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Acetaminophen (APAP) hepatotoxicity because of overdose is the most frequent cause of acute liver failure. The mechanisms of APAP hepatotoxicity are dominated by intracellular events including the formation of a reactive metabolite, hepatic glutathione depletion and protein binding. In response to overdose of APAP treatment, the liver elicits a healing process characterized by proliferation of hepatocytes, removal of necrotic tissue, and restoration of the hepatic microvasculature. However, the mechanisms of repair of the tissue damage during APAP hepatotoxicity are poorly understood. Vascular endothelial growth factor (VEGF) and its receptors, VEGFR1 and VEGFR2, promote the repair and regeneration of the liver after acute insult including liver resection and toxicants. This mini review focuses on the role of VEGF/VEGFRs signaling in liver injury and hepatic tissue repair during APAP hepatotoxicity. Rec.6/15/2012, Acc.7/10/2012, pp66-71

VEGF/VEGFR signaling in the liver repair from acetaminophen hepatotoxicity