ArticleSkeletal muscle2012
The superhealing MRL background improves muscular dystrophy.
Article in Skeletal muscle, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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
26 citing papers in PubMed, 32 citations in OpenAlex.
- A novel, rapidly progressive ataxia due to a spontaneous Myo5a mutation in mice impairs transport proteins and alters mitochondria.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The super-healing MRL strain promotes muscle growth in muscular dystrophy through a regenerative extracellular matrix.JCI insight · 2024Article
- Altered TGFB1 regulated pathways promote accelerated tendon healing in the superhealer MRL/MpJ mouse.Scientific reports · 2022Article
- The MRL/MpJ Mouse Strain Is Not Protected From Muscle Atrophy and Weakness After Rotator Cuff Tear.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2020Article
- Laminin-111 protein therapy enhances muscle regeneration and repair in the GRMD dog model of Duchenne muscular dystrophy.Human molecular genetics · 2019Article
- Sunitinib promotes myogenic regeneration and mitigates disease progression in the mdx mouse model of Duchenne muscular dystrophy.Human molecular genetics · 2019Article
- Hypoxia-inducible factor 1α (HIF-1α) is a major determinant in the enhanced function of muscle-derived progenitors from MRL/MpJ mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Markers of Accelerated Skeletal Muscle Regenerative Response in Murphy Roths Large Mice: Characteristics of Muscle Progenitor Cells and Circulating Factors.Stem cells (Dayton, Ohio) · 2019Article
- Skeletal Muscle Metabolism in Duchenne and Becker Muscular Dystrophy-Implications for Therapies.Nutrients · 2018Review
- Drug delivery and epimorphic salamander-type mouse regeneration: A full parts and labor plan.Advanced drug delivery reviews · 2018Review
- Skeletal muscle stem cells in comfort and stress.NPJ Regenerative medicine · 2018Review
- Genetic modifiers of Duchenne and facioscapulohumeral muscular dystrophies.Muscle & nerve · 2018Review
- Enhanced cartilage repair in 'healer' mice-New leads in the search for better clinical options for cartilage repair.Seminars in cell & developmental biology · 2017Review
- Functional improvement of dystrophic muscle by repression of utrophin: let-7c interaction.PloS one · 2017Article
- Hepatic Adaptations to a High Fat Diet in the MRL Mouse Strain are Associated with an Inefficient Oxidative Phosphorylation System.Jacobs journal of diabetes and endocrinology · 2016Article
- Degenerative and regenerative features of myofibers differ among skeletal muscles in a murine model of muscular dystrophy.Journal of muscle research and cell motility · 2016Article
- Diseases of the Nucleoskeleton.Comprehensive Physiology · 2016Review
- Observational
- Article
- The Murphy Roths Large (MRL) mouse strain is naturally resistant to high fat diet-induced hyperglycemia.Metabolism: clinical and experimental · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
unlabelled
backgroundMice from the MRL or "superhealing" strain have enhanced repair after acute injury to the skin, cornea, and heart. We now tested an admixture of the MRL genome and found that it altered the course of muscle pathology and cardiac function in a chronic disease model of skeletal and cardiac muscle. Mice lacking γ-sarcoglycan (Sgcg), a dystrophin-associated protein, develop muscular dystrophy and cardiomyopathy similar to their human counterparts with limb girdle muscular dystrophy. With disruption of the dystrophin complex, the muscle plasma membrane becomes leaky and muscles develop increased fibrosis.
methodsMRL/MpJ mice were bred with Sgcg mice, and cardiac function was measured. Muscles were assessed for fibrosis and membrane leak using measurements of hydroxyproline and Evans blue dye. Quantitative trait locus mapping was conducted using single nucleotide polymorphisms distinct between the two parental strains.
resultsIntroduction of the MRL genome reduced fibrosis but did not alter membrane leak in skeletal muscle of the Sgcg model. The MRL genome was also associated with improved cardiac function with reversal of depressed fractional shortening and the left ventricular ejection fraction. We conducted a genome-wide analysis of genetic modifiers and found that a region on chromosome 2 was associated with cardiac, diaphragm muscle and abdominal muscle fibrosis.
conclusionsThese data are consistent with a model where the MRL genome acts in a dominant manner to suppress fibrosis in this chronic disease setting of heart and muscle disease.
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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.