ArticleThe Biochemical journal2013
Nitric oxide signalling pathway in Duchenne muscular dystrophy mice: up-regulation of L-arginine transporters.
Article in The Biochemical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 39 citations in OpenAlex.
- Integrative multi-omics analysis reveals lipid/metabolite dysregulation and temporal decoupling in disease progression.Scientific reports · 2026Article
- Nitric Oxide Signaling in Cardiovascular Physiology and Pathology: Mechanisms, Dysregulation, and Therapeutic Frontiers.International journal of molecular sciences · 2026Review
- Type 2 diabetes-related sarcopenia: role of nitric oxide.Nutrition & metabolism · 2024Review
- Why is early-onset atrial fibrillation uncommon in patients with Duchenne muscular dystrophy? Insights from the mdx mouse.Cardiovascular research · 2024Article
- nNOS-derived NO modulates force production and iNO-derived NO the excitability in C2C12-derived 3D tissue engineering skeletal muscleFrontiers in physiology · 2022Article
- Cellular pathology of the human heart in Duchenne muscular dystrophy (DMD): lessons learned from in vitro modeling.Pflugers Archiv : European journal of physiology · 2021Review
- The multifaceted view of heart problem in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2021Review
- Therapeutic aspects of cell signaling and communication in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2021Review
- Cardiomyocyte depolarization triggers NOS-dependent NO transient after calcium release, reducing the subsequent calcium transient.Basic research in cardiology · 2021Article
- Cardioprotective Effect of Whole Body Periodic Acceleration in Dystrophic PhenotypeFrontiers in physiology · 2021Article
- Enhanced dimethylarginine degradation improves coronary flow reserve and exercise tolerance in Duchenne muscular dystrophy carrier mice.American journal of physiology. Heart and circulatory physiology · 2020Article
- Metabolic Alterations in Cardiomyocytes of Patients with Duchenne and Becker Muscular Dystrophies.Journal of clinical medicine · 2019Review
- Cardiac Pathophysiology and the Future of Cardiac Therapies in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2019Review
- Targeting angiogenesis in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2019Review
- Mutation-Based Therapeutic Strategies for Duchenne Muscular Dystrophy: From Genetic Diagnosis to Therapy.Journal of personalized medicine · 2019Review
- Article
- Enhancing Endogenous Nitric Oxide by Whole Body Periodic Acceleration Elicits Neuroprotective Effects in Dystrophic Neurons.Molecular neurobiology · 2018Article
- Voltage-Dependent Sarcolemmal Ion Channel Abnormalities in the Dystrophin-Deficient Heart.International journal of molecular sciences · 2018Review
- Combined use of protein biomarkers and network analysis unveils deregulated regulatory circuits in Duchenne muscular dystrophy.PloS one · 2018Article
- Dystrophic Cardiomyopathy: Complex Pathobiological Processes to Generate Clinical Phenotype.Journal of cardiovascular development and disease · 2017Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
DMD (Duchenne muscular dystrophy) is an incurable rapidly worsening neuromuscular degenerative disease caused by the absence of dystrophin. In skeletal muscle a lack of dystrophin disrupts the recruitment of neuronal NOS (nitric oxide synthase) to the sarcolemma thus affecting NO (nitric oxide) production. Utrophin is a dystrophin homologue, the expression of which is greatly up-regulated in the sarcolemma of dystrophin-negative fibres from mdx mice, a mouse model of DMD. Although cardiomyopathy is an important cause of death, little is known about the NO signalling pathway in the cardiac muscle of DMD patients. Thus we used cardiomyocytes and hearts from two month-old mdx and mdx:utrophin-/- (double knockout) mice (mdx:utr) to study key steps in NO signalling: L-arginine transporters, NOS and sGC (soluble guanylyl cyclase). nNOS did not co-localize with dystrophin or utrophin to the cardiomyocyte membrane. Despite this nNOS activity was markedly decreased in both mdx and mdx:utr mice, whereas nNOS expression was only decreased in mdx:utr mouse hearts, suggesting that utrophin up-regulation in cardiomyocytes maintains nNOS levels, but not function. sGC protein levels and activity remained at control levels. Unexpectedly, L-arginine transporter expression and function were significantly increased, suggesting a novel biochemical compensatory mechanism of the NO pathway and a potential entry site for therapeutics.
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