MITOCHONDRIAL Ca2+ UNIPORTER (MCU) IN HEPATOCYTES BUT NOT IN KUPFFER CELLS PROMOTES LIVER INJURY INDUCED BY ACETAMINOPHEN (APAP)
<div><p><b>Background: </b>Iron-catalyzed formation of reactive oxygen species (ROS) increases after APAP overdose and triggers the mitochondrial permeability transition (MPT). Previous studies show that iron translocation from lysosomes into mitochondria by MCU in hepatocytes promotes the MPT after APAP. Kupffer cells are liver resident macrophages that are involved in uptake, processing, and export of iron. Here, our Aim was to investigate and compare the roles of MCU in hepatocytes and Kupffer cells in APAP hepatotoxicity. </p>