ArticleSkeletal muscle2014
Incidence and severity of myofiber branching with regeneration and aging.
Article in Skeletal muscle, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed.
- A Borophosphate Glass Doped with Cobalt Oxide Improves Skeletal Muscle Structure and Function in Myopathic Mice.Journal of functional biomaterials · 2026Article
- Association Between Abnormal DNA Methylation and Altered Transcriptome in Muscle Five Years After Critical Illness.Journal of cachexia, sarcopenia and muscle · 2026Article
- Twisting Paths: The Paradox of Fiber Branching in Muscle Regeneration.International journal of molecular sciences · 2026Review
- Quantitative 3D assessment of muscle dystrophy through X-ray phase-contrast tomography.Scientific reports · 2025Article
- Bidirectional role of Costameres in the pathophysiology of mdx skeletal muscles.Human molecular genetics · 2025Article
- Intrinsic Muscle Stem Cell Dysfunction Contributes to Impaired Regeneration in the mdx Mouse.Journal of cachexia, sarcopenia and muscle · 2025Article
- Three-dimensional imaging studies in mice identify cellular dynamics of skeletal muscle regeneration.Developmental cell · 2024Article
- Hallmarks of ageing in human skeletal muscle and implications for understanding the pathophysiology of sarcopenia in women and men.Clinical science (London, England : 1979) · 2023Article
- Regenerating Myofibers after an Acute Muscle Injury: What Do We Really Know about Them?International journal of molecular sciences · 2023Review
- Use of a novel technique to assess impact of age-related denervation on mouse soleus muscle function.Biogerontology · 2023Article
- Detyrosinated microtubule arrays drive myofibrillar malformations inFrontiers in cell and developmental biology · 2023Article
- Inhibiting 5-lipoxygenase prevents skeletal muscle atrophy by targeting organogenesis signalling and insulin-like growth factor-1.Journal of cachexia, sarcopenia and muscle · 2022Article
- Article
- Three-dimensional mechanical characterization of murine skeletal muscle using quantitative micro-elastography.Biomedical optics express · 2022Article
- Loss of α-actinin-3 confers protection from eccentric contraction damage in fast-twitch EDL muscles from aged mdx dystrophic mice by reducing pathological fibre branching.Human molecular genetics · 2022Article
- All-trans retinoic acid changes muscle fiber type via increasing GADD34 dependent on MAPK signal.Life science alliance · 2022Article
- Gelsolin and dCryAB act downstream of muscle identity genes and contribute to preventing muscle splitting and branching in Drosophila.Scientific reports · 2021Article
- TGFβ signaling curbs cell fusion and muscle regeneration.Nature communications · 2021Article
- Lifespan Analysis of DystrophicFrontiers in physiology · 2021Article
- Enhancing Interrogation of Skeletal Muscle Samples for Informative Quantitative Data.Journal of neuromuscular diseases · 2021Review
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Authors and funding
2 authors.
Funding
Abstract
backgroundMyofibers with an abnormal branching cytoarchitecture are commonly found in muscular dystrophy and in regenerated or aged nondystrophic muscles. Such branched myofibers from dystrophic mice are more susceptible to damage than unbranched myofibers in vitro, suggesting that muscles containing a high percentage of these myofibers are more prone to injury. Little is known about the regulation of myofiber branching.
methodsTo gain insights into the formation and fate of branched myofibers, we performed in-depth analyses of single myofibers isolated from dystrophic and nondystrophic (myotoxin-injured or aged) mouse muscles. The proportion of branched myofibers, the number of branches per myofiber and the morphology of the branches were assessed.
resultsAged dystrophic mice exhibited the most severe myofiber branching as defined by the incidence of branched myofibers and the number of branches per myofiber, followed by myotoxin-injured, wild-type muscles and then aged wild-type muscles. In addition, the morphology of the branched myofibers differed among the various models. In response to either induced or ongoing muscle degeneration, branching was restricted to regenerated myofibers containing central nuclei. In myotoxin-injured muscles, the amount of branched myofibers remained stable over time.
conclusionWe suggest that myofiber branching is a consequence of myofiber remodeling during muscle regeneration. Our present study lays valuable groundwork for identifying the molecular pathways leading to myofiber branching in dystrophy, trauma and aging. Decreasing myofiber branching in dystrophic patients may improve muscle resistance to mechanical stress.
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