Abstract
The association of the CYP2J2 G-50T polymorphism with coronary artery disease has been explored, but the results remain controversial. Thus, a meta-analysis was conducted to provide a comprehensive estimate of this association. We selected ten articles encompassing 12 independent case-control studies with 7063 cases and 10,453 controls for this meta-analysis. Overall, we found significant associations between the CYP2J2 G-50T polymorphism and coronary artery disease risk in three genetic models (allele model: odds ratio (OR) = 1.19, 95% confidence interval (CI) = 1.05–1.34; homozygote model: OR = 2.25, 95% CI = 1.27–4.01; recessive model: OR = 2.17, 95% CI = 1.22–3.86). In these three genetic models, a significant association was observed in Caucasians but not in Asians when the data were stratified by ethnicity. However, no significant associations were found between the CYP2J2 polymorphism G-50T and coronary artery disease risk in heterozygote model and dominant model. In conclusion, our meta-analysis suggested that the CYP2J2 G-50T polymorphism was associated with coronary artery disease risk in the allele, homozygote and recessive models in Caucasians.
Highlights
Coronary artery disease (CAD) is a major cause of cardiovascular morbidity and mortality worldwide [1]
We found significant associations between the CYP2J2 G-50T polymorphism and coronary artery disease risk in three genetic models (allele model: odds ratio (OR) = 1.19, 95% confidence interval (CI) = 1.05–1.34; homozygote model: OR = 2.25, 95% CI = 1.27–4.01; recessive model: OR = 2.17, 95% CI = 1.22–3.86)
The G-50T polymorphism is one of the most relevant polymorphisms associated with CAD according to polymorphism frequency and functional importance [22]
Summary
Coronary artery disease (CAD) is a major cause of cardiovascular morbidity and mortality worldwide [1]. Epidemiological studies have demonstrated that CAD is the consequence of several risk factors, such as age, body mass index (BMI), smoking, less exercise, gender, diabetes, hypercholesterolemia and low intake of dietary fiber. In addition to these risks, it is undeniable that hereditary factors play a crucial role. Until now, both genome-wide association studies (GWASs) and candidate gene studies have stated that numerous genetic variants are associated with susceptibility to CAD in various populations [4, 5]
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