Fibrogenic Pathways in Metabolic Dysfunction Associated Fatty Liver Disease (MAFLD)

The prevalence of nonalcoholic fatty liver disease (NAFLD), recently also re-defined as metabolic dysfunction associated fatty liver disease (MAFLD), is rapidly increasing, affecting similar to 25% of the world population. MALFD/NAFLD represents a spectrum of liver pathologies including the more benign hepatic steatosis and the more advanced non-alcoholic steatohepatitis (NASH). NASH is associated with enhanced risk for liver fibrosis and progression to cirrhosis and hepatocellular carcinoma. Hepatic stellate cells (HSC) activation underlies NASH-related fibrosis. Here, we discuss the profibrogenic pathways, which lead to HSC activation and fibrogenesis, with a particular focus on the intercellular hepatocyte-HSC and macrophage-HSC crosstalk.

Automated summary

The prevalence of nonalcoholic fatty liver disease (NAFLD), also known as metabolic dysfunction associated fatty liver disease (MAFLD), is increasing globally. This disease spectrum includes benign hepatic steatosis and more advanced non-alcoholic steatohepatitis (NASH), which carries a higher risk of liver fibrosis, cirrhosis, and hepatocellular carcinoma. The activation of hepatic stellate cells (HSC) plays a key role in NASH-related fibrosis, and the intercellular interaction between hepatocytes and macrophages with HSC is a crucial factor.