ArticleThe American journal of pathology2006
Age-dependent effect of myostatin blockade on disease severity in a murine model of limb-girdle muscular dystrophy.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 95 citations in OpenAlex.
- Myostatin Research: From Molecular Understanding to Clinical Translation for Musculoskeletal and Metabolic Disorders.International journal of molecular sciences · 2026Review
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- SERCA1 Overexpression in Skeletal Muscle Attenuates Muscle Atrophy and Improves Motor Function in a Mouse Model of ALS.Journal of neuromuscular diseases · 2024Article
- Transcriptional Knock-down of mstn Encoding Myostatin Improves Muscle Quality of Nile Tilapia (Oreochromis niloticus).Marine biotechnology (New York, N.Y.) · 2023Article
- Histone Deacetylases: Molecular Mechanisms and Therapeutic Implications for Muscular Dystrophies.International journal of molecular sciences · 2023Review
- The landscape of cancer cachexia in advanced non-small cell lung cancer: a narrative review.Translational lung cancer research · 2023Review
- Transcriptomic Analysis ofGenes · 2021Article
- Antimyostatin Treatment in Health and Disease: The Story of Great Expectations and Limited Success.Cells · 2021Review
- EffectiveInternational journal of molecular sciences · 2020Article
- Advances in cancer cachexia: Intersection between affected organs, mediators, and pharmacological interventions.Biochimica et biophysica acta. Reviews on cancer · 2020Review
- GDF11 Decreases Pressure Overload-Induced Hypertrophy, but Can Cause Severe Cachexia and Premature Death.Circulation research · 2018Article
- Pharmacological inhibition of myostatin improves skeletal muscle mass and function in a mouse model of stroke.Scientific reports · 2017Article
- MMI-0100 Inhibits Cardiac Fibrosis in a Mouse Model Overexpressing Cardiac Myosin Binding Protein C.Journal of the American Heart Association · 2017Article
- Natural disease history of mouse models for limb girdle muscular dystrophy types 2D and 2F.PloS one · 2017Article
- Article
- Dystrophin-deficient dogs with reduced myostatin have unequal muscle growth and greater joint contractures.Skeletal muscle · 2016Article
- GDF11 does not rescue aging-related pathological hypertrophy.Circulation research · 2015Article
- RNA sequencing identifies upregulated kyphoscoliosis peptidase and phosphatidic acid signaling pathways in muscle hypertrophy generated by transgenic expression of myostatin propeptide.International journal of molecular sciences · 2015Article
- P38α MAPK underlies muscular dystrophy and myofiber death through a Bax-dependent mechanism.Human molecular genetics · 2014Article
- Limb-girdle muscular dystrophies: where next after six decades from the first proposal (Review).Molecular medicine reports · 2014Review
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5 authors at 3 institutions in 1 country.
Funding
Abstract
Myostatin (MSTN) is a muscle-specific secreted peptide that functions to limit muscle growth through an autocrine regulatory feedback loop. Loss of MSTN activity in cattle, mice, and humans leads to a profound phenotype of muscle overgrowth, associated with more and larger fibers and enhanced regenerative capacity. Deletion of MSTN in the mdx mouse model of Duchenne muscular dystrophy enhances muscle mass and reduces disease severity. In contrast, loss of MSTN activity in the dyW/dyW mouse model of laminin-deficient congenital muscular dystrophy, a much more severe and lethal disease model, does not improve all aspects of muscle pathology. Here we examined disease severity associated with myostatin (mstn-/-) deletion in mice nullizygous for delta-sarcoglycan (scgd-/-), a model of limb-girdle muscular dystrophy. Early loss of MSTN activity achieved either by monoclonal antibody administration or by gene deletion each improved muscle mass, regeneration, and reduced fibrosis in scgd-/- mice. However, antibody-mediated inhibition of MSTN in late-stage dystrophic scgd-/- mice did not improve disease. These findings suggest that MSTN inhibition may benefit muscular dystrophy when instituted early or if disease is relatively mild but that MSTN inhibition in severely affected or late-stage disease may be ineffective.
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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.