A Meta-Analysis on the Association Between TNFSF4 Polymorphisms (rs3861950 T > C and rs1234313 A > G) and Susceptibility to Coronary Artery Disease

Author:

Liu Shuyan,Wang Xiju,Yu Shoujun,Yan Miao,Peng Yue,Zhang Guilong,Xu Zhaowei

Abstract

Background: Coronary artery disease (CAD) remains the leading cause of mortality worldwide, and its susceptibility is closely associated with genetic modifications. The association between inflammation and CAD has been investigated in detail. This meta-analysis was conducted based on the PRISMA guidelines to evaluate the association between the tumor necrosis factor superfamily member 4 (TNFSF4) gene polymorphisms (rs3861950 T > C and rs1234313 A > G) and the risk of CAD.Methods: The selected criteria included 11 eligible articles containing 18 studies (nine studies included 7,395 cases and 5,296 controls for rs3861950 and nine studies with 6,951 cases and 4,959 controls for rs1234313). Correlations between the two polymorphisms and CAD were estimated by pooling the odds ratios (ORs) with 95% confidence interval (95% CI) in allelic, dominant, recessive, heterozygous, and homozygous models.Results: The pooled analyses demonstrated that the rs3861950 T > C polymorphism was significantly associated with an increased risk of CAD in the Asian population in the allelic model, dominant model, and homozygous model. Furthermore, subgroup analysis based on disease type showed that TNFSF4 rs3861950 T > C had a robust correlation with increased risk of cerebral infarction (CI) in the allelic model, dominant model, heterozygous model, and homozygous model. However, the rs1234313 A > G polymorphism mostly tended to decrease the risk of CAD in the Asian and Caucasian populations in the allelic and dominant model. This single nucleotide polymorphism (SNP) had a close relation to myocardial infarction (MI) susceptibility in the allelic model, dominant model, and heterozygous model.Conclusion: This meta-analysis identified two novel SNPs in TNFSF4 significantly associated with CAD susceptibility.

Funder

National Natural Science Foundation of China

Natural Science Foundation of Shandong Province

Publisher

Frontiers Media SA

Subject

Physiology (medical),Physiology

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