ArticleJournal of cachexia, sarcopenia and muscle2025
Intrinsic Muscle Stem Cell Dysfunction Contributes to Impaired Regeneration in the mdx Mouse.
Article in Journal of cachexia, sarcopenia and muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- GDF5 modulation of MuSC pool as a potential therapeutic benefit for DMD.Molecular therapy. Nucleic acids · 2026Article
- Mechanisms of Impaired Skeletal Muscle Regeneration and Therapeutic Approaches in Aging and Chronic Disease.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Regenerative Index: a method to assess muscle regeneration in patients with Duchenne muscular dystrophy.Skeletal muscle · 2026Article
- Wnt/Chemerin Signaling Involved in Exercise Training Preventing Diaphragm Dysfunction Induced by Cigarette Smoke.Biomedicines · 2026Article
- AAVcc47-The Yale journal of biology and medicine · 2026Article
- Voluntary running sustains the correction of inflammation-related gene expression conferred by AAV gene therapy in mdx mice.Molecular therapy. Advances · 2026Article
- The Evolutionarily Conserved TPM1 Super-Enhancer Drives Skeletal Muscle Regeneration via Mechanotransduction Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Regenerative Index reveals declining muscle regeneration in paediatric patients with Duchenne muscular dystrophy.bioRxiv : the preprint server for biology · 2026Article
- Lineage relationships in muscle stem cells: linking functional fate to molecular state.Frontiers in cell and developmental biology · 2026Review
- Genetic strategies for therapy of Duchenne muscular dystrophy.Molecular therapy. Nucleic acids · 2025Review
- Conditional Dmd ablation in muscle and brain causes profound effects on muscle function and neurobehavior.Communications biology · 2025Article
- Quantitative 3D assessment of muscle dystrophy through X-ray phase-contrast tomography.Scientific reports · 2025Article
- Intrinsic dysfunction in muscle stem cells lacking dystrophin begins during secondary myogenesis.Nature communications · 2025Article
- Cell therapy for Duchenne muscular dystrophy: promises, challenges, and controversies.Cellular and molecular life sciences : CMLS · 2025Review
- Bioactive lipid mediator class switching regulates myogenic cell progression and muscle regeneration.Nature communications · 2025Article
- Stem/progenitor cell-based therapy for Duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
backgroundDuchenne muscular dystrophy (DMD) is a devastating disease characterized by progressive muscle wasting that leads to diminished lifespan. In addition to the inherent weakness of dystrophin-deficient muscle, the dysfunction of resident muscle stem cells (MuSC) significantly contributes to disease progression.
methodsUsing the mdx mouse model of DMD, we performed an in-depth characterization of disease progression and MuSC function in dystrophin-deficient skeletal muscle using immunohistology, isometric force measurements, transcriptomic analysis and transplantation assays. We examined the architectural and functional changes in mdx skeletal muscle from 13 and 52 weeks of age and following acute cardiotoxin (CTX) injury. We also studied MuSC dynamics and function under homeostatic conditions, during regeneration post-acute injury, and following engraftment using a combination of histological and transcriptomic analyses.
resultsDystrophin-deficient skeletal muscle undergoes progressive changes with age and delayed regeneration in response to acute injury. Muscle hypertrophy, deposition of collagen and an increase in small myofibres occur with age in the tibialis anterior (TA) and diaphragm muscles in mdx mice. Dystrophic mdx mouse TA muscles become hypertrophic with age, whereas diaphragm atrophy is evident in 1-year-old mdx mice. Maximum tetanic force is comparable between genotypes in the TA, but maximum specific force is reduced by up to 38% between 13 and 52 weeks in the mdx mouse. Following acute injury, myofibre hyperplasia and hypotrophy and delayed recovery of maximum tetanic force occur in the mdx TA. We also find defective MuSC polarity and reduced numbers of myocytes in mdx muscle following acute injury. We observed a 50% and 30% decrease in PAX7
conclusionsOur study provides evidence that dystrophin deficiency in MuSCs and myofibres together contributes to progression of DMD. Ongoing muscle damage stimulates MuSC activation; however, aberrant intrinsic MuSC polarity and stem cell commitment deficits due to the loss of dystrophin impair muscle regeneration. Our study provides in vivo validation that dystrophin-deficient MuSCs undergo fewer asymmetric cell divisions, instead favouring symmetric expansion.
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