氧化应激
活性氧
黄嘌呤氧化酶
内皮功能障碍
一氧化氮
NADPH氧化酶
内皮
烟酰胺腺嘌呤二核苷酸磷酸
内科学
内分泌学
糖尿病
生物
化学
医学
生物化学
氧化酶试验
酶
作者
Ulrich Förstermann,Ning Xia,Huige Li
出处
期刊:Circulation Research
[Ovid Technologies (Wolters Kluwer)]
日期:2017-02-17
卷期号:120 (4): 713-735
被引量:935
标识
DOI:10.1161/circresaha.116.309326
摘要
Major reactive oxygen species (ROS)-producing systems in vascular wall include NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) oxidase, xanthine oxidase, the mitochondrial electron transport chain, and uncoupled endothelial nitric oxide (NO) synthase. ROS at moderate concentrations have important signaling roles under physiological conditions. Excessive or sustained ROS production, however, when exceeding the available antioxidant defense systems, leads to oxidative stress. Animal studies have provided compelling evidence demonstrating the roles of vascular oxidative stress and NO in atherosclerosis. All established cardiovascular risk factors such as hypercholesterolemia, hypertension, diabetes mellitus, and smoking enhance ROS generation and decrease endothelial NO production. Key molecular events in atherogenesis such as oxidative modification of lipoproteins and phospholipids, endothelial cell activation, and macrophage infiltration/activation are facilitated by vascular oxidative stress and inhibited by endothelial NO. Atherosclerosis develops preferentially in vascular regions with disturbed blood flow (arches, branches, and bifurcations). The fact that these sites are associated with enhanced oxidative stress and reduced endothelial NO production is a further indication for the roles of ROS and NO in atherosclerosis. Therefore, prevention of vascular oxidative stress and improvement of endothelial NO production represent reasonable therapeutic strategies in addition to the treatment of established risk factors (hypercholesterolemia, hypertension, and diabetes mellitus).
科研通智能强力驱动
Strongly Powered by AbleSci AI