Journal
SEMINARS IN LIVER DISEASE
Volume 41, Issue 4, Pages 461-475Publisher
THIEME MEDICAL PUBL INC
DOI: 10.1055/s-0041-1731707
Keywords
NAFLD; FXR; bile acids; microcholestasis
Categories
Ask authors/readers for more resources
NAFLD and NASH are common liver diseases, with their pathogenesis potentially involving disturbance in bile acid homeostasis and the FXR signaling pathway. FXR serves as a key regulator of bile acid metabolism, as well as having roles in metabolic regulation and immune modulation, making it a promising therapeutic target for NAFLD/NASH.
Nonalcoholic fatty liver disease (NAFLD) has become the most prevalent cause of liver disease, increasingly contributing to the burden of liver transplantation. In search for effective treatments, novel strategies addressing metabolic dysregulation, inflammation, and fibrosis are continuously emerging. Disturbed bile acid (BA) homeostasis and microcholestasis via hepatocellular retention of potentially toxic BAs may be an underappreciated factor in the pathogenesis of NAFLD and nonalcoholic steatohepatitis (NASH) as its progressive variant. In addition to their detergent properties, BAs act as signaling molecules regulating cellular homeostasis through interaction with BA receptors such as the Farnesoid X receptor (FXR). Apart from being a key regulator of BA metabolism and enterohepatic circulation, FXR regulates metabolic homeostasis and has immune-modulatory effects, making it an attractive therapeutic target in NAFLD/NASH. In this review, the molecular basis and therapeutic potential of targeting FXR with a specific focus on restoring BA and metabolic homeostasis in NASH is summarized.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available