ReviewThe Journal of physiology2014
Nitric oxide synthase deficiency and the pathophysiology of muscular dystrophy.
Review in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Effect of exercise training on nitric oxide and nitrate/nitrite (NOx) production: A systematic review and meta-analysis.Frontiers in physiology · 2022Pooled it
- Circuit training on oxidative stress and arterial health: a health promotion perspective for obese adult men.Frontiers in public health · 2025Trial
- Inspiratory muscle training in children with neuromuscular disorders.The South African journal of physiotherapy · 2024Trial
- Lipin1 restores nNOS sarcolemmal localization and improves fatigue resistance in Duchenne muscular dystrophy.American journal of physiology. Cell physiology · 2026Article
- Dystrophins DP71 and DP427 determine cell viability during proliferation and myofibre differentiation.Cell death & disease · 2026Article
- Histone deacetylases in Duchenne muscular dystrophy: a role in the mechanism of disease and a target for inhibition.Clinical epigenetics · 2025Review
- S-nitrosylation of cardiac myocyte proteins may underlie sex differences in cardiac disease.Frontiers in physiology · 2025Review
- High-dose systemic adeno-associated virus vector administration causes liver and sinusoidal endothelial cell injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Poor bone health in Duchenne muscular dystrophy: a multifactorial problem beyond corticosteroids and loss of ambulation.Frontiers in endocrinology · 2024Review
- High nitrate levels in skeletal muscle contribute to nitric oxide generation via a nitrate/nitrite reductive pathway in mice that lack the nNOS enzyme.Frontiers in physiology · 2024Article
- Genetic Neuromuscular Disorders and Health Services Access, Utilization, and Needs in Zambia.Pediatric neurology · 2023Article
- Histone Deacetylases: Molecular Mechanisms and Therapeutic Implications for Muscular Dystrophies.International journal of molecular sciences · 2023Review
- Endogenous and Exogenous Antioxidants in Skeletal Muscle Fatigue Development during Exercise.Antioxidants (Basel, Switzerland) · 2023Review
- The importance of dystrophin and the dystrophin associated proteins in vascular smooth muscle.Frontiers in physiology · 2022Review
- Immunometabolism of macrophages regulates skeletal muscle regeneration.Frontiers in cell and developmental biology · 2022Review
- Assessing the Use of the sGC Stimulator BAY-747, as a Potential Treatment for Duchenne Muscular Dystrophy.International journal of molecular sciences · 2021Article
- Innovative Therapeutic Approaches for Duchenne Muscular Dystrophy.Journal of clinical medicine · 2021Review
- Review
- Inspiratory muscle training in children and adolescents living with neuromuscular diseases: A pre-experimental study.The South African journal of physiotherapy · 2021Article
- Comparative proteomic analyses of Duchenne muscular dystrophy and Becker muscular dystrophy muscles: changes contributing to preserve muscle function in Becker muscular dystrophy patients.Journal of cachexia, sarcopenia and muscle · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The secondary loss of neuronal nitric oxide synthase (nNOS) that occurs in dystrophic muscle is the basis of numerous, complex and interacting features of the dystrophic pathology that affect not only muscle itself, but also influence the interaction of muscle with other tissues. Many mechanisms through which nNOS deficiency contributes to misregulation of muscle development, blood flow, fatigue, inflammation and fibrosis in dystrophic muscle have been identified, suggesting that normalization in NO production could greatly attenuate diverse aspects of the pathology of muscular dystrophy through multiple regulatory pathways. However, the relative importance of the loss of nNOS from the sarcolemma versus the importance of loss of total nNOS from dystrophic muscle remains unknown. Although most current evidence indicates that nNOS localization at the sarcolemma is not required to achieve NO-mediated reductions of pathology in muscular dystrophy, the question remains open concerning whether membrane localization would provide a more efficient rescue from features of the dystrophic phenotype.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.