Trends Cardiovasc Med. 1998 Feb;8(2):59-64. doi: 10.1016/S1050-1738(97)00133-3.
Reduction-oxidation (redox) reactions that generate reactive oxygen species (ROS) have been identified as important chemical processes that regulate signal transduction. Because increased ROS may be a risk factor for cardiovascular events such as unstable angina, myocardial infarction and sudden death, understanding the biological processes that generate ROS and the intracellular signals elicited by ROS will be important to gain insight into the pathogenesis of these diseases. In this review, we discuss the enzymes that generate ROS in cardiovascular tissues, the role of the mitogen-activated protein (MAP) kinase pathway in redox-sensitive signal transduction, and focus on tyrosine kinases as proximate "sensors" for redox-mediated signal events. The mechanisms by which these kinases regulate gene transcription are then discussed to provide insight into the pathogenic roles of ROS in hypertension, atherosclerosis and vascular remodeling.
氧化还原（redox）反应会生成活性氧物种（ROS），这些反应已被确定为调节信号转导的重要化学过程。由于增加的 ROS 可能是心血管事件（如不稳定型心绞痛、心肌梗死和猝死）的一个风险因素，因此了解生成 ROS 的生物过程以及 ROS 引发的细胞内信号对于深入了解这些疾病的发病机制非常重要。在这篇综述中，我们讨论了在心血管组织中生成 ROS 的酶、丝裂原活化蛋白（MAP）激酶途径在氧化还原敏感信号转导中的作用，并重点讨论了酪氨酸激酶作为氧化还原介导信号事件的直接“传感器”。然后讨论了这些激酶调节基因转录的机制，以深入了解 ROS 在高血压、动脉粥样硬化和血管重塑中的致病作用。
