ArticleBasic research in cardiology2012
Vascular endothelial dysfunction in Duchenne muscular dystrophy is restored by bradykinin through upregulation of eNOS and nNOS.
Article in Basic research in cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 46 citations in OpenAlex.
- Impact of dystrophin deficiency on vascular smooth muscle cell.Scientific reports · 2025Article
- Ambulatory electrocardiographic longitudinal monitoring in a canine model for Duchenne muscular dystrophy identifies decreased very low frequency power as a hallmark of impaired heart rate variability.Scientific reports · 2024Article
- 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
- Characterization of the Ang/Tie2 Signaling Pathway in the Diaphragm Muscle of DMD Mice.Biomedicines · 2023Article
- Spatial and Temporal Non-Uniform Changes in Left Ventricular Myocardial Strain in Dogs with Duchenne Muscular Dystrophy.Journal of cardiovascular development and disease · 2023Article
- Article
- Disrupted Calcium Homeostasis in Duchenne Muscular Dystrophy: A Common Mechanism behind Diverse Consequences.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
- Role of Matricellular CCN Proteins in Skeletal Muscle: Focus on CCN2/CTGF and Its Regulation by Vasoactive Peptides.International journal of molecular sciences · 2021Review
- Single-Cell Transcriptional Profiling Reveals Sex and Age Diversity of Gene Expression in Mouse Endothelial Cells.Frontiers in genetics · 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
- Clinical trial in a dish using iPSCs shows lovastatin improves endothelial dysfunction and cellular cross-talk in LMNA cardiomyopathy.Science translational medicine · 2020Article
- The hypertensive effect of sorafenib is abolished by sildenafil.Cardio-oncology (London, England) · 2020Article
- Canine Models of Inherited Musculoskeletal and Neurodegenerative Diseases.Frontiers in veterinary science · 2020Review
- Targeting angiogenesis in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2019Review
- Article
- Three-Dimensional Human iPSC-Derived Artificial Skeletal Muscles Model Muscular Dystrophies and Enable Multilineage Tissue Engineering.Cell reports · 2018Article
- Effects of a novel ACE inhibitor, 3-(3-thienyl)-l-alanyl-ornithyl-proline, on endothelial vasodilation and hepatotoxicity in l-NAME-induced hypertensive rats.Drug design, development and therapy · 2016Article
- Vascular endothelial dysfunction and pharmacological treatment.World journal of cardiology · 2015Review
- Calycosin and formononetin from astragalus root enhance dimethylarginine dimethylaminohydrolase 2 and nitric oxide synthase expressions in Madin Darby Canine Kidney II cells.Journal of natural medicines · 2013Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Little is known about the vascular function and expression of endothelial and neuronal nitric oxide synthases (eNOS and nNOS) in Duchenne muscular dystrophy (DMD). Bradykinin is involved in the regulation of eNOS expression induced by angiotensin-converting enzyme inhibitors. We characterized the vascular function and eNOS and nNOS expression in a canine model of DMD and evaluated the effects of chronic bradykinin treatment. Vascular function was examined in conscious golden retriever muscular dystrophy (GRMD) dogs with left ventricular dysfunction (measured by echocardiography) and in isolated coronary arteries. eNOS and nNOS proteins in carotid arteries were measured by western blot and cyclic guanosine monophosphate (cGMP) content was analyzed by radioimmunoassay. Compared with controls, GRMD dogs had an impaired vasodilator response to acetylcholine. In isolated coronary artery, acetylcholine-elicited relaxation was nearly absent in placebo-treated GRMD dogs. This was explained by reduced nNOS and eNOS proteins and cGMP content in arterial tissues. Chronic bradykinin infusion (1 μg/min, 4 weeks) restored in vivo and in vitro vascular response to acetylcholine to the level of control dogs. This effect was NO-mediated through upregulation of eNOS and nNOS expression. In conclusion, this study is the first to demonstrate that DMD is associated with NO-mediated vascular endothelial dysfunction linked to an altered expression of eNOS and nNOS, which can be overcome by bradykinin.
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