ReviewCell death and differentiation2015
Genetic evidence in the mouse solidifies the calcium hypothesis of myofiber death in muscular dystrophy.
Review in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
64 citing papers in PubMed, 106 citations in OpenAlex.
- An Unbiased Drug Screen in a Drosophila Model ofInternational journal of molecular sciences · 2026Article
- Microbiota dysbiosis influences immune system and muscle pathophysiology of dystrophin deficient mice.EMBO molecular medicine · 2026Article
- Dysferlin and the Regulation of CaCells · 2025Review
- SERCA Silencing Alleviates AßInternational journal of molecular sciences · 2025Article
- DWORF expression is reduced in a large animal model of Duchenne muscular dystrophy.Disease models & mechanisms · 2025Article
- Emerging roles for microproteins as critical regulators of endoplasmic reticulum function and cellular homeostasis.Seminars in cell & developmental biology · 2025Review
- 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
- Recycle, repair, recover: the role of autophagy in modulating skeletal muscle repair and post-exercise recovery.Bioscience reports · 2025Review
- Effects of aging on calcium channels in skeletal muscle.Frontiers in molecular biosciences · 2025Review
- Transcriptional changes of genes encoding sarcoplasmic reticulum calcium binding and up-taking proteins in normal and Duchenne muscular dystrophy dogs.BMC musculoskeletal disorders · 2024Article
- Cyclo His-Pro Attenuates Muscle Degeneration in Murine Myopathy Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Nanodysferlins support membrane repair and binding to TRIM72/MG53 but do not localize to t-tubules or stabilize CaMolecular therapy. Methods & clinical development · 2024Article
- MCU-independent CaScientific reports · 2024Article
- Pharmacotherapeutic Approaches to Treatment of Muscular Dystrophies.Biomolecules · 2023Review
- ANT-dependent MPTP underlies necrotic myofiber death in muscular dystrophy.Science advances · 2023Article
- Modulating fast skeletal muscle contraction protects skeletal muscle in animal models of Duchenne muscular dystrophy.The Journal of clinical investigation · 2023Article
- Inhibition of ATP synthase reverse activity restores energy homeostasis in mitochondrial pathologies.The EMBO journal · 2023Article
- Dwarf Open Reading Frame (DWORF) Gene Therapy Ameliorated Duchenne Muscular Dystrophy Cardiomyopathy in Aged mdx Mice.Journal of the American Heart Association · 2023Article
- Ion Channels of the Sarcolemma and Intracellular Organelles in Duchenne Muscular Dystrophy: A Role in the Dysregulation of Ion Homeostasis and a Possible Target for Therapy.International journal of molecular sciences · 2023Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Muscular dystrophy (MD) refers to a clinically and genetically heterogeneous group of degenerative muscle disorders characterized by progressive muscle wasting and often premature death. Although the primary defect underlying most forms of MD typically results from a loss of sarcolemmal integrity, the secondary molecular mechanisms leading to muscle degeneration and myofiber necrosis is debated. One hypothesis suggests that elevated or dysregulated cytosolic calcium is the common transducing event, resulting in myofiber necrosis in MD. Previous measurements of resting calcium levels in myofibers from dystrophic animal models or humans produced equivocal results. However, recent studies in genetically altered mouse models have largely solidified the calcium hypothesis of MD, such that models with artificially elevated calcium in skeletal muscle manifest fulminant dystrophic-like disease, whereas models with enhanced calcium clearance or inhibited calcium influx are resistant to myofiber death and MD. Here, we will review the field and the recent cadre of data from genetically altered mouse models, which we propose have collectively mostly proven the hypothesis that calcium is the primary effector of myofiber necrosis in MD. This new consensus on calcium should guide future selection of drugs to be evaluated in clinical trials as well as gene therapy-based approaches.
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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.