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Inflammatory mediators of liver ischemia-reperfusion injury Walsh KB; Toledo AH; Rivera-Chavez FA; Lopez-Neblina F; Toledo-Pereyra LHExp Clin Transplant 2009[Jun]; 7 (2): 78-93Liver 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.|Animals[MESH]|Humans[MESH]|Inflammation/*physiopathology[MESH]|Liver Diseases/*physiopathology[MESH]|Liver/blood supply/pathology/physiopathology[MESH]|Models, Animal[MESH]|Nitric Oxide/metabolism[MESH]|Reactive Oxygen Species/metabolism[MESH]|Reperfusion Injury/*physiopathology[MESH] |
