Cytoprotective role of heme oxygenase-1 in liver ischemia reperfusion injury.

Ischemia/reperfusion (I/R) injury is the main cause of graft dysfunction and failure in vascular occlusion both during liver surgery and during liver transplantation. The pathophysiology of hepatic ischemia-reperfusion includes a number of mechanisms including oxidant stress that contribute to various degrees to the overall organ damage. Heme oxygenases (HO) are essential enzymes which degrade heme into biliverdin-IXalpha, free divalent iron, and carbon monoxide (CO). Due to its anti-inflammatory, anti-apoptotic and, as recently described, anti-viral properties. The inducible HO isoform HO-1 is an important molecule which could find its way into therapy of acute and chronic liver injuries including acute liver failure, alcoholic or viral hepatitis, chronic inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma are life threatening diseases and as a consequence might result in the necessity of liver transplantation. Liver transplantation is limited by ischemia/reperfusion (I/R) injury, which is characterized by hypoxia and nutrient deficiency resulting in oxidative stress, apoptosis and immune activation. Induction of HO-1 and application predominantly of CO have been shown to interfere with liver I/R injury and to improve recipient and graft survival. HO-1 and its reaction products of heme degradation has been linked to cytoprotection, and as an inducible form of HO, serves a vital metabolic function as the rate-limiting step in the heme degradation pathway, and affords protection in models of liver I/R injury. HO-1 system is an important player in liver I/R injury condition, and may offer new targets for the management of this condition. This review aims to summarize cytoprotective role of heme oxygenase-1 (HO-1) and its products within the liver.