ArticleMuscle & nerve2018
Morphological and functional analyses of skeletal muscles from an immunodeficient animal model of limb-girdle muscular dystrophy type 2E.
Article in Muscle & nerve, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Whole-genome SNP allele frequency differences between Tibetan and Large white pigs reveal genes associated with skeletal muscle growth.BMC genomics · 2024Article
- MEK-inhibitors decrease Nfix in muscular dystrophy but induce unexpected calcifications, partially rescued with Cyanidin diet.iScience · 2024Article
- Preying dangerously: black widow spider venom resistance in sympatric lizards.Royal Society open science · 2022Article
- Extracellular vesicle-derived miRNAs improve stem cell-based therapeutic approaches in muscle wasting conditions.Frontiers in immunology · 2022Article
- Intramuscular adipocyte and fatty acid differences between high-fat and control rabbit groups subject to a restricted diet.Veterinary medicine and science · 2021Article
- Muscle Diversity, Heterogeneity, and Gradients: Learning from Sarcoglycanopathies.International journal of molecular sciences · 2021Review
- Growth Factor Screening in Dystrophic Muscles Reveals PDGFB/PDGFRB-Mediated Migration of Interstitial Stem Cells.International journal of molecular sciences · 2019Article
- Cross-sectional study into age-related pathology of mouse models for limb girdle muscular dystrophy types 2D and 2F.PloS one · 2019Article
- Pericytes in Muscular Dystrophies.Advances in experimental medicine and biology · 2019Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionLimb-girdle muscular dystrophy type 2E (LGMD2E) is caused by mutations in the β-sarcoglycan gene, which is expressed in skeletal, cardiac, and smooth muscles. β-Sarcoglycan-deficient (Sgcb-null) mice develop severe muscular dystrophy and cardiomyopathy with focal areas of necrosis.
methodsIn this study we performed morphological (histological and cellular characterization) and functional (isometric tetanic force and fatigue) analyses in dystrophic mice. Comparison studies were carried out in 1-month-old (clinical onset of the disease) and 7-month-old control mice (C57Bl/6J, Rag2/γc-null) and immunocompetent and immunodeficient dystrophic mice (Sgcb-null and Sgcb/Rag2/γc-null, respectively).
resultsWe found that the lack of an immunological system resulted in an increase of calcification in striated muscles without impairing extensor digitorum longus muscle performance. Sgcb/Rag2/γc-null muscles showed a significant reduction of alkaline phosphate-positive mesoangioblasts. DISCUSSION: The immunological system counteracts skeletal muscle degeneration in the murine model of LGMD2E. Muscle Nerve, 2018.
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