ArticleHuman molecular genetics2015
Muscle hypertrophy induced by myostatin inhibition accelerates degeneration in dysferlinopathy.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Therapeutic Peptides in Aesthetic, Metabolic and Endocrine Conditions: Effects, Safety, Clinical Applications, and Future Perspectives.International journal of molecular sciences · 2026Review
- Metabolic dysregulation contributes to the development of dysferlinopathy.Life science alliance · 2025Article
- Impact of Disease Severity and Disease-Modifying Therapies on Myostatin Levels in SMA Patients.International journal of molecular sciences · 2024Article
- Bioengineered Model of Human LGMD2B Skeletal Muscle Reveals Roles of Intracellular Calcium Overload in Contractile and Metabolic Dysfunction in Dysferlinopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Role of Myostatin in Rheumatoid Arthritis: A Review of the Clinical Impact.Diagnostics (Basel, Switzerland) · 2024Review
- Longitudinal Assessment of Creatine Kinase, Creatine/CreatinineNeurology · 2023Article
- Esophageal striated muscle hypertrophy and muscle fiber type transformation in MSTN knockout pigs.Transgenic research · 2022Article
- Anti-latent TGFβ binding protein 4 antibody improves muscle function and reduces muscle fibrosis in muscular dystrophy.Science translational medicine · 2021Article
- Antimyostatin Treatment in Health and Disease: The Story of Great Expectations and Limited Success.Cells · 2021Review
- ACVR2B antagonism as a countermeasure to multi-organ perturbations in metastatic colorectal cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2020Article
- Effects of aerobic and inspiratory training on skeletal muscle microRNA-1 and downstream-associated pathways in patients with heart failure.Journal of cachexia, sarcopenia and muscle · 2020Article
- Skeletal muscle: A review of molecular structure and function, in health and disease.Wiley interdisciplinary reviews. Systems biology and medicine · 2020Review
- Plasmid-Mediated Gene Therapy in Mouse Models of Limb Girdle Muscular Dystrophy.Molecular therapy. Methods & clinical development · 2019Article
- Functional muscle hypertrophy by increased insulin-like growth factor 1 does not require dysferlin.Muscle & nerve · 2019Article
- Treatment with Soluble Activin Receptor Type IIB Alters Metabolic Response in Chemotherapy-Induced Cachexia.Cancers · 2019Article
- Dusp6 is a genetic modifier of growth through enhanced ERK activity.Human molecular genetics · 2019Article
- Skeletal Muscle Hypertrophy, Insulin-like Growth Factor 1, Myostatin and Follistatin in Healthy and Sarcopenic Elderly Men: The Effect of Whole-body Resistance Training.International journal of preventive medicine · 2019Article
- The Limb-Girdle Muscular Dystrophies: Is Treatment on the Horizon?Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
- DNA-Mediated Gene Therapy in a Mouse Model of Limb Girdle Muscular Dystrophy 2B.Molecular therapy. Methods & clinical development · 2017Article
- Intermittent Glucocorticoid Dosing Improves Muscle Repair and Function in Mice with Limb-Girdle Muscular Dystrophy.The American journal of pathology · 2017Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Myostatin is a secreted signaling molecule that normally acts to limit muscle growth. As a result, there is extensive effort directed at developing drugs capable of targeting myostatin to treat patients with muscle loss. One potential concern with this therapeutic approach in patients with muscle degenerative diseases like muscular dystrophy is that inducing hypertrophy may increase stress on dystrophic fibers, thereby accelerating disease progression. To investigate this possibility, we examined the effect of blocking the myostatin pathway in dysferlin-deficient (Dysf(-/-)) mice, in which membrane repair is compromised, either by transgenic expression of follistatin in skeletal muscle or by systemic administration of the soluble form of the activin type IIB receptor (ACVR2B/Fc). Here, we show that myostatin inhibition by follistatin transgene expression in Dysf(-/-) mice results in early improvement in histopathology but ultimately exacerbates muscle degeneration; this effect was not observed in dystrophin-deficient (mdx) mice, suggesting that accelerated degeneration induced by follistatin transgene expression is specific to mice lacking dysferlin. Dysf(-/-) mice injected with ACVR2B/Fc showed significant increases in muscle mass and amelioration of fibrotic changes normally seen in 8-month-old Dysf(-/-) mice. Despite these potentially beneficial effects, ACVR2B/Fc treatment caused increases in serum CK levels in some Dysf(-/-) mice, indicating possible muscle damage induced by hypertrophy. These findings suggest that depending on the disease context, inducing muscle hypertrophy by myostatin blockade may have detrimental effects, which need to be weighed against the potential gains in muscle growth and decreased fibrosis.
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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.