1. Approaches for treatment of liver fibrosis in chronic hepatitis C
Pierre Bedossa, MD, PhD, Valerie Paradis, MD, PhD 
Clinics in Liver Disease 
Volume 7, Issue 1, Pages (February 2003)
DOI: /S (02)

2. Fig. 1
F0 = Normal liver stained with piciosirius red. Fibrous tissue is limited to portal tracts and central veins. F4 = Cirrhosis. Septa of collagen fibers accumulate within the tissue and delineate cirrhotic nodules.
Clinics in Liver Disease 2003 7, DOI: ( /S (02) )

3. Fig. 2
(A) Hepatic stellate cell within a normal liver. Hepatic stellate cell (arrow) is a lipid-laden cell within the Disse's space at the interface between hepatocyte and sinusoid. (B) Hepatic stellate cell after isolation. Hepatic stellate cell displays numerous cell processes.
Clinics in Liver Disease 2003 7, DOI: ( /S (02) )

4. Fig. 3
Schematic drawing of hepatic stellate cells in quiescent state (left side) and after activation (right side). Quiescent cells are laden with lipid vacuoles. After activation, these cells lose their vacuoles and transform into myofibroblasts with high protein synthesis activity.
Clinics in Liver Disease 2003 7, DOI: ( /S (02) )

5. Fig. 4
Phenotype features of hepatic stellate cell activation during liver injury. Following liver injury, hepatic stellate cells (HSC) undergo “activation”, which connotes a transition from quiescent vitamin A-rich cells into proliferative, fibrogenetic, and contractile myofibroblasts. The major phenotypic changes after activation include proliferation, contractility, fibrogenesis, matrix degradation, chemotaxis, retinoid loss, and white blood cell chemoattraction. Key mediators underlying these effects are shown.
Clinics in Liver Disease 2003 7, DOI: ( /S (02) )