Journal
CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
Volume 15, Issue 6, Pages 1277-1292Publisher
ELSEVIER INC
DOI: 10.1016/j.jcmgh.2023.02.010
Keywords
Hepatic Stellate Cell; NAFLD; Fibrosis; NASH
Categories
Ask authors/readers for more resources
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.
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/
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available