Foresight regarding drug candidates acting on the succinate-GPR91 signalling pathway for non-alcoholic steatohepatitis (NASH) treatment

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, and it is a liver manifes-tation of metabolic syndrome, with a histological spectrum from simple steatosis to non-alcoholic steatohepatitis (NASH). NASH can evolve into progressive liver fibrosis and eventually lead to liver cirrhosis. The pathological mechanism of NASH is multifactorial, involving a series of metabolic disorders and changes that trigger low-level inflammation in the liver and other organs. In the pathogenesis of NASH, the signal transduction pathway involving succinate and the succinate receptor (G-protein-coupled receptor 91, GPR91) regulates inflammatory cell activation and liver fibrosis. This review describes the mechanism of the succinate-GPR91 signalling pathway in NASH and summarizes the drugs that act on this pathway, with the aim of providing a new approach to NASH treatment.

Automated summary

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, which can progress to non-alcoholic steatohepatitis (NASH). The pathogenesis of NASH is complex, involving multiple factors such as metabolic disorders and inflammation. Research on the succinate-GPR91 signaling pathway provides a new direction for the treatment of NASH.