Meta-analysis of RAGE gene polymorphism and coronary heart disease risk

PLoS One. 2012;7(12):e50790. doi: 10.1371/journal.pone.0050790. Epub 2012 Dec 6.

Abstract

Background: Recent data from human and animal studies have shown an upregulated expression of advanced glycosylation end product-specific receptor (RAGE) in human atherosclerotic plaques 1 and in retina, messangial, and aortic vessels, suggesting an important role of RAGE in the pathogenesis of atherothrombotic diseases. In the past few years, the relationship between RAGE polymorphisms (-429T/C, -374T/A, and G82S) and coronary heart disease (CHD) has been reported in various ethnic groups; however, these studies have yielded contradictory results.

Methods: PubMed, ISI web of science, EMBASE and the Chinese National Knowledge Infrastructure databases were systematically searched to identify relevant studies. Data were abstracted independently by two reviewers. A meta-analysis was performed to examine the association between RAGE polymorphisms and susceptibility to CHD. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated.

Results: A total of 17 studies including 4343 patients and 5402 controls were involved in this meta-analysis. Overall, no significant results were observed for -429T/C (OR = 1.01, 95% CI: 0.92-1.12, P = 0.78), -374T/A (OR = 1.11, 95% CI: 0.98-1.26, P = 0.09) and G82S (OR = 1.12, 95% CI: 0.86-1.45, P = 0.41) polymorphism. In the stratified analyses according to ethnicity, sample size, CHD endpoint and Hardy-Weinberg status, no evidence of any gene-disease association was obtained.

Conclusions: This meta-analysis demonstrates that there is no association between the RAGE -429T/C, -374T/A and G82S polymorphisms and CHD.

Publication types

  • Meta-Analysis

MeSH terms

  • Coronary Disease / genetics*
  • Genetic Predisposition to Disease
  • Genotype
  • Humans
  • Polymorphism, Genetic
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic / genetics*
  • Risk

Substances

  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic

Grants and funding

No current external funding sources for this study.