Contribution of<i>eNOS</i>Variants to the Genetic Susceptibility of Coronary Artery Disease in a Tunisian Population

AliMarwa, Ben; Messaoudi, Safia; EzzineHouda,; MahjoubTouhami,

doi:10.1089/gtmb.2014.0261

Cited by 23 publications

(11 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This remained significant after adjustment for age, gender, diabetes, smoking, and hypertension. These findings suggest that the G894T (rs1799983) polymorphism of the NOS3 was associated with CAD in Tunisian patients (Ben Ali et al, 2015). In our study, the difference in the distribution of genotype frequencies of rs1799983 between CAD subjects and healthy controls was significant.…”

Section: Discussionsupporting

confidence: 47%

“…Genetic studies have consistently demonstrated a substantial genetic influence on the development of CAD, with inherited risk estimates in the range 20-60% (Kraus, 2000;Won et al, 2015;Yamada et al, 2015). Other studies have suggested that polymorphisms in the enzyme endothelial nitric oxide synthase (NOS3) may relate to CAD (Ben Ali et al, 2015;Gaunt and Davey Smith, 2015;Shim et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Association between NOS3 genetic variants and coronary artery disease in the Han population

Zhao¹,

Li²,

Lu³

2016

Genet. Mol. Res.

View full text Add to dashboard Cite

ABSTRACT. The enzyme endothelial nitric oxide synthase (NOS3) is an important mediator of atherosclerotic disease and is associated with coronary artery disease (CAD). There is growing evidence that polymorphisms in NOS3 influence the progression of CAD; however, there is also a controversy regarding the association of polymorphisms in the gene encoding NOS3 and CAD. To determine if the NOS3 genetic variants are associated with CAD in the Han Chinese, we examined the potential association between CAD and eight single nucleotide polymorphisms (rs1799983, rs2070744, rs11771443, rs3918188, rs2853796, rs7830, rs1541861, and rs2853792) of the NOS3 using the MassARRAY system. The allelic and genotypic frequencies of the rs1799983 (promoter regions) and rs2070744 (intron 1) polymorphisms in patients with CAD were significantly different from those in healthy controls. These patients had significantly higher frequencies of the rs1799983 T allele (χ 2 = 7.717, P = 0.007, OR = 1.649, 95%CI = 1.41-2.382) and the rs2070744 G allele (χ 2 = 4.548, P = 0.033, OR = 1.490,

show abstract

Section: Discussionsupporting

confidence: 47%

Section: Introductionmentioning

confidence: 99%

Association between NOS3 genetic variants and coronary artery disease in the Han population

Zhao¹,

Li²,

Lu³

2016

Genet. Mol. Res.

View full text Add to dashboard Cite

show abstract

“…These inconsistencies may be linked to the African population’s high genetic diversity and low levels of linkage disequilibrium among loci when compared to populations from other countries outside Africa [ 105 ]. Furthermore, studies suggest that from a genetic standpoint, there is no SNP-database that can be used to personalize treatments for HTN in an African population [ 47 , 106 , 107 ]. Inferring that the lack of genetic information with robust allele frequency distributions serves as a hurdle to implement corrective treatment and this may have important medical implications [ 108 ].…”

Section: Discussionmentioning

confidence: 99%

Hypertension in African Populations: Review and Computational Insights

Mabhida

Mashatola

Kaur

et al. 2021

Genes

View full text Add to dashboard Cite

Hypertension (HTN) is a persistent public health problem affecting approximately 1.3 billion individuals globally. Treatment-resistant hypertension (TRH) is defined as high blood pressure (BP) in a hypertensive patient that remains above goal despite use of ≥3 antihypertensive agents of different classes including a diuretic. Despite a plethora of treatment options available, only 31.0% of individuals have their HTN controlled. Interindividual genetic variability to drug response might explain this disappointing outcome because of genetic polymorphisms. Additionally, the poor knowledge of pathophysiological mechanisms underlying hypertensive disease and the long-term interaction of antihypertensive drugs with blood pressure control mechanisms further aggravates the problem. Furthermore, in Africa, there is a paucity of pharmacogenomic data on the treatment of resistant hypertension. Therefore, identification of genetic signals having the potential to predict the response of a drug for a given individual in an African population has been the subject of intensive investigation. In this review, we aim to systematically extract and discuss African evidence on the genetic variation, and pharmacogenomics towards the treatment of HTN. Furthermore, in silico methods are utilized to elucidate biological processes that will aid in identifying novel drug targets for the treatment of resistant hypertension in an African population. To provide an expanded view of genetic variants associated with the development of HTN, this study was performed using publicly available databases such as PubMed, Scopus, Web of Science, African Journal Online, PharmGKB searching for relevant papers between 1984 and 2020. A total of 2784 articles were reviewed, and only 42 studies were included following the inclusion criteria. Twenty studies reported associations with HTN and genes such as AGT (rs699), ACE (rs1799752), NOS3 (rs1799983), MTHFR (rs1801133), AGTR1 (rs5186), while twenty-two studies did not show any association within the African population. Thereafter, an in silico predictive approach was utilized to identify several genes including CLCNKB, CYPB11B2, SH2B2, STK9, and TBX5 which may act as potential drug targets because they are involved in pathways known to influence blood pressure. Next, co-expressed genes were identified as they are controlled by the same transcriptional regulatory program and may potentially be more effective as multiple drug targets in the treatment regimens for HTN. Genes belonging to the co-expressed gene cluster, ACE, AGT, AGTR1, AGTR2, and NOS3 as well as CSK and ADRG1 showed enrichment of G-protein-coupled receptor activity, the classical targets of drug discovery, which mediate cellular signaling processes. The latter is of importance, as the targeting of co-regulatory gene clusters will allow for the development of more effective HTN drug targets that could decrease the prevalence of both controlled and TRH.

show abstract

“…In several studies, these factors are consistently and independently related to CAD. 30 –32 The evidence is based on numerous prospective epidemiological studies and clinical observations in the general population. 33,34 Our previous study explains the pathophysiology mechanisms of diabetes, hypertension, and dyslipidemia in the contribution of CAD.…”

Section: Discussionmentioning

confidence: 99%

Association of FV G1691A Polymorphism but not A4070G With Coronary Artery Disease

Amara

Mrad

Sayeh

et al. 2017

Clin Appl Thromb Hemost

View full text Add to dashboard Cite

Coronary artery disease (CAD) is one of the chief causes of death in the world. Several hypotheses have been promoted as for the origin of the disease, among which are genetic predispositions and/or environmental factors. The aim of this study was to determine the effect of factor V (FV) gene polymorphisms (Leiden, G1691A [FVL] and HR2 A4070G) and to analyze their association with traditional risk factors in assessing the risk of CAD. Our study population included 200 Tunisian patients with symptomatic CAD and a control group of 300 participants matched for age and sex. All participants were genotyped for the FVL and HR2 polymorphisms. Multivariate logistic regression was applied to analyze independent factors associated with the risk of CAD. Our analysis showed that the FVL A allele frequency ( P < 10, odds ratio [OR] = 2.81, 95% confidence interval [CI] = 1.6-4.9) and GA genotype ( P < 10, OR = 4.03, 95% CI = 2.1-7.6) are significantly more prevalent among patients with CAD compared to those controls and may be predisposing to CAD. We further found that the FVL mutation is an independent risk factor whose effect is not modified by other factors (smoking, diabetes, hypertension, dyslipidemia, and a family history of CAD) in increasing the risk of the disease. However, analysis of FV HR2 variation does not show any statistically significant association with CAD. The FVL polymorphism may be an independent risk factor for CAD. However, further investigations on these polymorphisms and their possible synergisms with traditional risk factors for CAD could help to ascertain better predictability for CAD susceptibility.

show abstract

Contribution ofeNOSVariants to the Genetic Susceptibility of Coronary Artery Disease in a Tunisian Population

Cited by 23 publications

References 50 publications

Association between NOS3 genetic variants and coronary artery disease in the Han population

Association between NOS3 genetic variants and coronary artery disease in the Han population

Hypertension in African Populations: Review and Computational Insights

Association of FV G1691A Polymorphism but not A4070G With Coronary Artery Disease

Contact Info

Product

Resources

About