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Meta-Analysis
. 2020 Feb 11;21(1):29.
doi: 10.1186/s12881-020-0952-2.

Association of tumor necrosis factor-α gene polymorphisms and coronary artery disease susceptibility: a systematic review and meta-analysis

Rui Huang  1 , Su-Rui Zhao  1 , Ya Li  1 , Fang Liu  1 , Yue Gong  1 , Jun Xing  1 , Ze-Sheng Xu  2   3
Affiliations
Meta-Analysis

Association of tumor necrosis factor-α gene polymorphisms and coronary artery disease susceptibility: a systematic review and meta-analysis

Rui Huang et al. BMC Med Genet. .

Abstract

Background: The goal of this study was to review relevant case-control studies to determine the association of tumor necrosis factor-α (TNF-α) gene polymorphisms and coronary artery disease (CAD) susceptibility.

Methods: Using appropriate keywords, we identified relevant studies using PubMed, Cochrane, Embase, CNKI, VANFUN, and VIP. Key pertinent sources in the literature were also reviewed, and all articles published through April 2019 were considered for inclusion. Based on eligible studies, we performed a meta-analysis of association between 308G/A, 238G/A, 857C/T, 863C/A and 1031 T/C polymorphisms in TNF-α and risk of CAD.

Results: We found 25 studies that were consistent with this meta-analysis, including 7697 patients in the CAD group and 9655 control patients. TNF-α 308G/A locus A showed no significant association with CAD susceptibility by the five models in the analysis of the overall population, European, African, South Asian, and North Asian patients. TNF-α 863C/A locus A and 1031 T/C locus C exhibited no significant association with CAD susceptibility. TNF-α 238G/A locus A had no significant association with CAD susceptibility in the overall population. However, TNF-α 238G/A locus A showed significant association with higher CAD susceptibility in the subgroup of Europeans and north Asians. TNF-α 857C/T locus T had no significant association with CAD susceptibility in the analysis of the overall population and Europeans. In the north Asian population, TNF-α 857C/T locus T was associated with lower CAD susceptibility by the heterozygote model.

Conclusion: TNF-α 308G/A, 857C/T, 863C/A, and 1031 T/C has no significant association with CAD susceptibility. TNF-α 238G/A locus A has significant association with CAD susceptibility in Europeans and north Asians, but has no significant association in the overall population. Studies with a larger sample size are required to confirm the association between TNF-α 238G/A and CAD susceptibility.

Keywords: Coronary artery disease; Gene polymorphisms; Meta-analysis; Tumor necrosis factor-α.

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Conflict of interest statement

There is no competing interest.

Figures

Fig. 1
Fig. 1
Literature search and selection strategy
Fig. 2
Fig. 2
Risk of bias by domain (in bold) and question in twenty-six case-control studies using the Newcastle–Ottawa Scale
Fig. 3
Fig. 3
Forest plot for the dominant model of TNF-α 308G/A polymorphisms associated with CAD
Fig. 4
Fig. 4
Funnel plot analysis of the included studies onTNF-α 308G/A polymorphisms
Fig. 5
Fig. 5
Forest plot for the dominant model of TNF-α 238G/A polymorphisms associated with CAD
Fig. 6
Fig. 6
Forest plot for the dominant model of TNF-α 857C/T polymorphisms associated with CAD
Fig. 7
Fig. 7
Forest plot for the dominant model of TNF-α 863C/A polymorphisms associated with CAD
Fig. 8
Fig. 8
Forest plot for the dominant model of TNF-α 1031 T/C polymorphisms associated with CAD
See this image and copyright information in PMC

References

    1. Said MA, van de Vegte YJ, Zafar MM, van der Ende MY, Raja GK, Verweij N, et al. Contributions of interactions between lifestyle and genetics on coronary artery disease risk. Curr Cardiol Rep. 2019;21(9):89. doi: 10.1007/s11886-019-1177-x. - DOI - PMC - PubMed
    1. Musunuru K, Kathiresan S. Genetics of common. Complex Coronary Artery Disease Cell. 2019;177(1):132–145. - PubMed
    1. Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat Rev Genet. 2017;18(6):331–344. doi: 10.1038/nrg.2016.160. - DOI - PMC - PubMed
    1. Nedwin GE, Naylor SL, Sakaguchi AY, Smith D, Jarrett-Nedwin J, Pennica D, et al. Human lymphotoxin and tumor necrosis factor genes: structure, homology and chromosomal localization. Nucleic Acids Res. 1985;13(17):6361–6373. doi: 10.1093/nar/13.17.6361. - DOI - PMC - PubMed
    1. Christodoulidis G, Vittorio TJ, Fudim M, Lerakis S, Kosmas CE. Inflammation in coronary artery disease. Cardiol Rev. 2014;22(6):279–288. doi: 10.1097/CRD.0000000000000006. - DOI - PubMed

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