Quesnelle Kelly M, Bystrom Phillip V, Toledo-Pereyra Luis H
Western Michigan University Homer Stryker M.D. School of Medicine, Kalamazoo, MI, USA.
Arch Toxicol. 2015 May;89(5):651-7. doi: 10.1007/s00204-014-1437-x. Epub 2015 Jan 8.
Ischemia/reperfusion (IR) injury occurs when oxygen is rapidly reintroduced into ischemic tissue, resulting in cell death and necrotic tissue damage. This is a major concern during liver transplantation procedures since there is an inevitable interruption and subsequent restoration of circulation. IR injury in liver tissue is initiated through reactive oxygen species (ROS), which are generated by hepatocytes during IR insult. Although these ROS are thought to play a protective roll since they are known to activate several pathways involved in the hypoxic response, they also trigger a localized sterile immune response that results in the recruitment of Kupffer cells and neutrophils to the site of IR insult. These immune cells generate larger quantities of ROS that trigger apoptosis and oncotic necrosis in liver tissue. In this review, we will summarize what is currently known about the response of liver tissue to IR insult at the molecular level.
缺血/再灌注（IR）损伤发生在氧气迅速重新引入缺血组织时，导致细胞死亡和坏死组织损伤。这是肝移植手术中的一个主要问题，因为循环不可避免地会中断并随后恢复。肝组织中的IR损伤是通过活性氧（ROS）引发的，ROS是在IR损伤期间由肝细胞产生的。尽管这些ROS被认为起到保护作用，因为已知它们会激活参与缺氧反应的多种途径，但它们也会引发局部无菌免疫反应，导致库普弗细胞和中性粒细胞募集到IR损伤部位。这些免疫细胞产生大量ROS，引发肝组织中的细胞凋亡和胀亡性坏死。在本综述中，我们将总结目前在分子水平上关于肝组织对IR损伤反应的已知情况。
