Wassmann Sven, Wassmann Kerstin, Nickenig Georg
Medizinische Klinik II, Universitätsklinikum Bonn, Sigmund-Freud-Str. 25, D-53105 Bonn, Germany.
Curr Hypertens Rep. 2006 Apr;8(1):69-78. doi: 10.1007/s11906-006-0043-6.
Data from numerous studies demonstrate that oxidative stress plays an important role in the pathogenesis of vascular disease. Oxidative stress leads to many pathologic events, such as inactivation of nitric oxide, lipid oxidation, enhanced mitogenicity and apoptosis of vascular cells, and increased expression and activation of redox-sensitive genes, which contribute to atherogenesis at all stages of the disease. Multiple enzymes are expressed in vascular cells that are involved in the elimination and production of reactive oxygen species, including the superoxide dismutases, catalase, thioredoxin reductase, glutathione peroxidase, NAD(P)H oxidase, xanthine oxidase, myeloperoxidase, and endothelial nitric oxide synthase. Several agonists and pathologic conditions that predispose to vascular disease induce changes in the expression and activity levels of these antioxidant and oxidant enzyme systems, leading to modulation of vascular oxygen radical load. Identification of key enzymes and mechanisms of vascular oxidative stress is important for the development of novel, specific pharmacologic interventions.
大量研究数据表明，氧化应激在血管疾病的发病机制中起重要作用。氧化应激会引发许多病理事件，如一氧化氮失活、脂质氧化、血管细胞有丝分裂活性增强和凋亡，以及氧化还原敏感基因的表达和激活增加，这些都在疾病的各个阶段促进动脉粥样硬化的发生。血管细胞中表达多种参与活性氧清除和产生的酶，包括超氧化物歧化酶、过氧化氢酶、硫氧还蛋白还原酶、谷胱甘肽过氧化物酶、NAD(P)H氧化酶、黄嘌呤氧化酶、髓过氧化物酶和内皮型一氧化氮合酶。几种易导致血管疾病的激动剂和病理状况会引起这些抗氧化和氧化酶系统表达及活性水平的变化，从而导致血管氧自由基负荷的调节。识别血管氧化应激的关键酶和机制对于开发新型、特异性的药物干预措施很重要。
