Leopold Jane A, Loscalzo Joseph
Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
Drug Discov Today Ther Strateg. 2008 Mar;5(1):5-13. doi: 10.1016/j.ddstr.2008.02.001.
Oxidant stress has been implicated in the etiology and pathogenesis of atherothrombotic vascular disease. Elevated levels of reactive oxygen species, resulting from increased production and/or decreased antioxidant capacity, modulate the vessel wall phenotype to create an environment that facilitates the progression of atherosclerosis. Herein, we review a number of biochemical mechanisms by which oxidant stress mediates atherosclerotic lesion formation and progression.
氧化应激已被认为与动脉粥样硬化性血管疾病的病因和发病机制有关。由于活性氧生成增加和/或抗氧化能力降低导致的活性氧水平升高,会调节血管壁表型,从而营造出有利于动脉粥样硬化进展的环境。在此,我们综述了氧化应激介导动脉粥样硬化病变形成和进展的一些生化机制。