ArticleThe Journal of physiology2011
Lateral transmission of force is impaired in skeletal muscles of dystrophic mice and very old rats.
Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers.
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Who cites it
155 citing papers in PubMed, 230 citations in OpenAlex.
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- Eccentric Exercise and Muscle Damage: An Introductory Guide.Journal of functional morphology and kinesiology · 2026Review
- Pathogenic mechanisms and clinical insights intoJournal of neuromuscular diseases · 2025Article
- The Importance of Early Diagnosis and Treatment to Limit the Impact of Dystrophic Cardiomyopathy-We've Seen This Film Before, and We Didn't Like the Ending.Journal of cardiovascular development and disease · 2025Review
- Cell therapy for Duchenne muscular dystrophy: promises, challenges, and controversies.Cellular and molecular life sciences : CMLS · 2025Review
- Bidirectional role of Costameres in the pathophysiology of mdx skeletal muscles.Human molecular genetics · 2025Article
- Enhanced therapeutic potential of a microdystrophin with an extended C-terminal domain.Molecular therapy. Methods & clinical development · 2025Article
- Sarcospan protects against LGMD R5 via remodeling of the sarcoglycan complex composition in dystrophic mice.The Journal of clinical investigation · 2025Article
- Aging in the Skeletal Muscle Revealed by Molecular Immunohistochemical Imaging.International journal of molecular sciences · 2025Review
- The road toward AAV-mediated gene therapy of Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Padua Days on Muscle and Mobility Medicine, March 25-29, 2025, Hotel Petrarca, Euganean Thermae, Italy: Program and Abstracts.European journal of translational myology · 2025Article
- Acupuncture of the adductor magnus for the treatment of post-stroke equinovarus: an investigation of the mechanism of action based on the anterior deep line.Frontiers in neurology · 2025Review
- Article
- Comparative analysis of acute eccentric contraction-induced changes to the skeletal muscle transcriptome in young and aged mice and humans.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
95 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
The dystrophin–glycoprotein complex (DGC) provides an essential link from the muscle fibre cytoskeleton to the extracellular matrix. In dystrophic humans and mdx mice, mutations in the dystrophin gene disrupt the structure of the DGC causing severe damage to muscle fibres. In frog muscles, transmission of force laterally from an activated fibre to the muscle surface occurs without attenuation, but lateral transmission of force has not been demonstrated in mammalian muscles. A unique ‘yoke' apparatus was developed that attached to the epimysium of muscles midway between the tendons and enabled the measurement of lateral force. We now report that in muscles of young wild-type (WT) mice and rats, compared over a wide range of longitudinal forces, forces transmitted laterally showed little or no decrement. In contrast, for muscles of mdx mice and very old rats, forces transmitted laterally were impaired severely. Muscles of both mdx mice and very old rats showed major reductions in the expression of dystrophin. We conclude that during contractions, forces developed by skeletal muscles of young WT mice and rats are transmitted laterally from fibre to fibre through the DGC without decrement. In contrast, in muscles of dystrophic or very old animals, disruptions in DGC structure and function impair lateral transmission of force causing instability and increased susceptibility of fibres to contraction-induced injury.
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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.