ReviewInternational journal of molecular sciences2023
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.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Olesoxime Does Not Affect Mitochondrial Dysfunction and Skeletal Muscle Pathology in Dystrophin-Deficient mdx Mice.Bulletin of experimental biology and medicine · 2026Article
- Magnetic Mitohormesis as a Potential Non-Invasive Restorative Therapy for X-Linked Muscular Dystrophies.International journal of molecular sciences · 2026Review
- YAP Acts as a Negative Regulator of Mini Utrophin-Based Gene Therapy for Duchenne Muscular Dystrophy in Mdx Mice.International journal of molecular sciences · 2026Article
- Molecular Insights and Orthopedic Management in Muscular Dystrophies: A Comprehensive Review.International journal of molecular sciences · 2026Review
- Five key challenges for the plasma membrane insertion of nicotinic acetylcholine receptors in cellular model systems.Molecular and cellular biochemistry · 2026Review
- Emerging therapeutic strategies in muscular dystrophy: an updated review on pathogenesis and treatment advances.Molecular biology reports · 2026Review
- VBIT-4 Rescues Mitochondrial Dysfunction and Reduces Skeletal Muscle Degeneration in a Severe Model of Duchenne Muscular Dystrophy.International journal of molecular sciences · 2025Article
- Duchenne Muscular Dystrophy: Integrating Current Clinical Practice with Future Therapeutic and Diagnostic Horizons.International journal of molecular sciences · 2025Review
- Living with Duchenne Muscular Dystrophy Beyond the Physical Implications: Cognitive Features, Psychopathology Aspects, and Psychosocial Resources-A Narrative Review.Brain sciences · 2025Review
- A new method to evaluate staircase phenomenon in skeletal muscle using piezoelectric sensor.Clinical neurophysiology practice · 2025Article
- Cre recombinase affects calcium dynamics already in young mice.Frontiers in pharmacology · 2025Article
- The Gut Microbiota Involvement in the Panorama of Muscular Dystrophy Pathogenesis.International journal of molecular sciences · 2024Review
- Reduction of Mitochondrial Calcium Overload via MKT077-Induced Inhibition of Glucose-Regulated Protein 75 Alleviates Skeletal Muscle Pathology in Dystrophin-DeficientInternational journal of molecular sciences · 2024Article
- Correction of exon 2, exon 2-9 and exons 8-9 duplications in DMD patient myogenic cells by a single CRISPR/Cas9 system.Scientific reports · 2024Article
- Glucocorticoid Deflazacort Normalizes the Ultrastructure of Skeletal Muscles and the State of the Colon Microbiota in Dystrophin-Deficient Mice.Bulletin of experimental biology and medicine · 2024Article
- Exploring the Gut Microbiota-Muscle Axis in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2024Review
- Improved mitochondrial function in the hearts of sarcolipin-deficient dystrophin and utrophin double-knockout mice.JCI insight · 2024Article
- Mitochondrial Transplantation Therapy Ameliorates Muscular Dystrophy inBiomolecules · 2024Article
- How Can Proteomics Help to Elucidate the Pathophysiological Crosstalk in Muscular Dystrophy and Associated Multi-System Dysfunction?Proteomes · 2024Article
- Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is caused by the absence of the dystrophin protein and a properly functioning dystrophin-associated protein complex (DAPC) in muscle cells. DAPC components act as molecular scaffolds coordinating the assembly of various signaling molecules including ion channels. DMD shows a significant change in the functioning of the ion channels of the sarcolemma and intracellular organelles and, above all, the sarcoplasmic reticulum and mitochondria regulating ion homeostasis, which is necessary for the correct excitation and relaxation of muscles. This review is devoted to the analysis of current data on changes in the structure, functioning, and regulation of the activity of ion channels in striated muscles in DMD and their contribution to the disruption of muscle function and the development of pathology. We note the prospects of therapy based on targeting the channels of the sarcolemma and organelles for the correction and alleviation of pathology, and the problems that arise in the interpretation of data obtained on model dystrophin-deficient objects.
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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 Socratic graph.