ArticleProceedings of the National Academy of Sciences of the United States of America2009
Calcium influx is sufficient to induce muscular dystrophy through a TRPC-dependent mechanism.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.
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Who cites it
126 citing papers in PubMed, 216 citations in OpenAlex.
- An Unbiased Drug Screen in a Drosophila Model ofInternational journal of molecular sciences · 2026Article
- Magnetic Mitohormesis as a Potential Non-Invasive Restorative Therapy for X-Linked Muscular Dystrophies.International journal of molecular sciences · 2026Review
- Combination S100A1 and ARC gene therapy as a treatment for Duchenne muscular dystrophy cardiomyopathy.JCI insight · 2026Article
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Environmental Mixture Toxicity of Guanitoxin and Organophosphates in Zebrafish: from Developmental and Neurobehavioral Phenotypes to Transcriptomic Responses.Environmental science & technology · 2026Article
- Article
- Calcium Signaling in Cardiac Fibroblasts: Roles in Fibrosis and Therapeutic Implications.Cardiovascular drugs and therapy · 2026Review
- Inhibition of TRPC3-Nox2 Complex Formation Ameliorates Skeletal Muscle Atrophy.Antioxidants (Basel, Switzerland) · 2025Article
- Spatiotemporal analysis of dystrophin expression during muscle repair.Skeletal muscle · 2025Article
- DWORF expression is reduced in a large animal model of Duchenne muscular dystrophy.Disease models & mechanisms · 2025Article
- GsMTx4-blocked PIEZO1 channel promotes myogenic differentiation and alleviates myofiber damage in Duchenne muscular dystrophy.Skeletal muscle · 2025Article
- Metabolic dysregulation contributes to the development of dysferlinopathy.Life science alliance · 2025Article
- Reduced voltage-activated Ca2+ release flux in muscle fibers from a rat model of Duchenne dystrophy.The Journal of general physiology · 2025Article
- Effects of aging on calcium channels in skeletal muscle.Frontiers in molecular biosciences · 2025Review
- Histone deacetylase 6 inhibition promotes microtubule acetylation and facilitates autophagosome-lysosome fusion in dystrophin-deficient mdx mice.Acta physiologica (Oxford, England) · 2025Article
- Dystroglycan-HSPG interactions provide synaptic plasticity and specificity.Glycobiology · 2024Review
- Pharmacological Treatments and Therapeutic Targets in Muscle Dystrophies Generated by Alterations in Dystrophin-Associated Proteins.Medicina (Kaunas, Lithuania) · 2024Review
- A Novel MAO-B/SSAO Inhibitor Improves Multiple Aspects of Dystrophic Phenotype inAntioxidants (Basel, Switzerland) · 2024Article
- Exploring the Gut Microbiota-Muscle Axis in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2024Review
- MCU-independent CaScientific reports · 2024Article
66 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Muscular dystrophy is a general term encompassing muscle disorders that cause weakness and wasting, typically leading to premature death. Membrane instability, as a result of a genetic disruption within the dystrophin-glycoprotein complex (DGC), is thought to induce myofiber degeneration, although the downstream mechanism whereby membrane fragility leads to disease remains controversial. One potential mechanism that has yet to be definitively proven in vivo is that unregulated calcium influx initiates disease in dystrophic myofibers. Here we demonstrate that calcium itself is sufficient to cause a dystrophic phenotype in skeletal muscle independent of membrane fragility. For example, overexpression of transient receptor potential canonical 3 (TRPC3) and the associated increase in calcium influx resulted in a phenotype of muscular dystrophy nearly identical to that observed in DGC-lacking dystrophic disease models, including a highly similar molecular signature of gene expression changes. Furthermore, transgene-mediated inhibition of TRPC channels in mice dramatically reduced calcium influx and dystrophic disease manifestations associated with the mdx mutation (dystrophin gene) and deletion of the delta-sarcoglycan (Scgd) gene. These results demonstrate that calcium itself is sufficient to induce muscular dystrophy in vivo, and that TRPC channels are key disease initiators downstream of the unstable membrane that characterizes many types of muscular dystrophy.
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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.