ArticleNature communications2020
Exercise enhances skeletal muscle regeneration by promoting senescence in fibro-adipogenic progenitors.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
124 citing papers in PubMed, 1 synthesis or guideline pooled it, 169 citations in OpenAlex.
- Is exercise a senolytic medicine? A systematic review.Aging cell · 2021Pooled it
- Transcriptomic response of skeletal muscle to acute aerobic versus combined exercise in chronic kidney disease.PloS one · 2026Trial
- Review
- Cellular Remodeling of Skeletal Muscle Following Botulinum Toxin A Injection: A Single-Nucleus RNA Sequencing Study.Aesthetic plastic surgery · 2026Article
- Phase-transition failure in aged skeletal muscle regeneration.Biogerontology · 2026Review
- Woven dECM yarn scaffolds enable volumetric muscle loss regeneration via immunomodulation.Nature communications · 2026Article
- Comprehensive transcriptomic profiling reveals impaired polyamine metabolism as a contributor to age-related muscle decline.iScience · 2026Article
- Stem cells as an essential mediator of the exercise-tumorigenesis link.Nature reviews. Cancer · 2026Review
- Mechanisms of Impaired Skeletal Muscle Regeneration and Therapeutic Approaches in Aging and Chronic Disease.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Resident mesenchymal progenitor cells require autocrine IGF-I in homeostatic and regenerating skeletal muscle.Stem cell reports · 2026Article
- Cellular senescence and aging: molecular mechanisms and convergent pathways.Cellular and molecular life sciences : CMLS · 2026Review
- Fibro-Adipogenic Progenitor Cell Alterations in Skeletal Muscle: Pathological Dysfunction or Adaptive Reprogramming?International journal of molecular sciences · 2026Review
- The cellular ecosystem of skeletal muscle regeneration: molecular mechanisms, pathological disorders, and potential therapeutic strategies.Stem cell research & therapy · 2026Review
- Article
- Macrophage and fibro-adipogenic progenitor communication in skeletal muscle regeneration: tissue homeostasis and pathogenic remodeling.Journal of leukocyte biology · 2026Review
- Cellular senescence in skeletal muscle regeneration.Cell regeneration (London, England) · 2026Review
- The role of the cGAS/STING pathway in skeletal muscle regeneration: modulation of inflammation, macrophage polarization, and oxidative stress.Cellular & molecular biology letters · 2026Article
- Skeletal Fiber Type in Muscle Pain and Dysfunction.Biomedicines · 2026Review
- Piezo1-dependent activation of stromal cells ignites muscle inflammation in exercise and injury and is associated with inflammaging.Nature immunology · 2026Article
- RUNX2 Activation in Fibro/Adipogenic Progenitors Promotes Muscle Fibrosis in Muscular Dystrophy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
64 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.