The endothelial nitric oxide (eNOS) gene T-786C polymorphism may influence as a genetic risk factor cardiovascular diseases and shows association with cardiovascular mortality.
These results suggest that the Glu298Asp polymorphism in exon 7 of the eNOS gene is likely to be a risk factor for CVD in the eastern Taiwanese population.
The guanine to thymine polymorphism at position 894 of the eNOS gene (resulting in a change from glutamate to aspartate [Asp] at codon 298 [Asp298]) and the methylenetetrahydrofolate reductase (MTHFR) gene polymorphism (C677T) have been reported to be associated with atherosclerosis and cardiovascular disease.
With the development of molecular biological technology, the association between genes and diseases has drawn increasing attention of researchers; the endothelial nitric oxide synthase (eNOS) gene has been reported to be a candidate gene for cardiovascular disease (CHD).
Clear is that enhanced production of reactive oxygen species (ROS) and eNOS uncoupling are relatively important causes of reduced NO-bioactivity in cardiovascular disease states.
In this review, we discuss the basic biochemical mechanisms of NOS3 regulation and the clinical and pharmacogenetic impact of NOS3 polymorphisms on cardiovascular diseases.
NO is synthesized from l-arginine through the action of the nitric oxide synthase (NOS) family of enzymes, which includes three isoforms: endothelial NOS (eNOS), neuronal NOS (nNOS) and inducible NOS (iNOS). iNOS-derived NO has been associated with the pathogenesis and progression of several diseases, including liver diseases, insulin resistance, obesity and diseases of the cardiovascular system.
These results indicate that somatic delivery of the human eNOS gene induces a prolonged reduction of high blood pressure and raises the potential of using eNOS gene therapy for hypertension and cardiovascular diseases.
Endothelial nitric oxide synthase (eNOS)-uncoupling links obesity-associated insulin resistance and type-II diabetes to the increased incidence of cardiovascular disease.
The eNOS modulatory role of statins may have an imperative influence on the functional regulation of cardiovascular system and may offer new perspectives for the better use of statins in ameliorating cardiovascular disorders.
The current studies offer a new paradigm in which to study the non-cholesterol effects of SR-BI, HDL, and eNOS on the development of atherosclerosis and potentially other cardiovascular diseases.
Loss of endothelial BH<sub>4</sub> is observed in cardiovascular disease (CVD) states and results in decreased NO and increased superoxide (O<sub>2</sub><sup>-</sup>) generation via eNOS uncoupling.
The eNOS gene has a number of polymorphic sites, including SNPs, dinucleotide repeats and variable number tandem repeat sequences, and the opportunity exists to investigate polymorphic functional correlates as well as disease-specific associations, especially in cardiovascular disease, including coronary artery disease, and its most severe consequence, myocardial infarction.
This suggests a synergistic effect of the eNOS Asp298 allele and diabetes, and confirms the role of eNOS as an important pathological bottleneck for cardiovascular disease in patients with T2DM.
Cytochrome P450 2D6 (CYP2D6) and endothelial nitric oxide synthase (eNOS) are important in the cardiovascular disease susceptibility and drug response.
Another molecule, Sirtuin 1 (SIRT1), a histone/protein deacetylase, regulates endothelial nitric oxide synthase and is involved in different aspects of cardiovascular disease, aging and stress resistance.
Since NOS-III is also expressed in vascular cells, and cerebrovascular disease (CVD) frequently complicates the pathology of AD, we investigated the role of NOS-III in relation to CVD in AD.
Asymmetric dimethylarginine (ADMA), an endothelial nitric oxide synthase inhibitor, plays a crucial role in the pathogenesis of various cardiovascular diseases associated with endothelial dysfunction.
Cell-based eNOS gene therapy has both proangiogenic and antiatherogenic effects and should be further investigated for the development of efficient therapeutic neovascularization designed to treat ischemic cardiovascular disease.
Impaired endothelial function, characterized by an imbalance in endothelial Nitric Oxide Synthase (eNOS) activity, precedes and accelerates the development of CVD.
Many cardiovascular diseases are associated with reduced levels of bioactive nitric oxide (NO) and an uncoupling of oxygen reduction from NO synthesis in endothelial NO synthase (eNOS uncoupling).