Liver fibrosis can be considered as a dynamic and highly integrated cellular response to
chronic liver injury [1]. Whatever the etiology, the evolution of chronic liver disease (CLD) is
characterized by perpetuation of parenchymal necrosis, chronic hepatitis and qualitative as
well as quantitative alterations in extracellular matrix (ECM) composition, whereas activation
of hepatic stellate cells (HSC) and involvement of macrophages and Kupffer cells
predominate at cellular level [1±3]. At the molecular level, growth factors, cytokines and …