Hepatic stellate cells (HSCs) are one of the sinusoid constituent cells that play multiple roles in liver pathophysiology and, in particular, in liver fibrosis. In the intact liver, HSCs localise in the space between sinusoids and hepatocytes, so called space of Disse, embrace the sinusoids as liver specific pericytes to regulate sinusoidal blood flow by their contractility, and store lipid droplets largely containing vitamin A.¹ When the liver parenchyma suffers from chronic injury caused by various disease aetiologies, such as iron overload, alcohol consumption, infection by hepatitis B virus or hepatitis C virus (HCV), non-alcoholic steatohepatitis, autoimmune hepatitis, and bile duct obstruction, elimination of damaged hepatocytes causes HSCs to depart from the sinusoidal wall and become activated. This process is considered to be triggered by multiple peptide, lipid, and gaseous mediators that are released from hepatocytes, Kupffer cells, endothelial cells, and infiltrating inflammatory cells.^2–5

HSC activation accompanies their phenotypic transformation into myofibroblast (MFB)-like cells. The latter cell type exhibits expression of α smooth muscle actin and growth factor receptors, such as platelet derived growth factor receptor β (PDGF receptor β), production of contractile mediators, such as …