ReviewClinical epigenetics2021
Epigenetic modifications in muscle regeneration and progression of Duchenne muscular dystrophy.
Review in Clinical epigenetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 50 citations in OpenAlex.
- Identification of biomarkers associated with pathological dynamic progression in dystrophinopathies.Scientific reports · 2026Article
- Myotendinous Junction development and repair.Journal of orthopaedic translation · 2026Review
- Construction and Functional Analysis of the ceRNA Regulatory Network Associated with Muscle Development in Shaanbei White Cashmere Goats.Animals : an open access journal from MDPI · 2025Article
- Histone deacetylases in Duchenne muscular dystrophy: a role in the mechanism of disease and a target for inhibition.Clinical epigenetics · 2025Review
- Local Non-Coding Regulatory Elements in Muscular Dystrophies.International journal of molecular sciences · 2025Review
- Oestrogen suppresses the adipogenesis of fibro/adipogenic progenitors through reactivating the METTL3-ESR1-mediated loop in post-menopausal females.Clinical and translational medicine · 2025Article
- Stem/progenitor cell-based therapy for Duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2025Review
- Inhibition of Sesn2 has negative regulatory effects on the myogenic differentiation of C2C12 myoblasts.Molecular biomedicine · 2024Article
- Signaling pathways and regulatory networks in quail skeletal muscle development: insights from whole transcriptome sequencing.Poultry science · 2024Article
- Transcription FactorGenes · 2024Article
- Editorial: Mechanical and genetic signaling in striated muscle development, aging and disease.Frontiers in physiology · 2024Article
- Dystrophin- and Utrophin-Based Therapeutic Approaches for Treatment of Duchenne Muscular Dystrophy: A Comparative Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024Review
- 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
- Lysine methylation signaling in skeletal muscle biology: from myogenesis to clinical insights.The Biochemical journal · 2023Review
- Review
- Cellular pathogenesis of Duchenne muscular dystrophy: progressive myofibre degeneration, chronic inflammation, reactive myofibrosis and satellite cell dysfunction.European journal of translational myology · 2023Article
- Epitranscriptomics as a New Layer of Regulation of Gene Expression in Skeletal Muscle: Known Functions and Future Perspectives.International journal of molecular sciences · 2023Review
- Resolution of fibrosis in mdx dystrophic mouse after oral consumption of N-163 strain of Aureobasidium pullulans produced β-glucan.Scientific reports · 2023Article
- Long noncoding RNA lncMREF promotes myogenic differentiation and muscle regeneration by interacting with the Smarca5/p300 complex.Nucleic acids research · 2022Article
- Rho/SRF Inhibitor Modulates Mitochondrial Functions.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is a multisystemic disorder that affects 1:5000 boys. The severity of the phenotype varies dependent on the mutation site in the DMD gene and the resultant dystrophin expression profile. In skeletal muscle, dystrophin loss is associated with the disintegration of myofibers and their ineffective regeneration due to defective expansion and differentiation of the muscle stem cell pool. Some of these phenotypic alterations stem from the dystrophin absence-mediated serine-threonine protein kinase 2 (MARK2) misplacement/downregulation in activated muscle stem (satellite) cells and neuronal nitric oxide synthase loss in cells committed to myogenesis. Here, we trace changes in DNA methylation, histone modifications, and expression of regulatory noncoding RNAs during muscle regeneration, from the stage of satellite cells to myofibers. Furthermore, we describe the abrogation of these epigenetic regulatory processes due to changes in signal transduction in DMD and point to therapeutic treatments increasing the regenerative potential of diseased muscles based on this acquired knowledge.
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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.