Wu Meng-Yu, Yiang Giou-Teng, Liao Wan-Ting, Tsai Andy Po-Yi, Cheng Yeung-Leung, Cheng Pei-Wen, Li Chia-Ying, Li Chia-Jung
Department of Emergency Medicine, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei, Taiwan.
Department of Emergency Medicine, School of Medicine, Tzu Chi University, Hualien, Taiwan.
Cell Physiol Biochem. 2018;46(4):1650-1667. doi: 10.1159/000489241. Epub 2018 Apr 20.
Ischemia-reperfusion injury is associated with serious clinical manifestations, including myocardial hibernation, acute heart failure, cerebral dysfunction, gastrointestinal dysfunction, systemic inflammatory response syndrome, and multiple organ dysfunction syndrome. Ischemia-reperfusion injury is a critical medical condition that poses an important therapeutic challenge for physicians. In this review article, we present recent advances focusing on the basic pathophysiology of ischemia-reperfusion injury, especially the involvement of reactive oxygen species and cell death pathways. The involvement of the NADPH oxidase system, nitric oxide synthase system, and xanthine oxidase system are also described. When the blood supply is re-established after prolonged ischemia, local inflammation and ROS production increase, leading to secondary injury. Cell damage induced by prolonged ischemia-reperfusion injury may lead to apoptosis, autophagy, necrosis, and necroptosis. We highlight the latest mechanistic insights into reperfusion-injury-induced cell death via these different processes. The interlinked signaling pathways of cell death could offer new targets for therapeutic approaches. Treatment approaches for ischemia-reperfusion injury are also reviewed. We believe that understanding the pathophysiology ischemia-reperfusion injury will enable the development of novel treatment interventions.
缺血再灌注损伤与严重的临床表现相关，包括心肌冬眠、急性心力衰竭、脑功能障碍、胃肠功能障碍、全身炎症反应综合征和多器官功能障碍综合征。缺血再灌注损伤是一种危急的医学状况，给医生带来了重要的治疗挑战。在这篇综述文章中，我们介绍了聚焦于缺血再灌注损伤基本病理生理学的最新进展，尤其是活性氧物种和细胞死亡途径的参与情况。还描述了烟酰胺腺嘌呤二核苷酸磷酸氧化酶系统、一氧化氮合酶系统和黄嘌呤氧化酶系统的参与情况。长时间缺血后重新建立血液供应时，局部炎症和活性氧生成增加，导致继发性损伤。长时间缺血再灌注损伤诱导的细胞损伤可能导致凋亡、自噬、坏死和坏死性凋亡。我们重点介绍了通过这些不同过程对再灌注损伤诱导的细胞死亡的最新机制见解。细胞死亡的相互关联信号通路可为治疗方法提供新靶点。还综述了缺血再灌注损伤的治疗方法。我们相信，了解缺血再灌注损伤的病理生理学将有助于开发新的治疗干预措施。
