Abstract
Interleukin-13 (IL-13) has important functions in atherosclerosis, but its role in coronary artery disease (CAD) is unclear. Here, we studied the genetic role of IL-13 in CAD in a Chinese Han population using tag SNPs covering the whole IL13 gene (i.e., rs1881457, rs2069744 and rs20541) and a two-stage cohort containing 1863 CAD cases and 1841 controls. Traditional risk factors for CAD, such as age, BMI, and other factors, were used as covariates in logistic regression analysis. In the total population, we found that two haplotypes of IL13 (ATG and ATA, ordered rs1881457C-rs2069744T-rs20541A) significantly contributed to the risk of CAD with adjusted p values less than 0.05 (padj = 0.019 and padj = 0.042, respectively). In subgroup population analyses, the variant rs1881457C was found to significantly contribute to a nearly two fold increase in the risk of CAD in men (padj = 0.023, OR = 1.91, 95% CI: 1.09-3.33). The variant rs1881457C also significantly contributed to a nearly twofold risk of late-onset CAD (padj = 0.024, OR = 1.93, 95% CI: 1.09-3.42). In conclusion, IL13 might be involved in CAD via different mechanisms under different conditions in the Chinese Han population.
Highlights
SNPs covering the whole IL13 gene and a two-stage cohort containing 1863 CAD cases and 1841 controls
Later studies demonstrated that IL-13 can maintain metabolic homeostasis by inducing macrophage PPARδ or PPARβ expression in adipose tissue, which might promote the development of atherosclerosis[10,11]
We found the following results: two haplotypes in IL13 (ATG and ATA, ordered rs1881457C-rs2069744T-rs20541A) significantly contributed the risk of CAD; the promoter variant rs1881457C of IL13 contributed to the risk of CAD in male patients but was involved in the development of late-onset CAD; and, in contrast, rs1881457C did not influence the severity of CAD as determined by the Gensini scores
Summary
Jiang et al found that IL-13 is involved in glucose uptake and metabolism in skeletal muscle, which regulates glucose homeostasis in metabolic diseases[14]. In previous GWASs, such as analyses from the CARDIoGRAMplusC4D Consortium, two SNPs localized in the IL13 region were found to have no association with CAD and/or myocardial infarction (p = 0.260 for rs20541 and p = 0.975 for rs2069744) These data sets were mainly based on a European population, and the reported SNPs did not cover the whole IL13 region (UCSC). We assessed CAD severity using the Gensini score and examined whether the selected variants influenced this parameter. These data may elucidate the genetic function of IL-13 in CAD, which may help to determine the exact role of IL-13 in CAD
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