有害还是有益：瞬时受体电位阳离子通道M2型（TRPM2）在缺血/再灌注损伤中的作用
Detrimental or beneficial: the role of TRPM2 in ischemia/reperfusion injury.
作者信息
Zhan Kai-yu, Yu Pei-lin, Liu Chun-hui, Luo Jian-hong, Yang Wei
机构信息
Department of Neurobiology, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Collaborative Innovation Center for Brain Science, Zhejiang University School of Medicine, Hangzhou 310058, China.
Department of Toxicology, School of Public Health, Zhejiang University, Hangzhou 310058, China.
出版信息
Acta Pharmacol Sin. 2016 Jan;37(1):4-12. doi: 10.1038/aps.2015.141.
Ischemia/reperfusion (I/R) injury is the main cause of tissue damage and dysfunction. I/R injury is characterized by Ca(2+) overload and production of reactive oxygen species (ROS), which play critical roles in the process of I/R injury to the brain, heart and kidney, but the underlying mechanisms are largely elusive. Recent evidence demonstrates that TRPM2, a Ca(2+)-permeable cationic channel and ROS sensor, is involved in I/R injury, but whether TRPM2 plays a protective or detrimental role in this process remains controversial. In this review, we discuss the recent progress in understanding the role of TRPM2 in reperfusion process after brain, heart and kidney ischemia and the potential of targeting TRPM2 for the development of therapeutic drugs to treat I/R injury.
缺血/再灌注（I/R）损伤是组织损伤和功能障碍的主要原因。I/R损伤的特征是钙（Ca2+）超载和活性氧（ROS）生成，它们在脑、心脏和肾脏的I/R损伤过程中起关键作用，但其潜在机制在很大程度上仍不清楚。最近的证据表明，瞬时受体电位M型2通道（TRPM2），一种Ca2+通透阳离子通道和ROS传感器，参与I/R损伤，但TRPM2在此过程中起保护作用还是有害作用仍存在争议。在本综述中，我们讨论了在理解TRPM2在脑、心脏和肾脏缺血后再灌注过程中的作用方面的最新进展，以及靶向TRPM2开发治疗I/R损伤治疗药物的潜力。
Zotero 插件