Molecular crosstalk between the hepatitis c virus and the extracellular matrix in liver fibrogenesis and early carcinogenesis

Abstract

Chronic infection by the hepatitis C virus (HCV) is a major cause of liver diseases, predis-posing to fibrosis and hepatocellular carcinoma. Liver fibrosis is characterized by an overly abundant accumulation of components of the hepatic extracellular matrix, such as collagen and elastin, with consequences on the properties of this microenvironment and cancer initiation and growth. This review will provide an update on mechanistic concepts of HCV-related liver fibrosis/cirrhosis and early stages of carcinogenesis, with a dissection of the molecular details of the crosstalk during disease progression between hepatocytes, the extracellular matrix, and hepatic stellate cells.