**2. Potential Targets of Liver Fibrosis**

Activated HSCs are involved in the inflammatory response, fibrogenesis, and angiogenesis in liver fibrosis (Figure 1). They are at the center of liver fibrosis. Therefore, HSC-targeted strategies can be developed for the treatment of liver fibrosis. Alternative strategies include anti-inflammatory agents and inhibition of collagen deposition.

**Figure 1.** Hepatic stellate cell (HSC) activation. The pathways of HSC activation include initiation and perpetuation stages. Initiation is stimulated by reactive oxygen species (ROS), paracrine stimuli, and so on. The continuous stimulation could induce HSCs into myofibroblast cells, and the perpetuation phase occurs, which is involved in the change of HSC behavior, including proliferation, contractility, fibrogenesis, altered matrix degradation, chemotaxis, and inflammatory signaling. Abbreviations: CTGF, connective tissue growth factor; HSC, hepatic stellate cell; MMP, matrix metalloproteinase; NO, nitric oxide; PDGF, platelet-derived growth factor; TGF-β1, transforming growth factor β1; TIMP, tissue inhibitor of metalloproteinase; VEGF, vascular endothelial growth factor.
