ArticleJournal of cachexia, sarcopenia and muscle2019
Inhibition of myostatin improves muscle atrophy in oculopharyngeal muscular dystrophy (OPMD).
Article in Journal of cachexia, sarcopenia and muscle, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A Systematic Review of Oropharyngeal Dysphagia Models in Rodents.International journal of environmental research and public health · 2021Pooled it
- Oculopharyngeal Muscular Dystrophy: From Molecular Pathogenesis to Gene Therapy.Molecular neurobiology · 2026Review
- The genetic and clinical characteristics of oculopharyngeal muscular dystrophy patients in Israel.Orphanet journal of rare diseases · 2026Article
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Codon-optimized human Smad7 gene therapy enhances skeletal muscle mass and function in a murine model of Duchenne muscular dystrophy.Gene therapy · 2026Article
- Cisplatin-Induced Muscle Wasting and Atrophy: Molecular Mechanism and Potential Therapeutic Interventions.Journal of cachexia, sarcopenia and muscle · 2025Review
- Different outcomes of endurance and resistance exercise in skeletal muscles of Oculopharyngeal muscular dystrophy.Journal of cachexia, sarcopenia and muscle · 2024Article
- Impact of Disease Severity and Disease-Modifying Therapies on Myostatin Levels in SMA Patients.International journal of molecular sciences · 2024Article
- Novel Metabolomic Approach for Identifying Pathology-Specific Biomarkers in Rare Diseases: A Case Study in Oculopharyngeal Muscular Dystrophy (OPMD).Metabolites · 2023Article
- Longitudinal Assessment of Creatine Kinase, Creatine/CreatinineNeurology · 2023Article
- Myostatin is involved in skeletal muscle dysfunction in chronic obstructive pulmonary disease via Drp-1 mediated abnormal mitochondrial division.Annals of translational medicine · 2022Article
- Activation of the ubiquitin-proteasome system contributes to oculopharyngeal muscular dystrophy through muscle atrophy.PLoS genetics · 2022Article
- Statins induce skeletal muscle atrophy via GGPP depletion-dependent myostatin overexpression in skeletal muscle and brown adipose tissue.Cell biology and toxicology · 2021Article
- Recent Progress in Oculopharyngeal Muscular Dystrophy.Journal of clinical medicine · 2021Review
- Antimyostatin Treatment in Health and Disease: The Story of Great Expectations and Limited Success.Cells · 2021Review
- ActRIIB:ALK4-Fc alleviates muscle dysfunction and comorbidities in murine models of neuromuscular disorders.The Journal of clinical investigation · 2021Article
- Article
- Silencing COX-2 blocks PDK1/TRAF4-induced AKT activation to inhibit fibrogenesis during skeletal muscle atrophy.Redox biology · 2021Article
- Blocking myostatin: muscle mass equals muscle strength?Journal of cachexia, sarcopenia and muscle · 2020Article
- Ergogenic Effect of BCAAs and L-Alanine Supplementation: Proof-of-Concept Study in a Murine Model of Physiological Exercise.Nutrients · 2020Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOculopharyngeal muscular dystrophy (OPMD) is a late-onset muscle disease affecting one per 80 000 of the general population characterized by profound dysphagia and ptosis, and limb weakness at later stages. Affected muscles are characterized by increased fibrosis and atrophy. Myostatin is a negative regulator of muscle mass, and inhibition of myostatin has been demonstrated to ameliorate symptoms in dystrophic muscles.
methodsIn this study, we performed a systemic delivery of a monoclonal antibody to immunologically block myostatin in the A17 mouse model of OPMD. The mice were administered a weekly dose of 10 mg/kg RK35 intraperitonially for 10 weeks, following which histological analyses were performed on the samples.
resultsThis treatment significantly (P < 0.01) improved body mass (11%) and muscle mass (for the tibialis anterior and extensor digitorum longus by 19% and 41%) in the A17 mice treated with RK35 when compared to saline controls. Similarly, a significantly (P < 0.01) increased muscle strength (18% increase in maximal tetanic force) and myofibre diameter (17% and 44% for the tibialis anterior and extensor digitorum longus), and reduced expression of markers of muscle fibrosis (40% reduction in area of expression), was also observed. No change in the density of intranuclear inclusions (a hallmark of disease progression of OPMD) was however observed.
conclusionsOur study supports the clinical translation of such antibody-mediated inhibition of myostatin as a treatment of OPMD. This strategy has implications to be used as adjuvant therapies with gene therapy based approaches, or to stabilize the muscle prior to myoblast transplantation.
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