Cited by 44Metabolism, Diabetes, and CancerTelomeres, Telomerase, and SenescenceMuscle Physiology and Disorders

Exercise-induced AMPK activation is involved in delay of skeletal muscle senescence

Yoon, Kyeong Jin, Zhang, Didi, Kim, Seok-Jin, Lee, Min-Chul, Moon, Hyo Youl·2019·Biochemical and Biophysical Research Communications

Abstract

Accumulation of senescent cells leads to aging related phenotypes in various organs. Sarcopenia is a frequently observed aging-related disease, which is associated with the loss of muscle mass and functional disability. Physical activity represents the most critical treatment method for preventing decreased muscle size, mass and strength. However, the underlying mechanism as to how physical activity provides this beneficial effect on muscle function has not yet been fully understood. In particular, one unresolved question about aging is how the boost in catabolism induced by aerobic exercise affects skeletal muscle atrophy and other senescence phenotypes. Here we show that pre-activation of AMPK with the AMPK activator, AICAR can mitigate the diminished cellular viability of skeletal muscle cells induced by doxorubicin, which accelerates senescence through free radical production. Pre-incubation for 3 h with AICAR decreased doxorubicin-induced phosphorylation of AMPK in a differentiated skeletal muscle cell line. Accordingly, cellular viability of skeletal muscle cells was recovered in the cells pre-treated with AICAR then administered doxorubicin as compared to that of doxorubicin-only treatment. In accordance with the results of cellular experiments, we verified that 4 weeks of treadmill exercise decreased the senescence marker, p16 and p21 in 19-month-old mice compared to sedentary mice. In this study, we provide new evidence that prior activation of AMPK can reduce doxorubicin induced cell senescence phenotypes. The evidence in this paper suggest that aerobic exercise-activated catabolism in the skeletal muscle may prevent cellular senescence, partially through the cell cycle regulation.

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Crossref · 10.1016/j.bbrc.2019.03.086

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  • Four weeks of treadmill exercise reduced P21 protein level in the gastrocnemius muscle of 19-month-old mice compared with sedentary mice.

    “Four weeks of treadmill exercise was found to reduce P21 protein level in the gastrocnemius muscle of 19-month-old mice compared with sedentary mice (57).”

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Authors
Yoon, K. J., Zhang, D., Kim, S.-J., Lee, M.-C., & Moon, H. Y.
Affiliations
  • Seoul National University (KR)
  • CHA University (KR)
Corresponding author
Moon, Hyo Youl
Venue
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Published
2019-05
Volume
512
Issue
3
Pages
604-610
ISSN
0006-291X (ISSN-L)
OpenAlex
W2940404978
Cited by
44
References
39
Citations by year
2026: 5 · 2025: 4 · 2024: 6 · 2023: 4 · 2022: 8 · 2021: 8 · 2020: 8 · 2019: 1
FWCI
2.07
Type
journal article
Language
en
Open access
closed
Locations
  • Biochemical and Biophysical Research Communications (publishedVersion)
  • PubMed (publishedVersion)
  • Seoul National University Open Repository (Seoul National University) (submittedVersion)
Funders
  • National Research Foundation (700-20180020)
  • Korea Mouse Phenotype Center (2017M3A9D5A01052447)
  • Seoul National University
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Keywords
AMPK activation, cellular senescence, aerobic exercise, AICAR, doxorubicin-induced senescence, sarcopenia, treadmill exercise, p16, p21, cell cycle regulation, free radical generation, muscle atrophy, aging
MeSH terms
Aminoimidazole Carboxamide, Animals, Antibiotics, Antineoplastic, Cell Line, Doxorubicin, Enzyme Activation, Hypoglycemic Agents, Male, Mice, Inbred C57BL, Physical Conditioning, Animal, Ribonucleotides, Cellular Senescence, Muscle, Skeletal, Mice, AMP-Activated Protein Kinases

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