Recent developments in ischemic reperfusion injury in liver transplantation

Purpose of review Ischemic reperfusion injury creates a myriad of destructive processes that ultimately lead to graft loss and organ dysfunction. Recent findings The generation of reactive oxygen species produced subsequent to reperfusion and reoxygenation of ischemic tissue initiates cellular cascades that ultimately lead to inflammation and organ failure. Evidence suggests that Kupffer cells and T cells mediate the activation of neutrophilic inflammatory responses. Neutrophil infiltration in the injured liver is observed in parallel with increased expression of adhesion molecules on endothelial cells. One of the cellular cascades thought to be critical in ischemic reperfusion injury is the activation of toll-like receptors on Kupffer cells. The toll-like receptor system may provide the triggering signal for pro-inflammatory responses in the ischemic reperfusion injury sequence. The heme oxygenase system has been found to be a critical cytoprotective system that is activated during cellular stress and may provide a therapeutic option in the future. Summary Ischemic reperfusion injury creates an inflammatory environment that activates several key systems. Thus, a clear understanding of the molecular mechanisms involved in ischemic reperfusion injury is essential for the design of therapeutic strategies to improve the outcome of liver transplantation.