NFKB1 gene rs28362491 polymorphism is associated with the susceptibility of acute coronary syndrome

The acute coronary syndrome (ACS) is a complex disease where genetic and environmental factors are involved. NF-κB, a central regulator of inflammation, is involved in various inflammatory diseases. The aim of the present study was to explore the association between NFKB1 gene rs28362491 (-94ATTGins...

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Published inBioscience reports Vol. 39; no. 4
Main Authors Jin, Si-Yu, Luo, Jun-Yi, Li, Xiao-Mei, Liu, Fen, Ma, Yi-Tong, Gao, Xiao-Ming, Yang, Yi-Ning
Format Journal Article
LanguageEnglish
Published England Portland Press Ltd 30.04.2019
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Summary:The acute coronary syndrome (ACS) is a complex disease where genetic and environmental factors are involved. NF-κB, a central regulator of inflammation, is involved in various inflammatory diseases. The aim of the present study was to explore the association between NFKB1 gene rs28362491 (-94ATTGins/del) polymorphism and ACS. A total of 778 ACS patients and 1112 healthy subjects were included in our study. The TaqMan SNP genotyping assays was used to analyze the rs28362491 polymorphism. The lesion extent of coronary artery was assessed by Gensini Score and lesion vessel number in ACS patients. For total and males, the frequencies of the mutant DD genotype and D allele were significantly higher in ACS patients than that in control subjects (total: DD genotype: 18.0 vs 14.1%, P=0.009, D allele: 43.0 vs 37.9%, P=0.002, males: DD genotype: 20.6 vs 15.3%, P=0.042, D allele: 44.2 vs 38.8%, P=0.013). After multivariate logistic regression analysis, we found that individuals with mutant DD genotype had 1.329-fold higher risk of ACS compared with individuals with ID and II genotypes. Moreover, ACS patients with DD genotype were worse stenosis of coronary artery compared with patients carrying II or ID genotype. In conclusion, our study demonstrated that the mutant DD genotype of NFKB1 gene was associated with the risk and severity of ACS in Han population in Xinjiang, northwest of China.
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These authors contributed equally to this work.
ISSN:0144-8463
1573-4935
1573-4935
DOI:10.1042/BSR20182292