Modern concepts on pathogenetic mechanisms of liver fibrosis

Abstract

This review summarizes current data on the pathogenetic mechanisms of fibrosis in chronic liver diseases. Controlled inflammation and transdifferentiation of hepatic stellate cells into myofibroblasts is a key element of fibrogenesis, however, further study of the role of each of the macrophage populations is required. The initiation and progression of liver fibrosis is promoted by a complex interaction of different types of liver cells, mediated by cytokines, growth factors, miRNAs. Repeated cycles of apoptosis and regeneration of hepatocytes contribute to the pathogenesis of fibrosis. Modern experimental work has proven the role of mesenchymal stem cells in liver regeneration by inhibiting the expression of the proapoptotic BAX gene. The involution of liver fibrosis is associated with monocytes of the prorestorative phenotypeLY6Clow. On in vivo models, regression of fibrosis and utilization of the extracellular matrix depot by inhibition of mi-RNA-221-3p of hepatocytes have been proven.