ALCAT1 controls mitochondrial etiology of fatty liver diseases, linking defective mitophagy to steatosis

Abstract

Forced expression of ALCAT1 in primary hepatocytes led to multiple defects that are highly reminiscent of NAFLD, including steatosis, defective autophagy, and mitochondrial dysfunction, linking pathological cardiolipin remodeling by ALCAT1 to the pathogenesis of NAFLD.