Abstract
BackgroundNumerous case-control studies have investigated the association between GSTP1 Ile105Val polymorphism and CHD risk, but the results from published studies were inconclusive. The present meta-analysis was performed to derive a more precise estimation.MethodsPubMed, EMBASE, and Web of Science database searches were conducted to retrieve relevant articles.ResultsUltimately, 5,451 CHD cases and 5,561 controls from 15 studies were included. Pooled analysis did not yield any statistically significant association between GSTP1 Ile105Val polymorphism and CHD risk for the overall population (Val vs. Ile: OR, 1.05; 95% CI, 0.93 to 1.18; Val/Val vs. Ile/Ile: OR, 1.09; 95% CI, 0.83 to 1.42; Val/Ile vs. Ile/Ile: OR, 1.09; 95% CI, 0.93 to 1.28; Val/Val vs. Val/Ile+Ile/Ile: OR, 1.04; 95% CI, 0.83 to 1.30; Val/Val+Val/Ile vs. Ile/Ile: OR, 1.14; 95% CI, 0.97 to 1.33). Subgroup analyses and sensitivity analyses indicated that GSTP1 Ile105Val polymorphism was still not associated with an increased risk of CHD. After excluding studies detected by Galbraith plots as major sources of heterogeneity, these relationships were still not significant.ConclusionsThe overall results did not reveal a major role of the GSTP1 Ile105Val polymorphism in modulating CHD risk. Well-designed studies with large sample sizes are needed to validate our findings and explore the possible gene-gene or gene-environment interactions.
Highlights
Atherosclerosis is a major cause of coronary heart disease (CHD), a major public health problem, and a leading cause of morbidity and mortality in the world [1,2]
Pooled analysis did not yield any statistically significant association between glutathione S-transferase P1 (GSTP1) Ile105Val polymorphism and CHD risk for the overall population (Val vs. Ile: odds ratios (ORs), 1.05; 95% confidence intervals (95% CIs), 0.93 to 1.18; Val/Val vs. Ile/Ile: OR, 1.09; 95% CI, 0.83 to 1.42; Val/Ile vs. Ile/Ile: OR, 1.09; 95% CI, 0.93 to 1.28; Val/Val vs. Val/Ile+Ile/Ile: OR, 1.04; 95% CI, 0.83 to 1.30; Val/Val+Val/Ile vs. Ile/Ile: OR, 1.14; 95% CI, 0.97 to 1.33)
Subgroup analyses and sensitivity analyses indicated that GSTP1 Ile105Val polymorphism was still not associated with an increased risk of CHD
Summary
Atherosclerosis is a major cause of coronary heart disease (CHD), a major public health problem, and a leading cause of morbidity and mortality in the world [1,2]. Multiple traditional risk factors lead to CHD development, including age, a high-fat diet, smoking, alcohol, diabetes mellitus, hyperlipidemia, hypertension, and so on. An imbalance between antioxidant defenses and free radical generation, was implicated as potential pathophysiological mechanisms behind the pathogenesis and progression of CHD [3]. DNA damage, inflammation, smooth muscle cell proliferation, and lipid peroxidation, which are caused by increased production of reactive oxygen species (ROS), can result in atherosclerosis and, CHD [4]. DNA adducts have been detected in patients with severe CHD [5] and atherosclerotic plaques [6]. DNA adducts were considered to be related to atherogenic risk factors including old age, alcohol drinking status, smoking status, oxidative DNA damage, triglycerides, cholesterol, and arterial pressure. The present meta-analysis was performed to derive a more precise estimation
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