Nitric Oxide (NO) is an important molecule carrying number of different functions in humans. Published studies suggest that it may inhibit several key steps involved in the pathogenesis of atherosclerosis. Inhibition or reduction of NO due to Glu298Asp polymorphism may accelerate atherosclerosis. The aim of this study was to determine whether Glu298Asp polymorphism is implicated in the pathogenesis of coronary artery disease (CAD) among North Indian population from the state of Uttar Pradesh, India. We selected 253 CAD patients and 174 healthy, normotensive, non-diabetic controls, which were matched for gender and ethnicity. The Glu298Asp (rs1799983) variant was detected by genotyping subjects, using a polymerase chain reaction followed by restriction fragment length polymorphism. There was no significant difference found in the genotypic and allelic frequencies between patients and controls. Our study indicated that Glu298Asp polymorphism does not play any critical role in the pathogenesis of CAD, at least in North Indian population.
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http://dx.doi.org/10.1007/s11033-011-1412-z | DOI Listing |
Int J Mol Sci
January 2025
Department of Endocrinology, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540142 Targu Mures, Romania.
Differentiated thyroid cancer (DTC) is the most common endocrine malignancy, with genetic factors playing an important role in its development and progression. This study investigated the association between nitric oxide synthase 3 () gene polymorphisms (-786T>C or rs2070744 and Glu298Asp or c.894T>G or rs1799983) and the clinical characteristics and outcomes of DTC, aiming to evaluate their potential as biomarkers for prognosis.
View Article and Find Full Text PDFPlacenta
January 2025
Department of Obstetrics and Gynecology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan City, Taiwan. Electronic address:
Background: Preeclampsia (PE) is a serious condition characterized by hypertension and proteinuria after 20 weeks of gestation. The exact cause of PE is unknown but may involve abnormalities in the renin-angiotensin-aldosterone system (RAAS) and endothelial nitric oxide synthase (eNOS). Genetic variations in angiotensinogen (AGT), angiotensin-converting enzyme (ACE), and eNOS genes have been associated with PE.
View Article and Find Full Text PDFBioelectrochemistry
February 2025
Department of Chemistry and Biochemistry, Ohio University, Athens, OH, USA. Electronic address:
The impact of four clinically significant genetic variants of endothelial nitric oxide synthase (eNOS) polymorphisms on the concentrations of nitric oxide [NO] and peroxynitrite [ONOO] has been given scant consideration. This study utilized a [NO]/[ONOO] ratio to determine the extent of endothelial dysfunction caused by these variations in the eNOS gene. The single nucleotide polymorphisms (T-786C, C-665T, and Glu298Asp) and a variable number of tandem repeats (intron 4 a/b/c) were genotyped in human umbilical vein endothelial cells (HUVEC), using sanger sequencing and DNA electrophoresis, respectively.
View Article and Find Full Text PDFEpigenetics
December 2024
Department of Internal Medicine, Ribeirão Preto Medical School, University of São Paulo, São Paulo, Brazil.
The mechanisms by which the ageing process is associated to an unhealthy lifestyle and how they play an essential role in the aetiology of systemic arterial hypertension have not yet been completely elucidated. Our objective is to investigate the influence of NOS3 polymorphisms [-786T > C and (Glu298Asp)] on systolic blood pressure (SBP) and diastolic blood pressure (DBP) response, differentially methylated regions (DMRs), and physical fitness of adult and older women after a 14-week combined training intervention. The combined training was carried out for 14 weeks, performed 3 times a week, totalling 180 minutes weekly.
View Article and Find Full Text PDFBMC Cardiovasc Disord
March 2024
Cardiovascular Department, Gabriele Monasterio Foundation, Via G. Moruzzi 1, Pisa, Italy.
Background: The endothelial nitric oxide synthase (eNOS) gene deficiency is known to cause impaired coronary vasodilating capability in animal models. In the general clinical population, the eNOS gene polymorphisms, able to affect eNOS activity, were associated with cardiometabolic risk features and prevalence of coronary artery disease (CAD).
Aim: To investigate the association of eNOS Glu298Asp gene polymorphism, cardiometabolic profile, obstructive CAD and inducible myocardial ischemia in patients with suspected stable CAD.
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