Hepatic ischemia reperfusion injury (R/I) is a hepatic pathophysiologic process occurs post liver transplantation surgery. It also comprises complex systemic process affecting multiple tissues and organs. Hepatic I/R has serious impact on liver function, even producing irreversible failure, which may trigger multiple organ dysfunction. Many factors, including anaerobic metabolism, mitochondrial damage, oxidative stress and secretion of reactive oxygen species (ROS), intracellular calcium overload, cytokines and chemokines produced by Kupffer cells (KCs) and neutrophils are involved in the pathogenesis of hepatic I/R processes. There are many treatment options to combat hepatic I/R injury but none has shown clear beneficial clinical evidence. The purpose of this review is to provide insights into the mechanisms of hepatic I/R injury, indicating the potential factors/signaling pathways involved in this event and available therapeutic approaches that may help to improve controlling hepatic I/R during liver surgery.
ischemia/reperfusion, Kupffer cells, oxidative stress, mitochondrial damage, NF-kB, tumor necrosis factor