Hepatic stellate cells are non-parenchymal, contractile pericytes of the liver. Once activated hepatic stellate cells secret fibrosis factors in liver sinusoid and contribute to the fibrosis of the liver, which in turn causes portal hypertension and liver cirrhosis. Being in close proximity with hepatic endothelial cells in liver sinusoid, hepatic stellate cells might cross talk with endothelial cells to modulate endothelial functions. Hepatic stellate cell (HSC) represent 5–8% of all human liver cells and 13% of the volume of sinusoidal cells. Stellate cells are located in the perisinusoidal space of Disse beneath the endothelial barrier. Following acute or chronic liver injury, HSC are activated and undergo a process of trans-differentiation leading to a myofibroblastic phenotype. Upon stimulated the cells start trans-differentiating into activated stellate cells, which secrete fibrogenic factors in the liver. The trans-differentiation and activation of stellate cells are the inevitable step in most of the liver pathologies including cirrhosis.
Hepatic stellate cells are the major cell type involved in the formation of scar tissue, which is formed as a response to liver damage. HSCs can be stained with gold chloride and the characteristic feature in histological preparations includes lipid droplets in their cytoplasm. Cytoglobin is a specific marker for HSCs which distinguishes it from portal myofibroblasts in the damaged liver. Quiescent HSCs convert to activated state under liver damage. Proliferation, contractility and chemotaxis are the distinct features of activated HSCs. Liver fibrosis ultimately leads to senescence of HSCs, marked by p53 accumulation and increased SA-beta galactosidase staining.