ArticleProceedings of the National Academy of Sciences of the United States of America2019
Physical exertion exacerbates decline in the musculature of an animal model of Duchenne muscular dystrophy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Basal cytoplasmic calcium levels regulate C. elegans germ stem cell proliferation.Development (Cambridge, England) · 2026Article
- Basal cytoplasmic calcium levels regulatebioRxiv : the preprint server for biology · 2025Article
- Fibrillin-Related Proteins Control Calcium Homeostasis in Dystrophic Muscle Across Species.microPublication biology · 2025Article
- Longitudinal assessment of skeletal muscle functional mechanics in the DE50-MD dog model of Duchenne muscular dystrophy.Disease models & mechanisms · 2023Article
- Current care practices for patients with Duchenne muscular dystrophy in China.Brain & development · 2022Article
- Mitochonic Acid 5 Improves Duchenne Muscular Dystrophy and Parkinson's Disease Model ofInternational journal of molecular sciences · 2022Article
- Exercise and the Brain: Lessons From Invertebrate Studies.Frontiers in behavioral neuroscience · 2022Review
- Review
- Mitochondrial hydrogen sulfide supplementation improves health in theProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Transcriptome changes during the initiation and progression of Duchenne muscular dystrophy in Caenorhabditis elegans.Human molecular genetics · 2020Article
- Exercise protects proliferative muscle satellite cells against exhaustion via the Igfbp7-Akt-mTOR axis.Theranostics · 2020Article
- Swim exercise inProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Pluronic gel-based burrowing assay for rapid assessment of neuromuscular health in C. elegans.Scientific reports · 2019Article
- Mitochondrial dysfunction causes CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
Corrections and comments
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Authors and funding
19 authors at 3 institutions in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a genetic disorder caused by loss of the protein dystrophin. In humans, DMD has early onset, causes developmental delays, muscle necrosis, loss of ambulation, and death. Current animal models have been challenged by their inability to model the early onset and severity of the disease. It remains unresolved whether increased sarcoplasmic calcium observed in dystrophic muscles follows or leads the mechanical insults caused by the muscle's disrupted contractile machinery. This knowledge has important implications for patients, as potential physiotherapeutic treatments may either help or exacerbate symptoms, depending on how dystrophic muscles differ from healthy ones. Recently we showed how burrowing dystrophic (
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