Liver fibrosis, a major cause of morbidity and mortality worldwide, is a wound-healing response to repeated liver injury, driven by different causes such as chronic hepatitis, autoimmune disease, alcoholic and nonalcoholic fatty liver diseases.1 It results in impaired hepatic regenerative capacity that ultimately leads to cirrhosis and hepatocellular carcinoma.2 Liver fibrosis is characterized by excessive deposition of extracellular matrix (ECM), culminating to major changes in liver architecture where ECM acts as a reservoir for pro-inflammatory and pro-fibrogenic mediators.3 Hepatic stellate cells (HSCs) are the key fibrogenic effector cell type in the liver and the main ECM-producing cells.4 When hepatic injury persists, HSCs become activated and transform into myofibroblast-like cells.5 Activation of HSCs is promoted by tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β), and reactive oxygen species (ROS) produced by apoptotic hepatocytes and Kuppfer cells, which in turn, secrete pro-inflammatory cytokines and further perpetuating an inflammatory state.