ReviewJournal of neuromuscular diseases2016
Current Translational Research and Murine Models For Duchenne Muscular Dystrophy.
Review in Journal of neuromuscular diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 62 citations in OpenAlex.
- Systemic regeneration medicines for muscular dystrophy: progress and challenges in pro-regenerative drug development.Cell regeneration (London, England) · 2026Review
- NuMA1 controls myonuclear motility in striated skeletal muscle through AMPK activity and is impaired in Duchenne muscular dystrophy.Cell death & disease · 2026Article
- AAV-mediated gene transfer of a novel microdystrophin ameliorates pathology and enhances muscle function in a mouse model of DMD.Molecular therapy. Nucleic acids · 2026Article
- Neu5Gc-associated Serum Immunoglobulin G Glycosylation as a Diagnostic Biomarker for Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2026Article
- Beyond muscle: Delivering RNA therapeutics to the CNS in Duchenne muscular dystrophy.Journal of neuromuscular diseases · 2026Review
- Conditional Dmd ablation in muscle and brain causes profound effects on muscle function and neurobehavior.Communications biology · 2025Article
- Creation of DMD Muscle Cell Model Using CRISPR-Cas9 Genome Editing to Test the Efficacy of Antisense-Mediated Exon Skipping.Methods in molecular biology (Clifton, N.J.) · 2025Article
- An Overview of Recent Advances and Clinical Applications of Exon Skipping and Splice Modulation for Muscular Dystrophy and Various Genetic Diseases.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Tips to Design Effective Splice-Switching Antisense Oligonucleotides for Exon Skipping and Exon Inclusion.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Respiratory characterization of a humanized Duchenne muscular dystrophy mouse model.Respiratory physiology & neurobiology · 2024Article
- The Adiponectin Receptor Agonist, ALY688: A Promising Therapeutic for Fibrosis in the Dystrophic Muscle.Cells · 2023Article
- Restoring Dystrophin Expression by Skipping Exons 6 and 8 in Neonatal Dystrophic Dogs.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Characterization of Alzheimer's disease-like neuropathology in Duchenne's muscular dystrophy using the DBA/2J mdx mouse model.FEBS open bio · 2022Article
- Unraveling Muscle Impairment Associated With COVID-19 and the Role of 3D Culture in Its Investigation.Frontiers in nutrition · 2022Review
- Available In Vitro Models for Human Satellite Cells from Skeletal Muscle.International journal of molecular sciences · 2021Review
- AInternational journal of molecular sciences · 2021Article
- The pan HDAC inhibitor Givinostat improves muscle function and histological parameters in two Duchenne muscular dystrophy murine models expressing different haplotypes of the LTBP4 gene.Skeletal muscle · 2021Article
- Estimating myofiber cross-sectional area and connective tissue deposition with electrical impedance myography: A study in D2-mdx mice.Muscle & nerve · 2021Article
- Is Upregulation of Sarcolipin Beneficial or Detrimental to Muscle Function?Frontiers in physiology · 2021Article
- Mouse Models of Muscle Fibrosis.Methods in molecular biology (Clifton, N.J.) · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is an X-linked genetic disorder characterized by progressive muscle degeneration. Mutations in the DMD gene result in the absence of dystrophin, a protein required for muscle strength and stability. Currently, there is no cure for DMD. Since murine models are relatively easy to genetically manipulate, cost effective, and easily reproducible due to their short generation time, they have helped to elucidate the pathobiology of dystrophin deficiency and to assess therapies for treating DMD. Recently, several murine models have been developed by our group and others to be more representative of the human DMD mutation types and phenotypes. For instance, mdx mice on a DBA/2 genetic background, developed by Fukada et al., have lower regenerative capacity and exhibit very severe phenotype. Cmah-deficient mdx mice display an accelerated disease onset and severe cardiac phenotype due to differences in glycosylation between humans and mice. Other novel murine models include mdx52, which harbors a deletion mutation in exon 52, a hot spot region in humans, and dystrophin/utrophin double-deficient (dko), which displays a severe dystrophic phenotype due the absence of utrophin, a dystrophin homolog. This paper reviews the pathological manifestations and recent therapeutic developments in murine models of DMD such as standard mdx (C57BL/10), mdx on C57BL/6 background (C57BL/6-mdx), mdx52, dystrophin/utrophin double-deficient (dko), mdxβgeo, Dmd-null, humanized DMD (hDMD), mdx on DBA/2 background (DBA/2-mdx), Cmah-mdx, and mdx/mTRKO murine models.
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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.