ArticlePloS one2012
Dystrophin deficiency compromises force production of the extensor carpi ulnaris muscle in the canine model of Duchenne muscular dystrophy.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 35 citations in OpenAlex.
- Viscoelastic properties of dystrophin-deficient mouse skeletal muscles are resilient to isometric fatiguing exercise.Physiological reports · 2026Article
- Canine Model of Duchenne Muscular Dystrophy.Methods in molecular biology (Clifton, N.J.) · 2026Article
- DWORF expression is reduced in a large animal model of Duchenne muscular dystrophy.Disease models & mechanisms · 2025Article
- Transcriptional changes of genes encoding sarcoplasmic reticulum calcium binding and up-taking proteins in normal and Duchenne muscular dystrophy dogs.BMC musculoskeletal disorders · 2024Article
- SERCA2a overexpression improves muscle function in a canine Duchenne muscular dystrophy model.Molecular therapy. Methods & clinical development · 2024Article
- Longitudinal assessment of skeletal muscle functional mechanics in the DE50-MD dog model of Duchenne muscular dystrophy.Disease models & mechanisms · 2023Article
- RhoA/ROCK signalling activated by ARHGEF3 promotes muscle weakness via autophagy in dystrophic mdx mice.Journal of cachexia, sarcopenia and muscle · 2023Article
- Eccentric contraction-induced strength loss in dystrophin-deficient muscle: Preparations, protocols, and mechanisms.The Journal of general physiology · 2023Article
- Physiological Assessment of Muscle, Heart, and Whole Body Function in the Canine Model of Duchenne Muscular Dystrophy.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Extensor carpi ulnaris muscle shows unexpected slow-to-fast fiber-type switch in Duchenne muscular dystrophy dogs.Disease models & mechanisms · 2021Article
- Dystrophin deficiency impairs vascular structure and function in the canine model of Duchenne muscular dystrophy.The Journal of pathology · 2021Article
- Prednisolone rescues Duchenne muscular dystrophy phenotypes in human pluripotent stem cell-derived skeletal muscle in vitro.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Canine Models of Inherited Musculoskeletal and Neurodegenerative Diseases.Frontiers in veterinary science · 2020Review
- Questions Answered and Unanswered by the First CRISPR Editing Study in a Canine Model of Duchenne Muscular Dystrophy.Human gene therapy · 2019Article
- Discovery of Novel Therapeutics for Muscular Dystrophies using Zebrafish Phenotypic Screens.Journal of neuromuscular diseases · 2019Review
- The Dog Model in the Spotlight: Legacy of a Trustful Cooperation.Journal of neuromuscular diseases · 2019Article
- Nitric oxide-dependent attenuation of noradrenaline-induced vasoconstriction is impaired in the canine model of Duchenne muscular dystrophy.The Journal of physiology · 2018Article
- Dual AAV Gene Therapy for Duchenne Muscular Dystrophy with a 7-kb Mini-Dystrophin Gene in the Canine Model.Human gene therapy · 2018Article
- Non-invasive evaluation of muscle disease in the canine model of Duchenne muscular dystrophy by electrical impedance myography.PloS one · 2017Article
- Muscle dysfunction in a zebrafish model of Duchenne muscular dystrophy.Physiological genomics · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Loss of muscle force is a salient feature of Duchenne muscular dystrophy (DMD), a fatal disease caused by dystrophin deficiency. Assessment of force production from a single intact muscle has been considered as the gold standard for studying physiological consequences in murine models of DMD. Unfortunately, equivalent assays have not been established in dystrophic dogs. To fill the gap, we developed a novel in situ protocol to measure force generated by the extensor carpi ulnaris (ECU) muscle of a dog. We also determined the muscle length to fiber length ratio and the pennation angle of the ECU muscle. Muscle pathology and contractility were compared between normal and affected dogs. Absence of dystrophin resulted in marked histological damage in the ECU muscle of affected dogs. Central nucleation was significantly increased and myofiber size distribution was altered in the dystrophic ECU muscle. Muscle weight and physiological cross sectional area (PCSA) showed a trend of reduction in affected dogs although the difference did not reach statistical significance. Force measurement revealed a significant decrease of absolute force, and the PCSA or muscle weight normalized specific forces. To further characterize the physiological defect in affected dog muscle, we conducted eccentric contraction. Dystrophin-null dogs showed a significantly greater force loss following eccentric contraction damage. To our knowledge, this is the first convincing demonstration of force deficit in a single intact muscle in the canine DMD model. The method described here will be of great value to study physiological outcomes following innovative gene and/or cell therapies.
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Registered trials
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.