Chen Kai, Thomas Shane R, Keaney John F
Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.
Free Radic Biol Med. 2003 Jul 15;35(2):117-32. doi: 10.1016/s0891-5849(03)00239-9.
The notion that oxidative stress contributes to the pathogenesis of vascular disease was originally driven by observations that low-density lipoprotein (LDL) modification is a prominent feature of atherosclerosis. More recently, it has become clear that the relation between oxidative stress and vascular disease goes beyond LDL oxidation and involves cellular production of reactive oxygen species (ROS). Considerable data now indicate that ROS represent an important means of cellular signaling, although the precise mechanisms whereby ROS accomplish this function remain unclear. Emerging data point to protein thiol groups as important targets for post-translational protein modification by ROS. In this review, the data linking ROS to cell signaling is discussed and the notion that ROS mediate a vascular "injury" response is proposed.
氧化应激促成血管疾病发病机制这一观点最初源于低密度脂蛋白(LDL)修饰是动脉粥样硬化的一个显著特征这一观察结果。最近,氧化应激与血管疾病之间的关系已变得明确,它不仅限于LDL氧化,还涉及活性氧(ROS)的细胞生成。现在大量数据表明,ROS是细胞信号传导的一种重要方式,尽管ROS实现这一功能的确切机制仍不清楚。新出现的数据表明蛋白质硫醇基团是ROS进行翻译后蛋白质修饰的重要靶点。在这篇综述中,我们讨论了将ROS与细胞信号传导联系起来的数据,并提出了ROS介导血管“损伤”反应的观点。