Hepatic Stellate Cells: Dictating Outcome in Nonalcoholic Fatty Liver Disease

• Published in: Cellular and molecular gastroenterology and hepatology Vol. 15; no. 6; pp. 1277 - 1292
• Main Authors: Wiering, Leke, Subramanian, Pallavi, Hammerich, Linda
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.01.2023; Elsevier
• Subjects: Carcinoma, Hepatocellular - pathology; Fibrosis; Gastroenterology and Hepatology; Hepatic Stellate Cell; Hepatic Stellate Cells - pathology; Humans; Liver Cirrhosis - pathology; Liver Neoplasms - pathology; NAFLD; NASH; Non-alcoholic Fatty Liver Disease - pathology; Review; PGE2; NAFLD; IL; EGF; MBOAT7; EP4; GATA6; TCF21; GATA4; NASH; TNF; CTGF; TGF; Hepatic Stellate Cell; PPAR; BAMBI; CCL5; PDGF; Fibrosis; CCl4; CCL3; PDGFR; CCL2; platelet-derived growth factor; connective tissue growth fact; membrane-bound O-acyltransferase domain containing 7; nonalcoholic steatohepatitis; chemokine (C-C motif) ligand 2; prostaglandin E2 receptor 4; prostaglandin E2; platelet-derived growth factor receptor; interleukin; BMP and activin membrane-bound inhibitor; peroxisome proliferator activated receptor; chemokine (C-C motif) ligand 5; chemokine (C-C motif) ligand 3; carbon tetrachloride; transcription factor 21; CCl 4; nonalcoholic fatty liver disease; tumor necrosis factor; epidermal growth factor; transforming growth factor; GATA-binding factor 4; GATA-binding factor 6
• ISSN: 2352-345X; 2352-345X
• DOI: 10.1016/j.jcmgh.2023.02.010

Nonalcoholic fatty liver disease (NAFLD) is a fast growing, chronic liver disease affecting ∼25% 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/NASH.