ArticleCell reports2025
A mechanistic basis of fast myofiber vulnerability to neuromuscular diseases.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- MAFF is a transcription factor that regulates contraction-induced skeletal muscle transcription.Life science alliance · 2026Article
- TSPO PET selectively detects the denervated skeletal muscle district remodeling after experimental peripheral nerve injury.EJNMMI research · 2026Article
- Article
- PGC-1α pathway dysregulation disrupts myofiber specification in a mouse model of SBMA.JCI insight · 2026Article
- 0.33Science advances · 2026Article
- Spatial protein expression patterns across pathologically-associated fibers revealed molecular specialization in inclusion body myositis.Cell communication and signaling : CCS · 2026Article
- Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
Neuromuscular diseases such as amyotrophic lateral sclerosis and sarcopenia cause muscle atrophy, which preferentially affects fast-twitch glycolytic myofibers. The mechanisms underlying the susceptibility of fast myofibers to disease remain unclear. To investigate this, we analyzed the transcriptional profiles of myonuclei from denervated muscle fibers. We found that the fast muscle gene program and the transcription factor Maf were repressed upon denervation. Overexpression of Maf in mice prevented loss of muscle mass caused by denervation by repressing atrophic genes and restoring fast gene expression. Similar repression of fast genes and Maf was observed in muscles from mice and humans with amyotrophic lateral sclerosis. Notably, Maf overexpression in human skeletal muscle cells in vitro prevented muscle atrophy and activated the expression of fast muscle genes. Our findings highlight a key role for Maf in maintaining muscle mass and could offer a promising therapeutic strategy to preserve muscle function during disease, aging, and injury.
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Registered trials
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