Association of IL-10-1082A/G polymorphism with cardiovascular disease risk: Evidence from a case-control study to an updated meta-analysis

Mol Genet Genomic Med. 2019 Nov;7(11):e888. doi: 10.1002/mgg3.888. Epub 2019 Sep 30.

Abstract

Background: Previous studies have generated controversial results about the association of interleukin 10 (IL-10) gene polymorphisms (-1082G/A) in the progression of cardiovascular disease (CVD). Therefore, this study processed a systemic meta-analysis to verify this association.

Methods: The publication studies on the IL-10 (-1082G/A) polymorphism and CVDs risk were obtained by searching PubMed and Embase databases. We analyzed the genotype data for meta-analysis. The results were evaluated by odds ratios (ORs) and 95% confidence intervals (CIs). Meanwhile, our meta-analysis was also performed sensitivity analyses, heterogeneity test, and identification of publication bias.

Results: The present meta-analysis suggested that the risk with allele G is lower than with allele A for CVD. The G allele of IL-10 (-1082) could increase the risk of CVDs in the 31 case-control studies for all genetic models. (OR = 1.10, 95% CI: 1.04-1.15 for the allele model A vs. G; OR = 0.87, 95% CI: 0.72-1.04 for the dominant model GG+AG vs. AA; OR = 1.03, 95% CI: 1.02-1.05 for the recessive model GG vs. AG + AA; OR = 1.06, 95% CI = 1.03-1.10 for the homozygote comparison model GG vs. AA; and OR = 0.88, 95% CI = 0.73-1.06 for the heterozygote comparison model AG vs. AA).

Conclusions: In genetic models, the association between the IL-10 (-1082G/A) polymorphism and CVDs risk was significant. This meta-analysis proposes that the IL-10 (-1082G/A) polymorphism may serve as a risk factor for CVDs.

Keywords: an updated meta-analysis; cardiovascular disease; interleukin-10; polymorphism.

Publication types

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

MeSH terms

  • Cardiovascular Diseases / genetics*
  • Cardiovascular Diseases / pathology*
  • Case-Control Studies
  • Genetic Predisposition to Disease*
  • Humans
  • Interleukin-10 / genetics*
  • Polymorphism, Single Nucleotide*
  • Prognosis
  • Risk Factors

Substances

  • IL10 protein, human
  • Interleukin-10