Chen Qing-Jie, Lai Hong-Mei, Zhao Long, Ma Yi-Tong, Li Xiao-Mei, Zhai Hui, Zhou Yun, He Chun-Hui, Chen Bang-Dang, Liu Fen, Yang Yi-Ning
1 Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University , Urumqi, China .
2 Xinjiang Key Laboratory of Cardiovascular Disease Research , Urumqi, China .
Genet Test Mol Biomarkers. 2016 Mar;20(3):105-11. doi: 10.1089/gtmb.2015.0242. Epub 2016 Jan 22.
Inflammation plays an important role in the pathophysiology of coronary artery disease (CAD). NF-κB is a central regulator of inflammation. Thus the aim of this study was to conduct a systematic review and meta-analysis investigating whether the polymorphism in the NFKB1 promoter region (NFKB1-94ins(I)/del(D)ATTG, rs28362491) is associated with CAD susceptibility.
PubMed, Embase, Cochrane Library and CNKI databases were searched up to 30 July 2015. All observational case-control studies that investigated the association of NFKB1 I/D polymorphism and CAD risk were included. Two reviewers independently selected the studies and extracted the data.
A total of 7 studies were included in this meta-analysis. Comparison between alleles showed a 13% increased risk of CAD for D vs. I (OR = 1.13, 95% CI 1.06-1.19, PH = 0.318), and comparisons among genotypes showed a 26% increased risk of CAD for DD vs. II (OR = 1.26, 95% CI 1.12-1.43, PH = 0.125) and in the heterozygote model ID vs. II had an 11% increased risk (OR = 1.11, 95% CI 1.01-1.21, PH = 0.751). In the dominant model the risk of CAD risk was reduced by 13% (OR = 0.87, 95%CI 0.80-0.95, PH = 0.814) across the total population. Subgroup analysis by ethnicity indicated that the additive model was associated with a 21% increased risk for CAD in the Caucasian population (OR = 1.21, 95% CI 1.09-1.34, PH = 0.522), while the homozygote model gave a 47% increased risk for CAD in Asian population (OR = 1.47, 95% CI 1.21-1.78, PH = 0.314).
Our results indicated that the NFKB1-94ins/del ATTG polymorphism was associated with susceptibility to CAD in both Asian and Caucasian populations.
炎症在冠状动脉疾病（CAD）的病理生理学中起重要作用。核因子κB（NF-κB）是炎症的核心调节因子。因此，本研究的目的是进行一项系统评价和荟萃分析，以调查NFKB1启动子区域的多态性（NFKB1-94ins(I)/del(D)ATTG，rs28362491）是否与CAD易感性相关。
检索截至2015年7月30日的PubMed、Embase、Cochrane图书馆和中国知网数据库。纳入所有调查NFKB1 I/D多态性与CAD风险关联的观察性病例对照研究。两名研究者独立选择研究并提取数据。
本荟萃分析共纳入7项研究。等位基因比较显示，D等位基因与I等位基因相比，CAD风险增加13%（比值比[OR]=1.13，95%可信区间[CI]1.06-1.19，P值异质性检验[PH]=0.318）；基因型比较显示，DD基因型与II基因型相比，CAD风险增加26%（OR=1.26，95%CI 1.12-1.43，PH=0.125），杂合子模型ID与II相比，CAD风险增加11%（OR=1.11，95%CI 1.01-1.21，PH=0.751）。在显性模型中，总体人群的CAD风险降低13%（OR=0.87，95%CI 0.80-0.95，PH=0.814）。按种族进行的亚组分析表明，在白种人群中，相加模型与CAD风险增加21%相关（OR=1.21，95%CI 1.09-1.34，PH=0.522），而在亚洲人群中，纯合子模型使CAD风险增加47%（OR=1.47，95%CI 1.21-1.78，PH=0.314）。
我们的结果表明，NFKB1-94ins/del ATTG多态性与亚洲和白种人群的CAD易感性相关。
