title: Molecular responses to ischemia and reperfusion in the liver.
abstract: 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.
authors.affiliation: Western Michigan University Homer Stryker M.D. School of Medicine, Kalamazoo, MI, USA.
authors.forename: Kelly M
authors.initials: KM
authors.lastname: Quesnelle
authors.forename: Phillip V
authors.initials: PV
authors.lastname: Bystrom
authors.forename: Luis H
authors.initials: LH
authors.lastname: Toledo-Pereyra
mesh_terms: D006801:Humans; D007511:Ischemia / Q000209:etiology / Q000378:metabolism*; D007728:Kupffer Cells / Q000502:physiology; D008099:Liver / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D016031:Liver Transplantation / Q000009:adverse effects; D009336:Necrosis; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000209:etiology / Q000378:metabolism*
chemical_list: D017382:Reactive Oxygen Species