ReviewBritish journal of pharmacology2011
Therapeutic effect of enhancing endothelial nitric oxide synthase (eNOS) expression and preventing eNOS uncoupling.
Review in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 3 of them syntheses that pooled it.
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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.
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Who cites it
146 citing papers in PubMed, 3 syntheses or guidelines pooled it, 294 citations in OpenAlex.
- Pooled it
- Prognostic factors of Takotsubo cardiomyopathy: a systematic review.ESC heart failure · 2021Pooled it
- Association of endothelial nitric oxide synthase polymorphisms with an increased risk of erectile dysfunction.Asian journal of andrologyPooled it
- The effects of a motorized passive simulated jogging device on descent of the arterial pulse waveform dicrotic notch: A single arm placebo-controlled cross-over trial.Physiological reports · 2022Trial
- Unraveling the potential of gasotransmitters as neurogenic and neuroprotective molecules: focus on Alzheimer's and Parkinson's diseases.Redox report : communications in free radical research · 2026Review
- Therapeutic Modulation of Nitric Oxide Pathways to Address Insulin Resistance in Cardiovascular-Kidney-Metabolic Syndrome.International journal of molecular sciences · 2026Review
- Maternal Rumen-Protected Leucine Supplementation Enhances Placental Nutrient Transport Capacity and Increases Birth Weight in Hu Sheep.Veterinary sciences · 2026Article
- Oxidative Stress and the KEAP1/NRF2 Axis in Saphenous Vein: Implications for Graft Patency.Cells · 2026Review
- Oxidative Stress-Induced DNA Damage Response Pathways in Aortic Disease: Implications for Inflammation and Vascular Degeneration.International journal of molecular sciences · 2026Review
- Potent, Selective, and Brain Penetrant Ether-Linked 2-Aminopyridine Inhibitors of Human Neuronal Nitric Oxide Synthase with Excellent Oral Bioavailability.Journal of medicinal chemistry · 2026Article
- Genistein Restores Nitric Oxide Bioavailability and Attenuates Oxidative Stress in Angiotensin II-Induced Hypertensive Mice.Preventive nutrition and food science · 2026Article
- Pathological mechanisms and research progress of multilevel intervention therapy for coronary heart disease.Frontiers in immunology · 2026Review
- The relationship between vitamin D levels and erectile dysfunction: A mini-review.Clinical and experimental reproductive medicine · 2025Article
- The Role of Micronutrients in Atherosclerosis: Mechanisms and Clinical Application.Journal of cellular and molecular medicine · 2025Review
- Review
- Intracranial Aneurysm Biomarkers: A Convergence of Genetics, Inflammation, Oxidative Stress, and the Extracellular Matrix.International journal of molecular sciences · 2025Review
- Association of Endothelial Nitric Oxide Synthase Polymorphisms with Clinical Severity in Patients with COVID-19.Journal of clinical medicine · 2025Article
- The Role of Dietary Anthocyanins for Managing Diabetes Mellitus-Associated Complications.Current diabetes reviews · 2025Review
- CaInflammation and regeneration · 2024Review
- The Effects ofAnimals : an open access journal from MDPI · 2024Article
86 more citing papers are in PubMed but not listed here.
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) produced by the endothelium is an important protective molecule in the vasculature. It is generated by the enzyme endothelial NO synthase (eNOS). Similar to all NOS isoforms, functional eNOS transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH), via the flavins flavin adenine dinucleotide and flavin mononucleotide in the carboxy-terminal reductase domain, to the heme in the amino-terminal oxygenase domain. Here, the substrate L-arginine is oxidized to L-citrulline and NO. Cardiovascular risk factors such as diabetes mellitus, hypertension, hypercholesterolaemia or cigarette smoking reduce bioactive NO. These risk factors lead to an enhanced production of reactive oxygen species (ROS) in the vessel wall. NADPH oxidases represent major sources of this ROS and have been found upregulated in the presence of cardiovascular risk factors. NADPH-oxidase-derived superoxide avidly reacts with eNOS-derived NO to form peroxynitrite (ONOO(-)). The essential NOS cofactor (6R-)5,6,7,8-tetrahydrobiopterin (BH(4) ) is highly sensitive to oxidation by this ONOO(-). In BH(4) deficiency, oxygen reduction uncouples from NO synthesis, thereby converting NOS to a superoxide-producing enzyme. Among conventional drugs, compounds interfering with the renin-angiotensin-aldosterone system and statins can reduce vascular oxidative stress and increase bioactive NO. In recent years, we have identified a number of small molecules that have the potential to prevent eNOS uncoupling and, at the same time, enhance eNOS expression. These include the protein kinase C inhibitor midostaurin, the pentacyclic triterpenoids ursolic acid and betulinic acid, the eNOS enhancing compounds AVE9488 and AVE3085, and the polyphenolic phytoalexin trans-resveratrol. Such compounds enhance NO production from eNOS also under pathophysiological conditions and may thus have therapeutic potential.
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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.