Abstract
Hepatic ischemia-reperfusion injury is an underlying complication that occurs in clinical conditions such as hepatic resection surgery, liver transplantation and the states of shock. Such injury has classically been attributed to the joint deleterious action of both neutrophils and reactive oxygen species. However, there is increasing evidence that T lymphocytes are also key players in the acute reperfusion injury of diverse organs. They seem to act mainly by promoting the recruitment of inflammatory cells. The purpose of this review is to summarize the molecular and cellular mechanisms that participate in the pathophysiology of liver reperfusion injury.
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