Receptor interacting protein kinase 3 is a critical early mediator of acetaminophen‐induced hepatocyte necrosis in mice
Anup Ramachandran, Mitchell R. McGill, Yuchao Xie, Hong‐Min Ni, Wen‐Xing Ding, Hartmut Jaeschke – 6 June 2013 – Acetaminophen (APAP) overdose is a major cause of hepatotoxicity and acute liver failure in the U.S., but the pathophysiology is incompletely understood. Despite evidence for apoptotic signaling, hepatic cell death after APAP is generally considered necrotic in mice and in humans. Recent findings suggest that the receptor interacting protein kinase 3 (RIP3) acts as a switch from apoptosis to necrosis (programmed necrosis).