ArticleScientific reports2016
Analysis of the genetic association between IL27 variants and coronary artery disease in a Chinese Han population.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Recent Insights Into Targeting Interleukin-27 in Coronary Artery Disease.Journal of cardiovascular translational research · 2025Review
- Genetic variant rs2243115 of the IL-12/IL-35 pathway contributes to the risk of coronary artery disease.International journal of medical sciences · 2025Article
- Polymorphism of IL-12/IL-23 axis is associated with coronary heart disease.Journal of cellular and molecular medicine · 2024Article
- Association between interleukin-27 gene polymorphisms andInnate immunity · 2023Article
- Multiplex proteomics for prediction of major cardiovascular events in type 2 diabetes.Diabetologia · 2018Article
- IL-13 may be involved in the development of CAD via different mechanisms under different conditions in a Chinese Han population.Scientific reports · 2018Article
- Genetic Regulation of the Thymic Stromal Lymphopoietin (TSLP)/TSLP Receptor (TSLPR) Gene Expression and Influence of Epistatic Interactions Between IL-33 and the TSLP/TSLPR Axis on Risk of Coronary Artery Disease.Frontiers in immunology · 2018Article
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Authors and funding
23 authors at 9 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Interleukin-27 (IL-27) is an important cytokine in inflammatory diseases, including coronary artery disease (CAD). To explore the precise role of IL-27 in CAD, we investigated the genetic association between IL27 and CAD in the GeneID Chinese Han population. A two-stage case control association analysis was performed for 3075 CAD cases and 2802 controls. Logistic regression analysis was used to adjust the traditional risk factors for CAD. Results showed that a promoter variant, rs153109, tended to be marginally associated with CAD in the discovery population (Padj = 0.028, OR = 1.27, 95%CI: 1.03-1.58). However, this association was not replicated in the validation stage (Padj = 0.559, OR = 1.04, 95%CI: 0.90-1.21). In addition, when we classified the combined population into two subgroups according to the age at disease onset or disease state, we again obtained no significant associations. Finally, we estimated the severity of coronary stenosis using the Gensini Scoring system and determined that the rs153109 genotypes were still not associated with the Gensini scores of the CAD patients. In conclusion, our study failed to find an association between common variants in the functional region of IL27 and CAD in a Chinese Han population, which indicated that IL-27 might only be an inflammatory marker during the development of CAD.
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