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REVIEW |
Liver Group, Division of Infection, Inflammation, and Repair, University of Southampton, Southampton, UK
Correspondence to:
Correspondence to:
Dr D A Mann, Liver Group, Division of Infection, Inflammation, and Repair, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK;
dam2{at}soton.ac.uk
The hepatic stellate cell (HSC) is now well established as the key cellular element involved in the development of hepatic fibrosis and because of this there is considerable interest in establishing the molecular events that trigger and perpetuate HSC activation. HSC activation at the level of gene transcription requires the coordinated activity of several key transcriptional regulators of the HSC genome. The considerable advances that have been made in the past five years into the mechanisms by which specific families of transcription factors regulate the profibrogenic characteristics of the activated HSC are reviewed.
Keywords: transcriptional regulation; hepatic stellate cell; hepatic stellate cell activation; liver fibrosis
Abbreviations: HSC, hepatic stellate cells; 
-SMA, smooth muscle actin; ECM, extracellular matrix; NF
B, nuclear factor B; IL-6, interleukin 6; ICAM-1, intercellular adhesion molecule 1; TNF-, tumour necrosis factor ; TIMP-1, tissue inhibitor of metalloproteinase 1; MMP, matrix metalloproteinase; TGF, transforming growth factor; C/EBP, CCAAT/enhancer binding protein; bHLH, basic helix-loop-helix; M6P/IGFIIR, mannose 6-phosphate/insulin-like growth factor II; PPAR
, peroxisome proliferator activated receptor ; IB-, inhibitor of NFB
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