ArticleHuman molecular genetics2016
Effect of genetic background on the dystrophic phenotype in mdx mice.
Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers.
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Who cites it
162 citing papers in PubMed, 247 citations in OpenAlex.
- Direct Pharmacological Activation of AMPK Extends Lifespan in Yeast, Worms and Flies.Aging cell · 2026Article
- Engineering suppressor tRNAs for effective treatment of Duchenne muscular dystrophy.Science advances · 2026Article
- Combination S100A1 and ARC gene therapy as a treatment for Duchenne muscular dystrophy cardiomyopathy.JCI insight · 2026Article
- Engineered exosomes improve myocardial cell membrane integrity and heart function in dystrophic cardiomyopathy.Clinical and translational medicine · 2026Article
- Systemic regeneration medicines for muscular dystrophy: progress and challenges in pro-regenerative drug development.Cell regeneration (London, England) · 2026Review
- Pharmacological PIK3C2B inhibition rescues XLMTM phenotype in mouse models and identifies molecular markers of disease.JCI insight · 2026Article
- Stimulation of EGFR signaling in fibro-adipogenic precursors decreases adipogenesis in Duchenne muscular dystrophy.Skeletal muscle · 2026Article
- CAR-T cells targeting fibroblast activation protein eliminate pathological fibroblasts and preserve cardiac function in a Duchenne Muscular Dystrophy murine model.Stem cell research & therapy · 2026Article
- Data-driven prioritization of mouse strains for improved preclinical modeling of rare and common disease.bioRxiv : the preprint server for biology · 2026Article
- Fibrotic differentiation profile of skeletal and cardiac muscle fibroadipogenic progenitors in D2-mdx mouse.Journal of neuromuscular diseases · 2026Article
- A Borophosphate Glass Doped with Cobalt Oxide Improves Skeletal Muscle Structure and Function in Myopathic Mice.Journal of functional biomaterials · 2026Article
- Empagliflozin preserves cardiac function and modulates metabolism in a mouse model of Duchenne muscular dystrophy.bioRxiv : the preprint server for biology · 2026Article
- Humanin improves bone health in a glucocorticoid-treated mouse model of Duchenne muscular dystrophy.Biochemistry and biophysics reports · 2026Article
- Functional and structural pathologies in skeletal muscle of a rat model of Duchenne muscular dystrophy.Skeletal muscle · 2026Article
- Direct AMPK Activation Confers Mutation-Independent Therapeutic Benefit in Duchenne Muscular Dystrophy.Journal of cachexia, sarcopenia and muscle · 2026Article
- The D2.B10-DmdThe American journal of pathology · 2026Article
- Parkin overexpression attenuates muscle atrophy and improves mitochondrial bioenergetics but not histological features of Duchenne muscular dystrophy in mice.Scientific reports · 2026Article
- Volitional exercise elicits physiological and molecular improvements in the severe D2.mdx mouse model of Duchenne muscular dystrophy.The Journal of physiology · 2026Article
- The electrical tumor microenvironment: abnormalities and opportunities.Frontiers in oncology · 2026Review
- Genetic strategies for therapy of Duchenne muscular dystrophy.Molecular therapy. Nucleic acids · 2025Review
102 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
Genetic background significantly affects phenotype in multiple mouse models of human diseases, including muscular dystrophy. This phenotypic variability is partly attributed to genetic modifiers that regulate the disease process. Studies have demonstrated that introduction of the γ-sarcoglycan-null allele onto the DBA/2J background confers a more severe muscular dystrophy phenotype than the original strain, demonstrating the presence of genetic modifier loci in the DBA/2J background. To characterize the phenotype of dystrophin deficiency on the DBA/2J background, we created and phenotyped DBA/2J-congenic Dmdmdx mice (D2-mdx) and compared them with the original, C57BL/10ScSn-Dmdmdx (B10-mdx) model. These strains were compared with their respective control strains at multiple time points between 6 and 52 weeks of age. Skeletal and cardiac muscle function, inflammation, regeneration, histology and biochemistry were characterized. We found that D2-mdx mice showed significantly reduced skeletal muscle function as early as 7 weeks and reduced cardiac function by 28 weeks, suggesting that the disease phenotype is more severe than in B10-mdx mice. In addition, D2-mdx mice showed fewer central myonuclei and increased calcifications in the skeletal muscle, heart and diaphragm at 7 weeks, suggesting that their pathology is different from the B10-mdx mice. The new D2-mdx model with an earlier onset and more pronounced dystrophy phenotype may be useful for evaluating therapies that target cardiac and skeletal muscle function in dystrophin-deficient mice. Our data align the D2-mdx with Duchenne muscular dystrophy patients with the LTBP4 genetic modifier, making it one of the few instances of cross-species genetic modifiers of monogenic traits.
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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.