ArticleThe Journal of cell biology2001
A nitric oxide synthase transgene ameliorates muscular dystrophy in mdx mice.
Article in The Journal of cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 249 papers.
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Who cites it
249 citing papers in PubMed, 529 citations in OpenAlex.
- A phase 3 randomized placebo-controlled trial of tadalafil for Duchenne muscular dystrophy.Neurology · 2017Trial
- Combined isosorbide dinitrate and ibuprofen as a novel therapy for muscular dystrophies: evidence from Phase I studies in healthy volunteers.Drug design, development and therapy · 2014Trial
- Tadalafil alleviates muscle ischemia in patients with Becker muscular dystrophy.Science translational medicine · 2012Trial
- Myovascular Niche: The Role of Endothelial Cells in Skeletal Muscle Health and Disease.Circulation research · 2026Review
- Progress on cell therapy for skeletal muscle disorders.Advanced drug delivery reviews · 2026Review
- CTLA4-Ig reduces proliferation and inflammatory gene expression in muscle fibroblasts, corresponding to less fibrosis and inflammation inAmerican journal of physiology. Cell physiology · 2026Article
- Transcriptome analysis of injured muscle identifies new candidate genes for satellite cell growth and myofiber formation during early muscle regeneration.Animal bioscience · 2026Article
- Macrophage Infiltration, Activation, and Therapeutic Implication in Skeletal Muscle Injury and Repair.International journal of molecular sciences · 2026Review
- Hemizygous mutation ofAmerican journal of physiology. Cell physiology · 2025Article
- Review
- Profiles of Monocyte Subsets and Fibrosis-Related Genes in Patients with Muscular Dystrophy Undergoing Intermittent Prednisone Therapy.International journal of molecular sciences · 2025Article
- Anti-fibrotic, muscle-promoting antibody-drug conjugates for the improvement and treatment of DMD.iScience · 2025Article
- Pharmacology and macrophage modulation of HPGDS inhibitor PK007 demonstrate reduced disease severity in DMD-affected muscles of the mdx mouse model.Skeletal muscle · 2025Article
- Cytotoxic T-Lymphocyte-Associated Protein 4 Fused to a Modified Fragment of IgG1 Reduces Muscle Fiber Damage in a Model of Duchenne Muscular Dystrophy by Attenuating Proinflammatory Gene Expression in Myeloid Lineage Cells.The American journal of pathology · 2025Article
- Type 2 diabetes-related sarcopenia: role of nitric oxide.Nutrition & metabolism · 2024Review
- Recombinant ADAMTS1 promotes muscle cell differentiation and alleviates muscle atrophy by repressing NOTCH1.BMB reports · 2024Article
- Caveolin and NOS in the Development of Muscular Dystrophy.International journal of molecular sciences · 2024Review
- Review
- Recent Advances in Pre-Clinical Development of Adiponectin Receptor Agonist Therapies for Duchenne Muscular Dystrophy.Biomedicines · 2024Review
- A Novel MAO-B/SSAO Inhibitor Improves Multiple Aspects of Dystrophic Phenotype inAntioxidants (Basel, Switzerland) · 2024Article
189 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dystrophin-deficient muscles experience large reductions in expression of nitric oxide synthase (NOS), which suggests that NO deficiency may influence the dystrophic pathology. Because NO can function as an antiinflammatory and cytoprotective molecule, we propose that the loss of NOS from dystrophic muscle exacerbates muscle inflammation and fiber damage by inflammatory cells. Analysis of transgenic mdx mice that were null mutants for dystrophin, but expressed normal levels of NO in muscle, showed that the normalization of NO production caused large reductions in macrophage concentrations in the mdx muscle. Expression of the NOS transgene in mdx muscle also prevented the majority of muscle membrane injury that is detectable in vivo, and resulted in large decreases in serum creatine kinase concentrations. Furthermore, our data show that mdx muscle macrophages are cytolytic at concentrations that occur in dystrophic, NOS-deficient muscle, but are not cytolytic at concentrations that occur in dystrophic mice that express the NOS transgene in muscle. Finally, our data show that antibody depletions of macrophages from mdx mice cause significant reductions in muscle membrane injury. Together, these findings indicate that macrophages promote injury of dystrophin-deficient muscle, and the loss of normal levels of NO production by dystrophic muscle exacerbates inflammation and membrane injury in muscular dystrophy.
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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.