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载脂蛋白 C3 基因与脂蛋白脂肪酶基因协同作用决定冠心病严重程度。

Synergistic effect between lipoprotein lipase and apolipoprotein C3 genes in determining the severity of coronary artery disease.

机构信息

Cardiology Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.

出版信息

J Cardiovasc Transl Res. 2013 Jun;6(3):430-5. doi: 10.1007/s12265-013-9446-3. Epub 2013 Feb 2.

Abstract

A number of genetic variants have been identified in the lipoprotein lipase (LPL) gene. We aimed to investigate the possible associations between LPL gene and apolipoprotein C3 (APOC3) gene polymorphisms with coronary artery disease (CAD) and its severity, as well as the interaction between these polymorphisms and classical risk factors. The HindIII variant of LPL and APOC3 were genotyped in 156 CAD patients and 154 subjects as a control group. We found that the odds ratio (OR) estimating the effect of joint exposure to H2H2 genotype of LPL and S2S2 genotype of APOC3 was significantly higher than the OR estimating the effect of each factor in the absence of the other. The present study points to a synergistic interaction between H2H2 genotype of LPL gene and S2S2 genotype of APOC3 gene that leads to increased severity of CAD. Smoking, low HDL, and diabetes increased the severity of CAD in patients carrying these risky genotypes.

摘要

已有多种脂蛋白脂肪酶(LPL)基因突变被鉴定。我们旨在研究脂蛋白脂肪酶基因和载脂蛋白 C3(APOC3)基因突变与冠状动脉疾病(CAD)及其严重程度之间的可能关联,以及这些突变与经典危险因素之间的相互作用。在 156 名 CAD 患者和 154 名对照组受试者中,对 LPL 的 HindIII 变体和 APOC3 进行了基因分型。我们发现,联合暴露于 LPL 的 H2H2 基因型和 APOC3 的 S2S2 基因型的风险比值(OR)估计效应明显高于在不存在其他因素的情况下每个因素的 OR 估计效应。本研究指出脂蛋白脂肪酶基因的 H2H2 基因型和载脂蛋白 C3 基因的 S2S2 基因型之间存在协同相互作用,导致 CAD 的严重程度增加。吸烟、低 HDL 和糖尿病会增加携带这些高危基因型患者的 CAD 严重程度。

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