Leborgne L, Mazière J C, Mazière C, Andrejak M
Service de réanimation cardiaque, CHU Amiens Sud, avenue René Laennec, 80054 Amiens.
Arch Mal Coeur Vaiss. 2002 Sep;95(9):805-14.
Cardiovascular diseases are the main cause of mortality in the western world. It is widely accepted that atherosclerosis, the first etiology, is influenced by free radicals and the oxidizing stress that they cause. In the oxidative theory of atherosclerosis, the atheromatous lesion is initiated by oxidation of two density lipoproteins (LDL), a process still known as lipid peroxidation. Oxidized LDL have many effects on the cells of the vessel wall which, provide an explanation to most of the cellular and tissular changes observed in the plaque. The vascular complications of hypercholesterolaemia, diabetes, hyperhomocysteinemia, hypertension and smoking may, in part, be secondary to oxidizing stress that impairs endothelial function and modify the lipids in the intima of the vessels. The aim of this paper is to review the modes of free radical production, to determine the role of oxidizing stress in the development of atherosclerosis and to show how the different risk factors may initiate atheroma through oxidizing stress.
心血管疾病是西方世界主要的死亡原因。动脉粥样硬化作为首要病因,受到自由基及其引发的氧化应激影响,这一观点已被广泛接受。在动脉粥样硬化的氧化理论中,动脉粥样病变由两种低密度脂蛋白(LDL)的氧化引发,这一过程仍被称为脂质过氧化。氧化型LDL对血管壁细胞有诸多影响,这为斑块中观察到的大多数细胞和组织变化提供了解释。高胆固醇血症、糖尿病、高同型半胱氨酸血症、高血压和吸烟导致的血管并发症,部分可能是氧化应激的继发结果,氧化应激会损害内皮功能并改变血管内膜中的脂质。本文旨在综述自由基产生的方式,确定氧化应激在动脉粥样硬化发展中的作用,并展示不同风险因素如何通过氧化应激引发动脉粥样硬化。