Exercise enhances skeletal muscle regeneration by promoting senescence in fibro-adipogenic progenitors
Open accessAbstract
Idiopathic inflammatory myopathies cause progressive muscle weakness and degeneration. Since high-dose glucocorticoids might not lead to full recovery of muscle function, physical exercise is also an important intervention, but some exercises exacerbate chronic inflammation and muscle fibrosis. It is unknown how physical exercise can have both beneficial and detrimental effects in chronic myopathy. Here we show that senescence of fibro-adipogenic progenitors (FAPs) in response to exercise-induced muscle damage is needed to establish a state of regenerative inflammation that induces muscle regeneration. In chronic inflammatory myopathy model mice, exercise does not promote FAP senescence or resistance against tumor necrosis factor-mediated apoptosis. Pro-senescent intervention combining exercise and pharmacological AMPK activation reverses FAP apoptosis resistance and improves muscle function and regeneration. Our results demonstrate that the absence of FAP senescence after exercise leads to muscle degeneration with FAP accumulation. FAP-targeted pro-senescent interventions with exercise and pharmacological AMPK activation may constitute a therapeutic strategy for chronic inflammatory myopathy.
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An acute bout of 14 d of downhill running promoted a senescent phenotype in skeletal muscle fibroadipogenic progenitors from young wild-type mice but not from mice with chronic inflammatory myopathy.
“In a recent study, an acute bout of 14 d of downhill running promoted a senescent phenotype in skeletal muscle fibroadipogenic progenitors from young wild-type mice but not from mice with chronic inflammatory myopathy (58).”
From Exercise Counters the Age-Related Accumulation of Senescent Cells (2022) · cites this paper as [58]
Induction of senescence with exercise and pharmacological activation of AMPK using 5-aminoimidazole-4-carboxamide ribonucleotide improved muscle function, cross-sectional area, and regeneration in the chronic inflammatory myopathy model.
“Induction of senescence with exercise and pharmacological activation of AMPK using 5-aminoimidazole-4-carboxamide ribonucleotide improved muscle function, cross-sectional area, and regeneration in the chronic inflammatory myopathy model.”
From Exercise Counters the Age-Related Accumulation of Senescent Cells (2022) · cites this paper as [58]
In this context, senescent FAPs improved skeletal muscle fiber size and performance on treadmill and grip strength tests.
“senescent FAPs improved skeletal muscle fiber size and performance on treadmill and grip strength tests”
From Skeletal muscle aging, cellular senescence, and senotherapeutics: current knowledge and future directions (2021) · cites this paper as Saito et al., 2020
In young (3-months) mice, muscle damage caused by downhill treadmill running activated the expression of senescence markers, including p16 and p21 in FAPs.
“in young (3-months) mice muscle damage caused by downhill treadmill running activated the expression of senescence markers, including p16 and p21 in FAPs”
From Skeletal muscle aging, cellular senescence, and senotherapeutics: current knowledge and future directions (2021) · cites this paper as Saito et al., 2020
Senescent FAPs may improve muscle regeneration through their pro-inflammatory expression profile.
“possibly through the pro-inflammatory expression profile of FAPs which facilitates muscle regeneration”
From Skeletal muscle aging, cellular senescence, and senotherapeutics: current knowledge and future directions (2021) · cites this paper as Saito et al., 2020
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- Authors
- Saito, Y., Chikenji, T. S., Matsumura, T., Nakano, M., & Fujimiya, M.
- Affiliations
- Sapporo Medical University (JP)
- Corresponding author
- Chikenji, Takako S.
- Venue
- Nature Communications
- Published
- 2020-02-14
- Volume
- 11
- Issue
- 1
- Pages
- 889-889
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC7021787
- OpenAlex
- W3005549618
- Cited by
- 196
- References
- 72
- Citations by year
- 2026: 35 · 2025: 29 · 2024: 36 · 2023: 28 · 2022: 32 · 2021: 26 · 2020: 10
- FWCI
- 7.79
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Hokkaido University Collection of Scholarly and Academic Papers (Hokkaido University) (submittedVersion, cc-by)
- Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by)
- Funders
- Japan Society for the Promotion of Science (18K16668, 18K17722, 16K16430)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Epidemiology › Inflammatory Myopathies and Dermatomyositis
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Keywords
- physical activity, skeletal muscle regeneration, fibro-adipogenic progenitors, cellular senescence, exercise-induced muscle damage, AMPK activation, TNF-α, apoptosis resistance, muscle fibrosis, muscle degeneration
- MeSH terms
- Aging, Animals, Exercise Therapy, Female, Humans, Mice, Inbred BALB C, Mice, Inbred C57BL, Muscular Diseases, Regeneration, Apoptosis, Muscle, Skeletal, Mice, Mesenchymal Stem Cells
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