Liver cirrhosis is increasingly becoming the major cause of global health burden. It originates through a dynamic process of liver fibrogenesis and fibrosis. Excessive accumulation of extracellular matrix comprising collagen, glycoproteins and other components alter the organization of liver lobule into fibrotic histology. Fibrogensis deprive the hepatocytes from oxygen and nutrients supply leading to necrosis which impedes the metabolic exchange between blood and liver cells.
Fibrogenesis initiated as a response to liver injury is an integrated process involving complex molecular, cellular and histological changes towards the excessive accumulation of extracellular matrix. Molecules like growth factors, proinflammatory cytokines, chemokines, reactive oxygen species (ROS) and other mediators interact with Hepatic stellate cells (HSC), Kuffer cells and Hepatocytes ultimately reorganize liver histology through fibrogenesis, fibrinolysis and epithelial-mesenchymal transition (EMT).
Hepatic stellate cells (HSCs) play a central role in hepatic fibrogenesis. Progression of fibrosis is influenced by modifiable factors such as body mass index, alcohol, chronic liver injuries, hepatitis viruses etc., and non-modifiable factors specifically genetic determinants and autoimmune disorders initiates quiescent HSC into proliferative, contractile and fibrogenic myofibroblast phenotype. Transdifferentiation of HSCs synergistically with EMT of cholangiocytes and hepatocytes and myofibroblasts of bone marrow origin enhances the fibrogenic activity in the liver to several folds.
Hepatic fibrosis is reversible, its progression and regression involved definite signaling. Hence through this research topic we welcome original research papers and review articles dealing with hepatic fibrogenesis to get new insights towards the development of diagnostic (non invasive including serum and imaging modalities) and effective antifibrotic therapies.
Journal of Genomics & Gene Study