The accumulation of lipids is a histologic and biochemical hallmark of obesity-associated
nonalcoholic fatty liver disease (NAFLD). A subset of NALFD patients develops progressive
liver disease, termed nonalcoholic steatohepatitis, which is characterized by hepatocellular
apoptosis and innate immune system-mediated inflammation. These responses are
orchestrated by signaling pathways that can be activated by lipids, directly or indirectly. In
this review, we discuss palmitate-and lysophosphatidylcholine (LPC)-induced upregulation …