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

Arch Med Res. 2014 Jan;45(1):21-30. doi: 10.1016/j.arcmed.2013.12.001. Epub 2013 Dec 11.

Abstract

Background and aims: 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.

Methods: 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.

Results: 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).

Conclusions: 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.

Keywords: Connexin; Coronary artery disease; Myocardial infarction; Polymorphism Meta-analysis.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Case-Control Studies
  • Connexins / genetics*
  • Coronary Artery Disease / genetics*
  • Gap Junction alpha-4 Protein
  • Genetic Association Studies
  • Genetic Predisposition to Disease
  • Humans
  • Myocardial Infarction / genetics
  • Odds Ratio
  • Polymorphism, Genetic
  • Risk
  • Risk Factors

Substances

  • Connexins