ArticleBioMed research international2015
Biochemical and Functional Comparisons of mdx and Sgcg(-/-) Muscular Dystrophy Mouse Models.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 18 citations in OpenAlex.
- The D2.B10-DmdThe American journal of pathology · 2026Article
- Sarcospan protects against LGMD R5 via remodeling of the sarcoglycan complex composition in dystrophic mice.The Journal of clinical investigation · 2025Article
- Article
- Effects of Glucocorticoids in Murine Models of Duchenne and Limb-Girdle Muscular Dystrophy.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Long-Term Protective Effect of Human Dystrophin Expressing Chimeric (DEC) Cell Therapy on Amelioration of Function of Cardiac, Respiratory and Skeletal Muscles in Duchenne Muscular Dystrophy.Stem cell reviews and reports · 2022Article
- Non-Invasive Optical Motion Tracking Allows Monitoring of Respiratory Dynamics in Dystrophin-Deficient Mice.Cells · 2022Article
- Preserved Left Ventricular Function despite Myocardial Fibrosis and Myopathy in the Dystrophin-Deficient D2.B10-DmdOxidative medicine and cellular longevity · 2022Article
- Human dystrophin expressing chimeric (DEC) cell therapy ameliorates cardiac, respiratory, and skeletal muscle's function in Duchenne muscular dystrophy.Stem cells translational medicine · 2021Article
- Systemically Administered Homing Peptide Targets Dystrophic Lesions and Delivers Transforming Growth Factor-β (TGFβ) Inhibitor to Attenuate Murine Muscular Dystrophy Pathology.Pharmaceutics · 2021Article
- Theoretical Analysis of S, M and N Structural Proteins by the Protein-RNA Recognition Code Leads to Genes/proteins that Are Relevant to the SARS-CoV-2 Life Cycle and Pathogenesis.Frontiers in genetics · 2021Article
- Gene therapy with secreted acid alpha-glucosidase rescues Pompe disease in a novel mouse model with early-onset spinal cord and respiratory defects.EBioMedicine · 2020Article
- Metabolic Alterations in Cardiomyocytes of Patients with Duchenne and Becker Muscular Dystrophies.Journal of clinical medicine · 2019Review
- Natural disease history of the D2FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Skeletal Muscle Metabolism in Duchenne and Becker Muscular Dystrophy-Implications for Therapies.Nutrients · 2018Review
- NADPH oxidase mediates microtubule alterations and diaphragm dysfunction in dystrophic mice.eLife · 2018Article
- Severe murine limb-girdle muscular dystrophy type 2C pathology is diminished by FTY720 treatment.Muscle & nerve · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mouse models have provided an essential platform to investigate facets of human diseases, from etiology, diagnosis, and prognosis, to potential treatments. Muscular dystrophy (MD) is the most common human genetic disease occurring in approximately 1 in 2500 births. The mdx mouse, which is dystrophin-deficient, has long been used to model this disease. However, this mouse strain displays a rather mild disease course compared to human patients. The mdx mice have been bred to additional genetically engineered mice to worsen the disease. Alternatively, other genes which cause human MD have been genetically disrupted in mice. We are now comparing disease progression from one of these alternative gene disruptions, the γ-sarcoglycan null mouse Sgcg(-/-) on the DBA2/J background, to the mdx mouse line. This paper aims to assess the time-course severity of the disease in the mouse models and determine which is best for MD research. The Sgcg(-/-) mice have a more severe phenotype than the mdx mice. Muscle function was assessed by plethysmography and echocardiography. Histologically the Sgcg(-/-) mice displayed increased fibrosis and variable fiber size. By quantitative Evan's blue dye uptake and hydroxyproline content two key disease determinants, membrane permeability and fibrosis respectively, were also proven worse in the Sgcg(-/-) mice.
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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.