ReviewJournal of neuromuscular diseases2016
Excitation-Contraction Coupling Alterations in Myopathies.
Review in Journal of neuromuscular diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Molecular genetics of skeletal muscle diseases associated with abnormal excitation-contraction coupling.Journal of human genetics · 2026Review
- Human induced pluripotent stem cell-derived cardiomyocytes and their use in a cardiac organ-on-a-chip to assay electrophysiology, calcium and contractility.Nature protocols · 2025Review
- The role of 3D printing in skeletal muscle-on-a-chip models: Current applications and future potential.Materials today. Bio · 2025Article
- Limited pre-clinical relevance of the heterozygous RYR1-I4895T/+ mouse model due to its mild phenotype.Journal of neuromuscular diseases · 2025Article
- Comparative transcriptome analysis of pectoralis major muscles affected by white striping, wooden breast and spaghetti meat in male and female broiler chickens.BMC genomics · 2025Article
- RyR1 Is Involved in the Control of Myogenesis.Cells · 2025Article
- Article
- Functional benefit of CRISPR-Cas9-induced allele deletion forMolecular therapy. Nucleic acids · 2024Article
- Defective excitation-contraction coupling and mitochondrial respiration precede mitochondrial CaNature communications · 2023Article
- Introduction to the Special Issue "Skeletal Muscle Atrophy: Mechanisms at a Cellular Level".Cells · 2023Article
- Huntingtin regulates calcium fluxes in skeletal muscle.The Journal of general physiology · 2023Article
- Article
- Variants in ASPH cause exertional heat illness and are associated with malignant hyperthermia susceptibility.Nature communications · 2022Article
- Structure-function relationships and modifications of cardiac sarcoplasmic reticulum Ca2+-transport.Physiological research · 2021Review
- Loss of dysferlin or myoferlin results in differential defects in excitation-contraction coupling in mouse skeletal muscle.Scientific reports · 2021Article
- Longer electromechanical delay in paretic triceps surae muscles during voluntary isometric plantarflexion torque generation in chronic hemispheric stroke survivors.Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology · 2021Article
- In vivo RyR1 reduction in muscle triggers a core-like myopathy.Acta neuropathologica communications · 2020Article
- CaCells · 2019Review
- Ryanodine Receptor 1-Related Myopathies: Diagnostic and Therapeutic Approaches.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the complex series of events leading to muscle contraction, the initial electric signal coming from motor neurons is transformed into an increase in calcium concentration that triggers sliding of myofibrils. This process, referred to as excitation-contraction coupling, is reliant upon the calcium-release complex, which is restricted spatially to a sub-compartment of muscle cells ("the triad") and regulated precisely. Any dysfunction in the calcium-release complex leads to muscle impairment and myopathy. Various causes can lead to alterations in excitation-contraction coupling and to muscle diseases. The latter are reviewed and classified into four categories: (i) mutation in a protein of the calcium-release complex; (ii) alteration in triad structure; (iii) modification of regulation of channels; (iv) modification in calcium stores within the muscle. Current knowledge of the pathophysiologic mechanisms in each category is described and discussed.
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Registered trials
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