Literature DB >> 22170599

Association of C47T polymorphism in SOD2 gene with coronary artery disease: a case-control study and a meta-analysis.

Changwei Tian1, Tongtao Liu, Shengxia Fang, Xunbo Du, Chongqi Jia.   

Abstract

Oxidative damage promotes atherosclerosis. SOD2 is an important antioxidant enzyme. A case-control study and a meta-analysis were performed to assess the association of C47T polymorphism in SOD2 gene with premature, late-onset and overall coronary artery disease (CAD) risk. A hospital-based case-control study was conducted with 269 premature CAD cases, 278 late-onset CAD cases and 299 healthy controls. Polymerase chain reaction (PCR) and Pyrosequencing were used to detect the polymorphism. Multinomial logistic regression model was performed to estimate odds ratio (OR) with 95% confidence intervals (CIs) and adjust potential confounders. A meta-analysis was performed using eight outcomes including our result. Fixed or random effect pooled measure was selected on the basis of homogeneity test among studies. Heterogeneity among studies was evaluated using I (2). Meta-regression was used to explore potential sources of between-study heterogeneity. Publication bias was estimated using Peters's linear regression test. In our case-control study, compared with the TT as the reference, the mutant genotype of CC + TC was significantly associated with a reduced premature CAD risk both in univariate (OR = 0.60, 95% CI = 0.41-0.87) and multivariate (OR = 0.59, 95% CI = 0.40-0.87) logistic regressions, but not with late-onset CAD risk. After excluding one article that deviated from Hardy-Weinberg equilibrium in controls, this meta-analysis showed a significant association of the C allele with reduced risk of CAD in dominant (FEM: OR = 0.69, 95% CI = 0.61-0.78), recessive (OR = 0.64, 95% CI = 0.50-0.82), and codominant (FEM: OR = 0.73, 95% CI = 0.65-0.80) models. Our study suggested that the mutant genotype of CC + TC was significantly associated with a reduced CAD risk.

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Year:  2011        PMID: 22170599     DOI: 10.1007/s11033-011-1324-y

Source DB:  PubMed          Journal:  Mol Biol Rep        ISSN: 0301-4851            Impact factor:   2.316


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