Heistad Donald D, Wakisaka Yoshinobu, Miller Jordan, Chu Yi, Pena-Silva Ricardo
Departments of Internal Medicine, University of Iowa Carver College of Medicine, 52242-1081, USA.
Circ J. 2009 Feb;73(2):201-7. doi: 10.1253/circj.cj-08-1082. Epub 2008 Dec 26.
Oxygen radicals, and other reactive oxygen species, may play an important role in the pathophysiology of atherosclerosis, stroke, and other cardiovascular diseases. Mechanisms that account for oxidative stress in different cardiovascular diseases are diverse; for example, increases in activity of NAD(P)H oxidase, "uncoupling" of nitric oxide synthase, and maladaptive changes in expression of antioxidants can all contribute to increases in oxidative stress. Very different patterns of pro-and antioxidant mechanisms that contribute to increases in oxygen radicals in atherosclerotic plaques, hemorrhagic strokes, and aortic valve stenosis have been observed. A disappointment, in relation to the hypothesis that oxygen radicals contribute to cardiovascular risk, is that many studies indicate that antioxidant vitamins fail to reduce the risk of cardiovascular disease. Better understanding of mechanisms that lead to increases in oxidative stress in different cardiovascular diseases may lead to more effective antioxidant prevention or treatment of diseases.
氧自由基及其他活性氧物质可能在动脉粥样硬化、中风和其他心血管疾病的病理生理学中发挥重要作用。不同心血管疾病中导致氧化应激的机制多种多样;例如,NAD(P)H氧化酶活性增加、一氧化氮合酶的“解偶联”以及抗氧化剂表达的适应性改变都可能导致氧化应激增加。在动脉粥样硬化斑块、出血性中风和主动脉瓣狭窄中,导致氧自由基增加的促氧化和抗氧化机制模式差异很大。与氧自由基导致心血管风险这一假说相关的一个令人失望的情况是,许多研究表明抗氧化维生素并不能降低心血管疾病风险。更好地理解导致不同心血管疾病中氧化应激增加的机制,可能会带来更有效的抗氧化疾病预防或治疗方法。