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.
Taken together, our results show that the 27 nt repeat polymorphism of the intron 4 in the eNOS gene increases susceptibility to cardiovascular diseases after MeHg exposure by modulating nitric oxide levels.
A single nucleotide polymorphism in the eNOS gene, where thymine (T) replaces guanine (G) at position 894 predicting substitution of glutamate for aspartate at codon 298 (Glu298Asp), has been associated with increased CVD risk due to effects on nitric oxide synthesis and subsequently vascular reactivity.
A single nucleotide polymorphism G894T within exon 7 of endothelial nitric oxide synthase (eNOS-7) gene, resulting in a replacement of glutamic acid by aspartic acid, has been studied as a putative candidate gene for cardiovascular diseases.
It was postulated that Hg exposure might decrease circulating nitrite concentrations and that variants in the eNOS gene might enhance the adverse effects of Hg resulting in increased risk of cardiovascular disease.
These data indicate that CAC dysfunction seen in high-risk patients can be partially reversed by eNOS overexpression, suggesting that ex vivo gene delivery may improve the efficacy of autologous cell therapy for cardiovascular disease.
Presence of endothelial nitric oxide synthase (eNOS) gene polymorphism has been associated with cardiovascular disease (CVD) whereas exercise training (EX) promotes beneficial effects on CVD which is related to increased nitric oxide levels (NO).
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.
Biomarkers of CVD risk, plasma fatty acid composition, and NOS3 single nucleotide polymorphism (SNP) genotype (rs11771443, rs1800783, rs1800779, rs1799983, rs3918227, and rs743507) were determined in 450 individuals with the MetS from the LIPGENE dietary intervention cohort.
Endothelial nitric oxide synthase gene polymorphisms, either independently or through gene environmental interactions, are associated with cardiovascular diseases in multiple ethnic populations.
However, the genetic background may also affect NO formation in the cardiovascular system, and recent studies have shown that genetic polymorphisms in the eNOS gene modify endogenous NO formation and the risk of developing cardiovascular diseases.
Thus, our findings revealed a critical function of Akt in mediating genistein-stimulated eNOS activity in PAECs, partially accounting for the beneficial effects of genistein on the development of cardiovascular diseases observed in animal models.
Both the thymidine to cytosine transition mutation (T(-786)-->C) in the promoter region and the missense mutation in the exon 7 coding region of the eNOS gene (G(894)-->T) have been associated with several cardiovascular disease states.
The endothelial nitric oxide (eNOS) gene T-786C polymorphism may influence as a genetic risk factor cardiovascular diseases and shows association with cardiovascular mortality.
The susceptibility to nephropathy and CVD depends to some extent on genetic factors, therefore polymorphisms in the gene coding for endothelial NO-synthase, NOS3, can affect the risk of developing these diseases.
Several polymorphisms in the eNOS gene have been described, some of them being linked with the increased risk of cardiovascular disease, coronary heart disease (CHD), and coronary spasm.
However, we found that eNOSG894T polymorphism was associated with the presence and severity of renal disease and with CVD in CRD patients (P=0.028, P=0.018, P=0.016 respectively).
The -786T>C, but not the Glu298>Asp variant of NOS3, may correlate with BP but do not appear to be associated with incident cardiovascular events in patients with established cardiovascular disease.
The present study was performed in an attempt to better understand whether metabolic, endothelial, and angiographic findings characteristic of subjects with cardiovascular disease and in-stent restenosis are related to NOS3 variants.
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).