Transcriptional Regulation of Metabolic Pathways via Lipid-Sensing Nuclear Receptors PPARs, FXR, and LXR in NASH

Nonalcoholic fatty liver disease comprises a wide spectrum of liver injuries from simple steatosis to steatohepatitis and cirrhosis. Nonalcoholic steatohepatitis (NASH) is defined when liver steatosis is associated with inflammation, hepatocyte damage, and fibrosis. A genetic predisposition and environmental insults (ie, dietary habits, obesity) are putatively responsible for NASH progression. Here, we present the impact of the lipid-sensing nuclear receptors in the pathogenesis and treatment of NASH. In detail, we discuss the pros and cons of the putative transcriptional action of the fatty acid sensors (peroxisome proliferator-activated receptors), the bile acid sensor (farnesoid X receptor), and the oxysterol sensor (liver X receptors) in the pathogenesis and bona fide treatment of NASH.

Automated summary

Nonalcoholic fatty liver disease encompasses a spectrum of liver injuries, from simple steatosis to steatohepatitis and cirrhosis. Nonalcoholic steatohepatitis (NASH) is characterized by liver steatosis, inflammation, hepatocyte damage, and fibrosis. Genetic predisposition and environmental factors such as dietary habits and obesity may contribute to the progression of NASH. The role of lipid-sensing nuclear receptors in the pathogenesis and treatment of NASH, including peroxisome proliferator-activated receptors, farnesoid X receptor, and liver X receptors, is discussed in this study.