ArticleThe Journal of pathology2011
Nitrosative stress elicited by nNOSµ delocalization inhibits muscle force in dystrophin-null mice.
Article in The Journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 97 citations in OpenAlex.
- Sodium nitrate alleviates functional muscle ischaemia in patients with Becker muscular dystrophy.The Journal of physiology · 2015Trial
- Evaluation of protein expression and oxidative stress index in Duchenne muscular dystrophy.Pediatric research · 2026Article
- When barriers fail: the role of endothelial dysfunction in rare pediatric neuromuscular diseases.Frontiers in medicine · 2026Review
- Impact of dystrophin deficiency on vascular smooth muscle cell.Scientific reports · 2025Article
- Type 2 diabetes-related sarcopenia: role of nitric oxide.Nutrition & metabolism · 2024Review
- The Gut Microbiota Involvement in the Panorama of Muscular Dystrophy Pathogenesis.International journal of molecular sciences · 2024Review
- Acute microtubule changes linked to DMD pathology are insufficient to impair contractile function or enhance contraction-induced injury in healthy muscle.bioRxiv : the preprint server for biology · 2024Article
- Down-regulation of neuronal form of Nitric oxide synthase in the Nurse cell ofHelminthologia · 2024Article
- Microbes, metabolites and muscle: Is the gut-muscle axis a plausible therapeutic target in Duchenne muscular dystrophy?Experimental physiology · 2023Review
- Curcumin Administration Improves Force ofAntioxidants (Basel, Switzerland) · 2023Article
- Microdystrophin Gene Addition Significantly Improves Muscle Functionality and Diaphragm Muscle Histopathology in a Fibrotic Mouse Model of Duchenne Muscular Dystrophy.International journal of molecular sciences · 2023Article
- Lifelong Outcomes of Systemic Adeno-Associated Virus Micro-Dystrophin Gene Therapy in a Murine Duchenne Muscular Dystrophy Model.Human gene therapy · 2023Article
- The Implication of Hinge 1 and Hinge 4 in Micro-Dystrophin Gene Therapy for Duchenne Muscular Dystrophy.Human gene therapy · 2023Article
- nNOS-derived NO modulates force production and iNO-derived NO the excitability in C2C12-derived 3D tissue engineering skeletal muscleFrontiers in physiology · 2022Article
- Multiomic Approaches to Uncover the Complexities of Dystrophin-Associated Cardiomyopathy.International journal of molecular sciences · 2021Review
- Dystrophin deficiency impairs vascular structure and function in the canine model of Duchenne muscular dystrophy.The Journal of pathology · 2021Article
- Cellular pathology of the human heart in Duchenne muscular dystrophy (DMD): lessons learned from in vitro modeling.Pflugers Archiv : European journal of physiology · 2021Review
- Duchenne muscular dystrophy.Nature reviews. Disease primers · 2021Review
- Review
- Rapid, redox-mediated mechanical susceptibility of the cortical microtubule lattice in skeletal muscle.Redox biology · 2020Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The mechanism of force reduction is not completely understood in Duchenne muscular dystrophy (DMD), a dystrophin-deficient lethal disease. Nitric oxide regulates muscle force. Interestingly, neuronal nitric oxide synthase µ (nNOSµ), a major source of muscle nitric oxide, is lost from the sarcolemma in DMD muscle. We hypothesize that nNOSµ delocalization contributes to force reduction in DMD. To test this hypothesis, we generated dystrophin/nNOSµ double knockout mice. Genetic elimination of nNOSµ significantly enhanced force in dystrophin-null mice. Pharmacological inhibition of nNOS yielded similar results. To further test our hypothesis, we studied δ-sarcoglycan-null mice, a model of limb-girdle muscular dystrophy. These mice had minimal sarcolemmal nNOSµ delocalization and muscle force was less compromised. Annihilation of nNOSµ did not improve their force either. To determine whether nNOSµ delocalization itself inhibited force, we corrected muscle disease in dystrophin-null mice with micro-dystrophins that either restored or did not restore sarcolemmal nNOSµ. Similar muscle force was obtained irrespective of nNOSµ localization. Additional studies suggest that nNOSµ delocalization selectively inhibits muscle force in dystrophin-null mice via nitrosative stress. In summary, we have demonstrated for the first time that nitrosative stress elicited by nNOSµ delocalization is an important mechanism underlying force loss in DMD.
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