Several studies have suggested that ALDH2 polymorphism plays an important role in the progress of CAD through multiple mechanisms, including the regulation of alcohol consumption, inflammation, endothelial progenitor cells, oxidative stress, asymmetric dimethylarginine, endothelial nitric oxide synthase, and other CAD-promoting factors.
The nitric oxide (NO) synthase 3 (NOS3) gene is responsible for the synthesis of endothelial NO synthase (eNOS) in humans and some genetic polymorphisms are considered "polymorphisms associated with risk" for the development of coronary artery diseases, such as acute coronary syndrome.
The results of overall analysis revealed significant positive associations between CAD risk and eNOS 4b/a polymorphism in homozygote comparisons (OR = 1.47, 95% CI = 1.16-1.87), heterozygote comparisons (OR = 1.14, 95% CI = 1.02-1.27) and dominant models (OR = 1.18, 95% CI = 1.06-1.33).
The combined results of overall analysis showed significant positive associations between CAD risk and eNOS -786T>C polymorphism in dominant model (OR=1.45, 95% CI=1.27-1.65), recessive model (OR=1.37, 95% CI=1.20-1.56), homozygote comparison (OR=1.64, 95% CI=1.31-2.04), heterozygote comparison (TC vs. TT, OR=1.39, 95% CI=1.23-1.57; CC vs. TC, OR=1.20, 95% CI=1.04-1.37) and allele comparison (OR=1.35, 95% CI=1.21-1.50).
Multiple logistic regression analysis revealed a significant and independent association of eNOST-786C polymorphism and other putative risk factors with CAD/TVD in T2DM individuals.
Association between the endothelial nitric oxide synthase gene Glu298Asp polymorphism and coronary heart disease: a meta‑analysis of 39 case‑control studies.
Our findings, for the first time, indicate that NOS3 T allele strongly interacts with CETP B1 allele to augment the risk of CAD and T2DM in the population of Western Iran.
The G894T polymorphism on endothelial nitric oxide synthase gene is associated with increased coronary heart disease among Asia population: evidence from a Meta analysis.
Glu298Asp polymorphism of the endothelial nitric oxide synthase (eNOS) gene (NOS3) has been characterized as a risk factor of hypertension and coronary artery disease.
Recent genetic studies have shown an association between the -786TC polymorphism in the endothelial nitric oxide synthase gene (NOS3) and coronary artery diseases, but any possible association with hypertension has been controversial.
Therefore, this study was planned to determine (a) role of endothelium-derived nitric oxide (NO) and endothelin as coronary artery disease (CAD) risk markers and (b) intergenotypic variation of endothelial nitric oxide synthase (eNOS) Glu298Asp polymorphism in CAD.The endothelin, NO and eNOS genotypes were determined in 60 patients with documented history of CAD.
The objective of this study is to assess the effect of lentiviral overexpression of endothelial nitric oxide synthase (eNOS) on the activity of CACs from patients with CAD and cardiac risk factors.
The aim of this research was to discover whether the T-786C polymorphism in the promoter 5'-flanking region of the gene for endothelial nitric oxide synthase (eNOS) is associated with CAD.
Polymorphisms in the endothelial nitric oxide synthase ( eNOS ) gene (- 786T > C and 894G > T ) enhance endothelial dysfunction and have been studied in relation to coronary artery disease (CAD).
This study, for the first time, suggests an independent association of 894G>T and -786T>C polymorphisms of endothelial nitric oxide synthase gene with coronary artery disease in a Saudi population.
The polymorphism Glu298Asp of endothelial nitric oxide (eNOS) gene has been associated with hypertension and coronary artery disease in several populations worldwide, but results are still controversial.
According to the linkage-disequilibrium levels of SNPs, the haplotypes were constructed and the results showed that the frequencies of the constructed haplotypes of ecNOS, PC-1 and ACE genes were associated with CAD.