ArticleEuropean journal of translational myology2023
Cellular pathogenesis of Duchenne muscular dystrophy: progressive myofibre degeneration, chronic inflammation, reactive myofibrosis and satellite cell dysfunction.
Article in European journal of translational myology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 15 citations in OpenAlex.
- Preventing Cardiomyopathy in Duchenne Muscular Dystrophy: Long-Term Follow-Up of Patients in the Randomised, Placebo-Controlled Drug-Trial of Perindopril and Bisoprolol.European journal of neurology · 2025Trial
- 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
- The Multi-System Roles of Dp71 Dystrophin Isoforms in Duchenne Muscular Dystrophy.Muscles (Basel, Switzerland) · 2026Review
- PPMO-based exon skipping therapy improves respiratory function in theMolecular therapy. Nucleic acids · 2026Article
- Metrnl and macrophage polarization: role in skeletal muscle homeostasis and therapeutic potential.Frontiers in immunology · 2026Review
- Histone deacetylases in Duchenne muscular dystrophy: a role in the mechanism of disease and a target for inhibition.Clinical epigenetics · 2025Review
- Ubiquitination-targeted therapies improve BMD iPSC myogenic cell engraftment and dystrophin expressionMolecular therapy. Methods & clinical development · 2025Article
- Epigenetic small molecule screening identifies a new HDACi compound for ameliorating Duchenne muscular dystrophy.Molecular therapy. Nucleic acids · 2025Article
- Modulatory Effects ofAntioxidants (Basel, Switzerland) · 2025Review
- 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
- Dysregulated ATX-LPA and YAP/TAZ signaling in dystrophic SgcdSkeletal muscle · 2025Article
- Estrogen receptor-α ablation reverses muscle fibrosis and inguinal hernias.The Journal of clinical investigation · 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
- Histone deacetylase inhibition with givinostat: a multi-targeted mode of action with the potential to halt the pathological cascade of Duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2024Review
- Uncovering the Embryonic Origins of Duchenne Muscular Dystrophy.WIREs mechanisms of diseaseArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy is a highly progressive muscle wasting disease of early childhood and characterized by complex pathophysiological and histopathological changes in the voluntary contractile system, including myonecrosis, chronic inflammation, fat substitution and reactive myofibrosis. The continued loss of functional myofibres and replacement with non-contractile cells, as well as extensive tissue scarring and decline in tissue elasticity, leads to severe skeletal muscle weakness. In addition, dystrophic muscles exhibit a greatly diminished regenerative capacity to counteract the ongoing process of fibre degeneration. In normal muscle tissues, an abundant stem cell pool consisting of satellite cells that are localized between the sarcolemma and basal lamina, provides a rich source for the production of activated myogenic progenitor cells that are involved in efficient myofibre repair and tissue regeneration. Interestingly, the self-renewal of satellite cells for maintaining an essential pool of stem cells in matured skeletal muscles is increased in dystrophin-deficient fibres. However, satellite cell hyperplasia does not result in efficient recovery of dystrophic muscles due to impaired asymmetric cell divisions. The lack of expression of the full-length dystrophin isoform Dp427-M, which is due to primary defects in the DMD gene, appears to affect key regulators of satellite cell polarity causing a reduced differentiation of myogenic progenitors, which are essential for myofibre regeneration. This review outlines the complexity of dystrophinopathy and describes the importance of the pathophysiological role of satellite cell dysfunction. A brief discussion of the bioanalytical usefulness of single cell proteomics for future studies of satellite cell biology is provided.
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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.