Targeting Metabolism to Modify Cirrhosis: Lessons From FGF21 Therapy in MASH

Metabolic dysfunction–associated steatohepatitis (MASH) has emerged as one of the leading causes of cirrhosis worldwide.1 Notably, up to one quarter of patients already have stage 4 fibrosis at the time of diagnosis.2 In this population, therapeutic priorities shift from resolving steatohepatitis to preventing hepatic decompensation, hepatocellular carcinoma, liver transplantation, and liver-related mortality. At the same time, non–liver-related causes of death – particularly cardiovascular disease and extrahepatic malignancy – contribute substantially to overall mortality.