Sestrin2, AMPKα2, mitochondrial function, skeletal muscle, mitochondrial fission and fusion, mitochondrial biogenesis, mitophagy, muscle atrophy, aging, gastrocnemius, chronic inflammation
- MeSH terms
- Sestrins, Aging, Animals, Cells, Cultured, Disease Models, Animal, Male, Mice, Inbred C57BL, Mitochondria, Nuclear Proteins, Physical Conditioning, Animal, Muscle, Skeletal, Myoblasts, Mice, Muscle Strength, AMP-Activated Protein Kinases, Sarcopenia
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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