Inflammatory mediators of liver ischemia-reperfusion injury.
Liver ischemia and reperfusion--which cause liver damage that is significant in a variety of diseases, injuries, and procedures (including but not limited to trauma and transplant)--have been the focus of many investigations in recent years. Although the mechanisms of ischemia-reperfusion injury are numerous and complex, many advances in treatment have been made. The following review considers recent advances in the understanding of hepatic ischemia-reperfusion injury and focuses on inflammatory mediators of significance. To provide a unique analysis and evaluation, we emphasized the most recent pertinent investigations of the last decade. Specific topics addressed include reactive oxygen species, nitric oxide, toll-like receptors, ischemic preconditioning, T cells, heme oxygenase-1, heat shock proteins, erythropoietin, selectins, protein kinases, matrix metalloproteinases, and cytokines.
Walsh
Kyle B
KB
Michigan State University College of Human Medicine, East Lansing, Michigan 49008, USA.
Toledo
Alexander H
AH
Rivera-Chavez
Fernando A
FA
Lopez-Neblina
Fernando
F
Toledo-Pereyra
Luis H
LH
D000818:Animals; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D008099:Liver / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D008107:Liver Diseases / Q000503:physiopathology*; D023421:Models, Animal; D009569:Nitric Oxide / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000503:physiopathology*
D017382:Reactive Oxygen Species; D009569:Nitric Oxide