Abstract
The IL-33/ST2 signaling pathway plays an important role in coronary artery disease (CHD); however, few studies have explored how variants in IL-33/ST2 genes influence CHD risk. Here, we examined the association between genetic variants in IL-33, ST2, and IL-1RAcP of the IL-33/ST2 axis and the risk of CHD. We conducted a case-controlled study with 1146 CHD cases and 1146 age- and sex-frequency-matched controls. Twenty-eight single nucleotide polymorphisms (SNPs) in IL-33, ST2, and IL-1RAcP were genotyped by Sequenom MassArray and TaqMan assay. Logistic regression was used to analyze these associations. The SNP rs4624606 in IL-1RAcP was nominally associated with CHD risk. The AA genotype was associated with a 1.85-fold increased risk of CHD (95% confidence interval (CI) = 1.01–3.36; p = 0.045) compared to the TT genotype. Further analysis showed that AA carriers also had a higher risk of CHD than TT + TA carriers (odds ratio (OR) = 1.85; 95% CI = 1.85–3.35; p = 0.043). However, no significant association was observed between variants in IL-33/ST2 genes and CHD risk. Further studies are needed to replicate our results in other ethnic groups with larger sample size.
Highlights
Coronary heart disease (CHD) is a complex chronic inflammatory process mediated by the innate and acquired immune systems and involves pro- and anti-inflammatory cytokines [1]
Considering the role of inflammation in CHD, we hypothesized that polymorphisms in Interleukin 33 (IL-33)/ST2 might be associated with CHD risk
CHD cases were more likely have a history of hypertension, diabetes mellitus (DM), and a family history of CHD
Summary
Coronary heart disease (CHD) is a complex chronic inflammatory process mediated by the innate and acquired immune systems and involves pro- and anti-inflammatory cytokines [1]. Other studies have reported that IL-33 promotes adhesion molecules and inflammatory activation in human endothelial cells and may, in such way, enhance the development of atherosclerotic lesions in the vessel wall [11,12]. The mechanisms of these contradictory effects of IL-33 are not yet completely understood yet. Considering the role of inflammation in CHD, we hypothesized that polymorphisms in IL-33/ST2 might be associated with CHD risk. We performed a genetic association analysis of IL-33/ST2 and CHD risk in a case-control study of the Han Chinese population
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