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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >Variants in the Atherogenic ALOX5AP, THBD, and KNG1 Genes Potentiate the Risk of Ischemic Stroke via a Genetic Main Effect and Epistatic Interactions in a Chinese Population
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Variants in the Atherogenic ALOX5AP, THBD, and KNG1 Genes Potentiate the Risk of Ischemic Stroke via a Genetic Main Effect and Epistatic Interactions in a Chinese Population

机译：体内Alox5ap，THBD和KNG1基因的变体通过遗传的主要疗法和中国人群中的认证互动提高了缺血性卒中的风险

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Background: Ischemic stroke (IS) is a multifactorial disease that displays a strong genetic predisposition. However, the genetic architecture of IS has yet to be fully elucidated. It was hypothesized that epistasis between genes in multiple atherothrombotic pathways may play a vital role in determining the susceptibility to IS. The aim of the present study was to investigate the contributions of the hypothesized genetic factors to IS and the interactions between these genetic factors in a Chinese population. Methods: In this study, 351 cases with IS and 417 control subjects from a Chinese population were genotyped for single-nucleotide polymorphisms (SNPs) in 12 genes hypothesized to be involved in atherosclerosis, coagulation, and related pathways. We examined SNP main effects and epistatic interactions between these polymorphic loci. Results: rs710446 of the KNG1 gene was associated with IS susceptibility based on an additive genetic model (rs710446: P = .012; odds ratio [OR], 1.247; 95% confidence interval [CI], 1.050-1.481) after adjusting for covariates. Furthermore, an epistatic interaction between the ALOX5AP, THBD, and KNG1 gene was also identified in association with stroke susceptibility (P .001 after 1000 permutations). Based on the chi-squared test, the OR of the high-risk combination of the three-locus model increased the risk of IS by 2.53-fold (95% CI, 1.60-4.01; P .0001). Conclusions: Our findings support the association of the epistatic interactions of ALOX5AP, THBD, and KNG1 and present novel evidence for the main effect of KNG1 gene on IS susceptibility, suggesting a modulation of stroke risk by a genetic main effect and gene-gene interactions.
机译：背景：缺血性卒中（是）是一种展示强大的遗传易感性的多因素疾病。然而，尚未完全阐明的遗传架构。它被假设在多个动脉粥样硬化途径中基因之间的外观可能在确定易感性方面起着至关重要的作用。本研究的目的是调查假设的遗传因素的贡献以及中国人群中这些遗传因素之间的相互作用。方法：在本研究中，351例，来自中国人群的351例和417个对照受试者对12个基因的单核苷酸多态性（SNP）进行基因分型，其假设涉及动脉粥样硬化，凝血和相关途径。我们检查了这些多晶型基因座之间的SNP主要效果和背景相互作用。结果：KNG1基因的RS710446与基于添加剂遗传模型的易感性有关（RS710446：P = .012;赔率比[或]，1.247; 95％置信区间[CI]，1.050-1.481）调整协变量后。此外，还与中风敏感性结合的Alox5ap，ThBD和Kng1基因之间的伪造相互作用（在1000次排列后的P＆LT;。基于Chi平方测试，三对基因座模型的高风险组合增加了2.53倍（95％CI，1.60-4.01; P＆ .0001）。结论：我们的研究结果支持Alox5AP，THBD和KNG1的背景相互作用的关联，并提出了KNG1基因的主要效果的新依据是易感性，表明遗传主要疗法和基因 - 基因相互作用的调节。

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