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氧化型低密度脂蛋白与肾素-血管紧张素系统在冠状动脉疾病中的相互作用。

Interaction of oxidized low-density lipoprotein and the renin-angiotensin system in coronary artery disease.

作者信息

Chen Jiawei, Mehta Jawahar L

机构信息

Division of Cardiovascular Medicine, University of Arkansas for Medical Sciences, 4301 W. Markham Street, Slot 532, Little Rock, AR 72205, USA.

出版信息

Curr Hypertens Rep. 2006 May;8(2):139-43. doi: 10.1007/s11906-006-0010-2.

DOI:10.1007/s11906-006-0010-2
PMID:16672147
Abstract

Hyperlipidemia and hypertension are frequently observed in patients with coronary artery disease. It has been proposed that an interaction between low-density lipoprotein, especially its oxidized form (ox-LDL), and renin-angiotensin system (RAS) activation is a major determinant of atherogenesis. Ox-LDL accumulation in the blood vessels enhances the expression and activation of RAS components; on the other hand, activation of RAS stimulates the accumulation of LDL and its oxidation into ox-LDL in the blood vessels. Individually ox-LDL and RAS activation induce oxidative stress and inflammatory cascade, whereas their combination exerts a synergistic effect. This concept of cross-talk between ox-LDL/hyperlipidemia and RAS activation has been proven in laboratory animals. Clinical trials also suggest that blockade of hyperlipidemia and RAS may have a synergistic salutary effect on the outcome of patients with hypertension and/or manifestations of atherosclerosis. This concept needs to be evaluated further in large clinical studies.

摘要

高脂血症和高血压在冠状动脉疾病患者中经常出现。有人提出,低密度脂蛋白,尤其是其氧化形式(氧化型低密度脂蛋白)与肾素-血管紧张素系统(RAS)激活之间的相互作用是动脉粥样硬化发生的主要决定因素。血管中氧化型低密度脂蛋白的积累会增强RAS成分的表达和激活;另一方面,RAS的激活会刺激血管中低密度脂蛋白的积累及其氧化为氧化型低密度脂蛋白。单独的氧化型低密度脂蛋白和RAS激活会诱导氧化应激和炎症级联反应,而它们的组合则发挥协同作用。氧化型低密度脂蛋白/高脂血症与RAS激活之间这种相互作用的概念已在实验动物中得到证实。临床试验还表明,对高脂血症和RAS的阻断可能对高血压患者的预后和/或动脉粥样硬化表现产生协同有益作用。这一概念需要在大型临床研究中进一步评估。

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