Abstract
BackgroundThe association of rs28362491 polymorphism in NF-κB1 gene and coronary artery disease (CAD) risk was reported in several studies with inconsistent outcomes. This study aimed to comprehensively collect and synthesize the existing evidence to appraise whether rs28362491 was correlated to CAD susceptibility.MethodsDatabases of Web of Science, EMBASE, PubMed, Wanfang, and CNKI were retrieved from inception to August 1, 2019 without any restriction on language. The strengths of association between rs28362491 polymorphism and CAD were presented as odds ratios (ORs) and 95% confidence intervals (CIs).ResultsThirteen case-control studies with 17 individual cohorts containing 9378 cases and 10,738 controls were incorporated into this meta-analysis. The findings indicated that rs28362491 polymorphism was significantly correlated to CAD risk in five genetic models: D vs. I, OR = 1.16, 95%CI 1.11–1.21, P<0.01; DD vs. II, OR = 1.37, 95%CI 1.25–1.49, P<0.01; DI vs. II, OR = 1.11, 95%CI 1.05–1.18, P<0.01; DD + DI vs. II, OR = 1.17, 95%CI 1.11–1.24, P<0.01; DD vs. DI + II, OR = 1.29, 95%CI 1.15–1.43, P<0.01. After stratification by ethnicity and gender, significant association still existed between rs28362491 and CAD, especially in the dominant model.ConclusionsThe findings suggest that the mutant D allele in rs28362491 locus may increase the risk of CAD, and carriers of D allele appear to be more susceptible to CAD.
Highlights
The association of rs28362491 polymorphism in NF-κB1 gene and coronary artery disease (CAD) risk was reported in several studies with inconsistent outcomes
After stratification by ethnicity and gender, significant association still existed between rs28362491 and CAD, especially in the dominant model
The findings suggest that the mutant D allele in rs28362491 locus may increase the risk of CAD, and carriers of D allele appear to be more susceptible to CAD
Summary
The association of rs28362491 polymorphism in NF-κB1 gene and coronary artery disease (CAD) risk was reported in several studies with inconsistent outcomes. A range of environmental factors like smoking [5], unhealthy diet and lifestyle [6], lack of physical activity [7], and low socioeconomic status [8], have been reported to stimulate the occurrence and progression of CAD. The large majority of CAD, are multifactorial with both environmental and heritable contributions [9]. Twin studies revealed the heritability estimates for CAD ranged from 41 to 77% [12]. The importance of genetic factors in CAD resulted in extensive identification of considerable candidate genes and numerous single-nucleotide polymorphisms (SNPs) that were related to this condition [13]
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