Beyond LDL oxidation: ROS in vascular signal transduction

被引:134
作者
Chen, K [1 ]
Thomas, SR [1 ]
Keaney, JF [1 ]
机构
[1] Boston Univ, Sch Med, Whitaker Cardiovasc Inst, Boston, MA 02118 USA
关键词
free radicals; signal transduction; protein thiols; oxidation-reduction;
D O I
10.1016/S0891-5849(03)00239-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. (C) 2003 Elsevier Inc.
引用
收藏
页码:117 / 132
页数:16
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