ReviewProteomics2022
Proteomic profiling of impaired excitation-contraction coupling and abnormal calcium handling in muscular dystrophy.
Review in Proteomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 21 citations in OpenAlex.
- Emerging Roles of Dystroglycan in Cardiac Remodeling, Fibrosis, and Heart Failure.International journal of molecular sciences · 2026Review
- Proteomic Profiling of Myofiber Repair Annexins and Their Role in Duchenne Muscular Dystrophy.Proteomics · 2026Review
- Magnetic Mitohormesis as a Potential Non-Invasive Restorative Therapy for X-Linked Muscular Dystrophies.International journal of molecular sciences · 2026Review
- AAV-Delivered RNAi Targeting Mutant LDB3 Prevents and Reverses Myofibrillar Myopathy through Mechanosignaling Restoration.bioRxiv : the preprint server for biology · 2026Article
- Comparative proteomic analysis of skin wound healing responses to biomaterial treatments identifies key pathways which govern differential regenerative outcomes.Biomaterials · 2026Article
- Integrated effects of altered action potentials and calcium release on skeletal muscle force generation in transgenic Huntington's disease mice.Pflugers Archiv : European journal of physiology · 2026Article
- Alterations of urinary proteomic profiles are correlated with return to sport after anterior cruciate ligament reconstruction.BMC sports science, medicine & rehabilitation · 2026Article
- (Z)-Endoxifen as a Potential Modulator of Utrophin Pathways in Duchenne Muscular Dystrophy: A Mechanistic and Transcriptomic Perspective.Degenerative neurological and neuromuscular disease · 2026Review
- Serum protein biomarker signature of Duchenne muscular dystrophy.European journal of translational myology · 2025Article
- Padua Days on Muscle and Mobility Medicine, March 25-29, 2025, Hotel Petrarca, Euganean Thermae, Italy: Program and Abstracts.European journal of translational myology · 2025Article
- Stem/progenitor cell-based therapy for Duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2025Review
- How Can Proteomics Help to Elucidate the Pathophysiological Crosstalk in Muscular Dystrophy and Associated Multi-System Dysfunction?Proteomes · 2024Article
- Hallmarks of ageing in human skeletal muscle and implications for understanding the pathophysiology of sarcopenia in women and men.Clinical science (London, England : 1979) · 2023Article
- Cellular pathogenesis of Duchenne muscular dystrophy: progressive myofibre degeneration, chronic inflammation, reactive myofibrosis and satellite cell dysfunction.European journal of translational myology · 2023Article
- Mass spectrometry-based proteomic characterization of the middle-aged mouse brain for animal model research of neuromuscular diseases.European journal of translational myology · 2023Article
- Extracellular Matrix Proteomics: TheBiomolecules · 2023Review
- 2023 Padua Days of Muscle and Mobility Medicine: post-meeting Book of Abstracts.European journal of translational myology · 2023Article
- Abstracts of the 2023 Padua Days of Muscle and Mobility Medicine (2023Pdm3) to be held March 29 - April 1 at the Galileian Academy of Padua and at the Petrarca Hotel, Thermae of Euganean Hills, Padua, Italy.European journal of translational myology · 2023Article
- Proteomic profiling of impaired excitation-contraction coupling and abnormal calcium handling in muscular dystrophy.Proteomics · 2022Review
- Proteomic Identification of Markers of Membrane Repair, Regeneration and Fibrosis in the Aged and Dystrophic Diaphragm.Life (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The X-linked inherited neuromuscular disorder Duchenne muscular dystrophy is characterised by primary abnormalities in the membrane cytoskeletal component dystrophin. The almost complete absence of the Dp427-M isoform of dystrophin in skeletal muscles renders contractile fibres more susceptible to progressive degeneration and a leaky sarcolemma membrane. This in turn results in abnormal calcium homeostasis, enhanced proteolysis and impaired excitation-contraction coupling. Biochemical and mass spectrometry-based proteomic studies of both patient biopsy specimens and genetic animal models of dystrophinopathy have demonstrated significant changes in the concentration and/or physiological function of essential calcium-regulatory proteins in dystrophin-lacking voluntary muscles. Abnormalities include dystrophinopathy-associated changes in voltage sensing receptors, calcium release channels, calcium pumps and calcium binding proteins. This review article provides an overview of the importance of the sarcolemmal dystrophin-glycoprotein complex and the wider dystrophin complexome in skeletal muscle and its linkage to depolarisation-induced calcium-release mechanisms and the excitation-contraction-relaxation cycle. Besides chronic inflammation, fat substitution and reactive myofibrosis, a major pathobiochemical hallmark of X-linked muscular dystrophy is represented by the chronic influx of calcium ions through the damaged plasmalemma in conjunction with abnormal intracellular calcium fluxes and buffering. Impaired calcium handling proteins should therefore be included in an improved biomarker signature of Duchenne muscular dystrophy.
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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.