Liver fibrosis is characterised by the excessive deposition of extracellular matrix (ECM) in response to chronic and sustained liver damage, triggering a prolonged wound healing response. The accumulation of ECM proteins disrupts the normal hepatic architecture, resulting in the development of fibrotic scars and nodules of regenerated hepatocytes, ultimately progressing to cirrhosis. While the acute wound healing response can be transiently initiated, its progression to fibrosis requires chronic exposure to damaging agents, including viral infections, autoimmune disorders, alcohol and drug abuse, cholestatic conditions, and metabolic diseases.

Cirrhosis represents an advanced stage of liver disease characterised by distorted liver parenchyma, nodule formation, hepatic dysfunction or insufficiency and reduced intrahepatic blood flow leading to portal hypertension.1–3

Hepatic stellate cells (HSCs), also termed Ito cells, lipocytes, fat storing or perisinusoidal cells, play a pivotal role in liver fibrosis regardless of its aetiology. They act as major producers of ECM and amplify the fibrogenic response.1 2 In a healthy liver, HSCs reside in the space of Disse in between hepatocytes and liver sinusoidal endothelial cells (LSEC). On liver injury, HSCs undergo activation and differentiation into myofibroblast-like cells, a process that is characterised by proliferation, contraction, inflammation and gain of fibrogenic capabilities. Activated HSCs migrate throughout the liver and thereby accumulate in damaged areas where they are replacing injured …