Hepatic encephalopathy describes the array of neurological complications that arise due to liver insufficiency and/or portal-systemic shunt. The pathogenesis of hepatic encephalopathy shares a longstanding association with hyperammonemia and inflammation. Recently, aberrant bile acid signaling has been implicated in the development of key features of hepatic encephalopathy due to acute liver failure including neuronal dysfunction, neuroinflammation and blood-brain barrier permeability. This review summarizes the findings of recent studies demonstrating a role for bile acids in hepatic encephalopathy and speculates on the possible downstream consequences of bile acid signaling.
Keywords: ASBT, Apical Sodium-Dependent Bile Acid Transporter; CCL2, Chemokine Ligand 2; CCR2, Chemokine Receptor 2; Cyp46A1, Cytochrome p450 46A1; FXR, Farnesoid X Receptor; GR, Glucocorticoid Receptor; NTCP, Sodium Taurocholate Cotransporting Polypeptide; PXR, Pregnane X Receptor; S1P2R, Sphingosine 1 Phosphate Receptor 2; TGR5, Takeda G-Protein Receptor 5; Takeda G-protein coupled receptor 5 (TGR5); VDR, Vitamin D Receptor; blood–brain barrier; farnesoid X receptor; neuroinflammation; sphingosine-1-phosphate receptor 2.