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炎症基因多态性与缺血性心脏病：人群关联研究综述

Inflammatory gene polymorphisms and ischaemic heart disease: review of population association studies.

作者信息

Andreotti F, Porto I, Crea F, Maseri A

机构信息

Institute of Cardiology, Catholic University, Rome, Italy.

出版信息

Heart. 2002 Feb;87(2):107-12. doi: 10.1136/heart.87.2.107.

DOI:10.1136/heart.87.2.107
PMID:11796541
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1766990/
Abstract

Inflammation and genetics are both prominent mechanisms in the pathogenesis of atherosclerosis and arterial thrombosis. Accordingly, a number of population studies have explored the association of ischaemic heart disease with gene polymorphisms of the inflammatory molecules tumour necrosis factors (TNF) alpha and beta, transforming growth factors (TGF) beta1 and 2, interleukin (IL) 1 and its receptor antagonist (IL 1ra), CD14 (the receptor for lipopolysaccharide), P and E selectins, and platelet endothelial cell adhesion molecule (PECAM) 1. Although they are very preliminary and partly conflicting, the data provide some evidence that alterations in the genetics of the inflammatory system may modify the risk of ischaemic heart disease.

摘要

炎症和基因都是动脉粥样硬化和动脉血栓形成发病机制中的重要机制。因此，一些人群研究探讨了缺血性心脏病与炎性分子肿瘤坏死因子（TNF）α和β、转化生长因子（TGF）β1和2、白细胞介素（IL）1及其受体拮抗剂（IL-1ra）、CD14（脂多糖受体）、P和E选择素以及血小板内皮细胞黏附分子（PECAM）1的基因多态性之间的关联。尽管这些研究非常初步且部分相互矛盾，但数据提供了一些证据，表明炎症系统基因的改变可能会改变缺血性心脏病的风险。

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