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      The Connexin37 gene C1019T polymorphism and risk of coronary artery disease: a meta-analysis.

      Archives of medical research
      Case-Control Studies, Connexins, genetics, Coronary Artery Disease, Genetic Association Studies, Genetic Predisposition to Disease, Humans, Myocardial Infarction, Odds Ratio, Polymorphism, Genetic, Risk, Risk Factors

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          Abstract

          Mounting data have emerged suggesting that the Connexin37 C1019T polymorphism increases susceptibility to coronary artery disease (CAD). However, previous studies yielded conflicting results. In the current study, a comprehensive meta-analysis was performed to investigate whether the C1019T polymorphism is associated with CAD risk. A total of 11 studies examining the C1019T polymorphism and CAD were identified using MEDLINE, Embase, CNKI, Wanfang and CBM, in which 5535 CAD patients and 5626 controls were analyzed. A random-effects model was used to calculate odd ratios and confidence intervals, while addressing between-study heterogeneity. Publication bias was weighed using the Egger's test, Begg-Mazemdar test and funnel plot. In genetic models with striking heterogeneity, the risk of CAD was not associated with the C1019T polymorphism (allele comparison: p = 0.34, OR = 1.11, 95% CI 0.90-1.36). Stratification by disease endpoints indicated that the 1019T allele was significantly associated with myocardial infarction (MI) (allele comparison: p <0.001, OR = 1.59, 95% CI 1.24-2.03). Further meta-regression analysis indicated that a large proportion of heterogeneity was probably due to the varying proportions of diabetes mellitus (DM) across studies (p = 0.014). Our results indicated that the C1019T polymorphism may be a moderate risk factor for MI and that DM was likely a potential source of between-study heterogeneity. Copyright © 2014 IMSS. Published by Elsevier Inc. All rights reserved.

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