Clinical Advancements in the Targeted Therapies against Liver Fibrosis

Figure 1

Hepatic injury initiated by chronic viral infections, excessive alcohol consumption, metabolic disorders, or autoimmune insult leads to the development of liver fibrosis. Hepatocellular damage instigates the recruitment of inflammatory cells and release of profibrogenic factors that result in the transdifferentiation of the resident quiescent liver fibroblast (hepatic stellate cells, HSCs) to the highly activated, proliferative, motile, and contractile myofibroblast phenotype. ECM accumulation, angiogenesis, and inflammation lead to progressive fibrosis ultimately culminating into cirrhosis associated with loss of liver function and portal hypertension, or hepatocellular carcinoma.