Hepatic Stellate Cells: Dictating Outcome in Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) is a fast growing, chronic liver disease affecting w25% of the global population. Nonalcoholic fatty liver disease severity ranges from the less severe simple hepatic steatosis to the more advanced nonalcoholic steatohepatitis (NASH). The presence of NASH predisposes individuals to liver fibrosis, which can further progress to cirrhosis and hepatocellular carcinoma. This makes hepatic fibrosis an important indicator of clinical outcomes in patients with NASH. Hepatic stellate cell activation dictates fibrosis development during NASH. Here, we discuss recent advances in the analysis of the profibrogenic pathways and mediators of hepatic stellate cell activation and inactivation, which ultimately determine the course of disease in nonalcoholic fatty liver disease/

Automated summary

Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease with a wide range of severity, from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH). NASH can lead to liver fibrosis, cirrhosis, and hepatocellular carcinoma, making hepatic fibrosis an important predictor of outcomes. Recent advancements in understanding the activation and inactivation of hepatic stellate cells, which drive fibrosis development, have shed light on the disease progression in NAFLD/NASH.