Chang Tuanjie, Wu Lingyun
Department of Pharmacology, College of Medicine, University of Saskatchewan, 107 Wiggins Road, Saskatoon, SK S7N 5E5, Canada.
Can J Physiol Pharmacol. 2006 Dec;84(12):1229-38. doi: 10.1139/y06-077.
Pathogenic mechanisms for essential hypertension are unclear despite striking efforts from numerous research teams over several decades. Increased production of reactive oxygen species (ROS) has been associated with the development of hypertension and the role of ROS in hypertension has been well documented in recent years. In this context, it is important to better understand pathways and triggering factors for increased ROS production in hypertension. This review draws a causative linkage between elevated methylglyoxal level, methylglyoxal-induced production of ROS, and advanced glycation end products in the development of hypertension. It is proposed that elevated methylglyoxal level and resulting protein glycation and ROS production may be the upstream links in the chain reaction leading to the development of hypertension.
尽管几十年来众多研究团队付出了巨大努力，但原发性高血压的发病机制仍不清楚。活性氧（ROS）生成增加与高血压的发生有关，近年来ROS在高血压中的作用已有充分文献记载。在此背景下，更好地了解高血压中ROS生成增加的途径和触发因素很重要。本综述阐述了甲基乙二醛水平升高、甲基乙二醛诱导的ROS生成以及晚期糖基化终产物在高血压发生过程中的因果联系。有人提出，甲基乙二醛水平升高以及由此导致的蛋白质糖基化和ROS生成可能是导致高血压发生的连锁反应中的上游环节。
