ArticleJournal of cachexia, sarcopenia and muscle2024
Ryanodine receptor dysfunction causes senescence and fibrosis in Duchenne dilated cardiomyopathy.
Article in Journal of cachexia, sarcopenia and muscle, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Review
- Senescence dynamics define therapeutic windows for Duchenne muscular dystrophy in DBA/2-mdx mice.Skeletal muscle · 2026Article
- Clinical challenges of an Xp21 contiguous gene deletion syndrome in a newborn and 15 months of follow-up - case report.Frontiers in endocrinology · 2026Article
- A Nomogram Integrating Clinical and Cardiac Imaging for Predicting Short-Term Left Ventricular Ejection Fraction Decline in Patients with Duchenne Muscular Dystrophy.International journal of general medicine · 2026Article
- Potentiation of ryanodine receptor-mediated calcium release by MAPK is responsible for epidermal transformation and carcinogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Extracellular activation of HCN4 by a subtype-specific nanobody.Nature communications · 2025Article
- Calcium handling remodeling in dilated cardiomyopathy: From molecular mechanisms to targeted therapies.Channels (Austin, Tex.) · 2025Review
- The role of cellular senescence in cardiovascular disease.Cell death discovery · 2025Review
- Conduction defects and arrhythmias inFrontiers in physiology · 2025Article
- Ryanodine receptor dysfunction causes senescence and fibrosis in Duchenne dilated cardiomyopathy.Journal of cachexia, sarcopenia and muscle · 2024Article
Corrections and comments
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Authors and funding
22 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundDuchenne muscular dystrophy (DMD) is an X-linked disorder characterized by progressive muscle weakness due to the absence of functional dystrophin. DMD patients also develop dilated cardiomyopathy (DCM). We have previously shown that DMD (mdx) mice and a canine DMD model (GRMD) exhibit abnormal intracellular calcium (Ca
methodsHere, we used hiPSC-CMs from DMD patients selected by Speckle-tracking echocardiography and canine DMD cardiac biopsies to assess key early-stage Duchenne DCM features.
resultsDystrophin deficiency was associated with RyR2 remodelling and SR Ca
conclusionsWe identified key cellular damages that are established earlier than cardiac clinical pathology in DMD patients, with major perturbation of the cardiac ECC. Our results demonstrated that cardiac fibrosis and premature senescence are induced by RyR2 mediated SR Ca
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Registered trials
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