Renin-angiotensin system: Genes to bedside

Renin-angiotensin system: Genes to bedside
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DOI:
10.1016/s0002-8703(97)70089-9
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发表时间:
1997-09-01
影响因子:
4.8
通讯作者:
Re, RN
Re, RN
中科院分区:
医学2区
文献类型:
--
作者:
Malik, FS;Lavie, CJ;Re, RN

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动脉粥样硬化及其血管后遗症导致相当高的发病率和死亡率。动脉粥样硬化的发病机制涉及多种危险因素,医学界仍在继续寻找其他危险因素。肾素-血管紧张素系统(RAS)是一种多酶、多部位轴,作为动脉粥样硬化的重要介质已被广泛研究。最近,基于组织的血管紧张素系统被认为是 RAS 最重要的途径。人类血管紧张素转换酶(ACE)(RAS 的两种酶之一)基因的遗传多态性被发现与急性冠状动脉事件、心源性猝死、血管成形术后血管再狭窄以及特发性和肥厚性心肌病的高风险密切相关。临床和动物数据支持血管紧张素 II 是 RAS 和 ACE 酶级联中的最终共同途径,是生成血管紧张素 II 的关键酶。 ACE 基因多态性似乎可以改变细胞和游离 ACE 水平的表达,并且可以代表心血管疾病的遗传标记。
Atherosclerosis and its vascular sequela are responsible for considerable morbidity and mortality rates. Several risk Factors have been implicated in the pathogenesis of atherosclerosis, and the search for other risk factors continues on the medical horizon. Renin-angiotensin system (RAS), a multienzyme, multilocale axis, has been extensively studied as an important mediator of atherosclerosis. Recently, the tissue-based angiotensin system has been suggested as the most significant pathway of RAS. A genetic polymorphism in the human gene for the angiotensin-converting enzyme (ACE), one of the two enzymes of RAS, has been found to have a strong association with higher risk for acute coronary events, sudden cardiac death, vascular restenosis after angioplasty, and idiopathic and hypertrophic cardiomyopathy. Clinical and animal data support angiotensin II to be the final common pathway in the enzyme cascade of RAS and ACE as the key enzyme in the generation of Angiotensin II. ACE gene polymorphism appears to modify expression of cellular and free ACE levels and could represent a genetic marker for cardiovascular disease.