Sterol O-acyltransferase 2 chaperoned by apolipoprotein J facilitates hepatic lipid accumulation following viral and nutrient stresses

Abstract

Sun et al. show that hepatitis C virus or free-fatty acids increase lipid droplets and apolipoprotein J (ApoJ) expression while ApoJ silencing alleviates hepatic lipid accumulation. This study suggests that hepatic ApoJ may activate sterol O-acyltransferase 2 to supply cholesteryl-ester for lipid loads, thus presenting ApoJ as a promising target for treating stress-induced steatosis.