Marian A J
Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA.
Curr Opin Cardiol. 1998 May;13(3):171-8.
Myocardial infarction (MI) is a complex phenotype caused by interaction of a number of genetic and environmental factors. A genetic susceptibility to MI was observed in a familial aggregation and studies in twins. Advances in molecular genetics have led to identification of a number of potential genetic risk factors for MI, such as variants of genes involved in vascular homeostasis, thrombosis, and lipid metabolism. Functional variants of angiotensin-1-converting enzyme (ACE), beta-fibrinogen, plasminogen activator inhibitor-1, methylenetetrahydrofolate reductase, glycoprotein Illa, and many apolipoprotein genes are considered excellent candidate risk factors for MI. Interaction of the susceptibility genes with modifier genes, environmental factors, and conventional risk factors results in the final phenotype of MI. Understanding the complex interaction between these factors is expected to provide significant insights into the pathogenesis of MI and lead to development of genetic-based risk stratification, prevention, and treatment.
心肌梗死(MI)是一种由多种遗传和环境因素相互作用引起的复杂表型。在家族聚集性研究和双胞胎研究中观察到对MI的遗传易感性。分子遗传学的进展已导致鉴定出许多MI潜在的遗传危险因素,例如参与血管稳态、血栓形成和脂质代谢的基因变体。血管紧张素转换酶(ACE)、β-纤维蛋白原、纤溶酶原激活物抑制剂-1、亚甲基四氢叶酸还原酶、糖蛋白IIIa以及许多载脂蛋白基因的功能性变体被认为是MI的优秀候选危险因素。易感性基因与修饰基因、环境因素和传统危险因素之间的相互作用导致了MI的最终表型。了解这些因素之间的复杂相互作用有望为MI的发病机制提供重要见解,并导致基于遗传的风险分层、预防和治疗的发展。