文献类型：期刊文献

英文题名：Association between NOS3 gene polymorphisms and genetic susceptibility to congenital heart Disease: A systematic review and meta-analysis

作者：Yi, Kang[1,2];Wang, Wei[2,3];Zhang, Xin[1,2,4];Dong, Xin[2,5];Fan, Zhengye[2,6];Ma, Yuhu[2,7];Gao, Jie[2,8];Li, Xinyao[2,9];You, Tao[1,2,10]

第一作者：Yi, Kang

通信作者：You, T[1]

机构：[1]Gansu Prov Hosp, Dept Cardiovasc Surg, Lanzhou, Gansu, Peoples R China;[2]Gansu Int Sci & Technol, Cooperat Base Diag & Treatment Congenital Heart Di, Lanzhou, Gansu, Peoples R China;[3]China Med Univ, Hosp 1, Dept Cardiac Surg, Shenyang, Liaoning, Peoples R China;[4]Gansu Univ Chinese Med, Sch Clin Med 1, Lanzhou, Gansu, Peoples R China;[5]Gansu Prov Hosp, Dept Ultrasound, Lanzhou, Gansu, Peoples R China;[6]First Peoples Hosp Longnan, Dept Cardiothorac Surg, Longnan, Gansu, Peoples R China;[7]Sichuan Univ, Dept Neurosurg, West China Hosp, Chengdu, Peoples R China;[8]SunYat Sen Univ, Affiliated Hosp 1, Dept Gastroenterol, Guangzhou, Peoples R China;[9]China Med Univ, Shengjing Hosp, Dept Obstet & Gynecol, Ctr Reprod Med, Shenyang, Liaoning, Peoples R China;[10]Gansu Prov Hosp, Dept Cardiovasc Surg, 204 Donggang West Rd, Lanzhou 730000, Gansu, Peoples R China

第一机构：Gansu Prov Hosp, Dept Cardiovasc Surg, Lanzhou, Gansu, Peoples R China

通信机构：[1]corresponding author), Gansu Prov Hosp, Dept Cardiovasc Surg, 204 Donggang West Rd, Lanzhou 730000, Gansu, Peoples R China.

年份：2024

卷号：173

外文期刊名：CYTOKINE

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001113276700001)】；

基金：Natural Science Foundation of Gansu Province (21JR1RA027) ; Health industry scientific research project of Gansu Province (GSWSKY2016-04) .

语种：英文

外文关键词：Nitric Oxide Synthase Type III; Congenital Heart Disease; Single Nucleotide Polymorphism; Meta-analysis; Systematic review

摘要：Background: Endothelial nitric oxide (NO) produced by endothelial Nitric Oxide Synthase (eNOS) can promote the expression of pro-angiogenic cytokines and is favorable for angiogenesis. However, the relationship between NOS3 gene polymorphisms and genetic susceptibility to congenital heart disease (CHD) was still unclear. Methods: We searched five databases including Pubmed, Cochrane Library, Embase, Web of Science, CNKI, and Wan Fang, to find all studies on NOS3 gene polymorphisms and CHD. Rstudio was used to merge the data included in the study to obtain OR, 95%CI, and forest plots. Results: Five relevant literatures were included, including three sites of NOS3 gene, rs1799983 (G894T), rs2070744 (T-786C), and rs7830 (G10T). Several models including the homozygous model of rs1799983 (G894T) gene polymorphism (TT VS GG: OR = 1.602, 95%CI: 1.098 similar to 2.337, P = 0.027), rs7830 (G10T) gene polymorphism allele model (A VS C: OR = 1.171, 95%CI: 1.029 similar to 1.333, P = 0.017), homozygous model (AA VS CC: OR = 1.474, 95%CI: 1.122 similar to 1.936, P = 0.005) and implicit model (AA VS CC + AC: OR = 1.451, 95%CI: 1.133 similar to 1.859, P = 0.003) indicated that there was a correlation. The results of the combined analysis of each gene model of rs2070744 (T-786C) gene polymorphism sites were not statistically significant, and their P values were all>0.05. Conclusion: rs1799983 (G894T) and rs7830 (G10T) polymorphic sites might play a role in the susceptibility of sporadic congenital heart disease and increase the risk of CHD. Yet, it is still necessary to expand the sample size and conduct more prospective/retrospective studies to confirm whether the rs2070744 (T-786C) polymorphism tended to increase the incidence of CHD.