ArticleNature communications2025
Intrinsic dysfunction in muscle stem cells lacking dystrophin begins during secondary myogenesis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Congenital Clubfoot as an Early Manifestation of Duchenne Muscular Dystrophy?Muscles (Basel, Switzerland) · 2026Article
- Antisense oligonucleotide selection scheme for rare Duchenne muscular dystrophy mutations: Application toMolecular therapy. Nucleic acids · 2026Article
- Regenerative Index: a method to assess muscle regeneration in patients with Duchenne muscular dystrophy.Skeletal muscle · 2026Article
- Duchenne Muscular Dystrophy: Contemporary Therapeutic Options and Real-World Challenges in Treatment Selection.Muscles (Basel, Switzerland) · 2026Review
- 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
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Loss of dystrophin causes Duchenne Muscular Dystrophy (DMD), a neuromuscular disease characterized by muscle fragility and muscle stem cell (MuSC) impairment. Conventional understanding is that DMD manifests after birth from cumulative muscle damage. Here, examination of mdx mouse embryos lacking dystrophin reveals no impairment of the primary myogenic program. By contrast, histological and single cell RNA-sequencing analysis during secondary myogenesis uncovers an increase in the proportion of fetal (f) MuSCs and a marked reduction in myogenic progenitors and myocytes, leading to fewer smaller-caliber myofibers. Wild type fMuSCs express full-length dystrophin that interacts with MARK2, whereas mdx fMuSCs downregulate MARK2 and NUMB, exhibiting reduced PARD3 polarization. Strikingly, deletion of the Numb Associated Kinase, AAK1, rescues polarization of NUMB and myogenic progenitor generation in mdx fetal muscle. Together, our results elucidate an acute disease pathology during DMD fetal development and the potential for therapeutic intervention by targeting AAK1.
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Registered trials
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