Fibrosis is a common response to hepatic damage, which is characterized by producing and depositing extracellular matrix (ECM) . Excessive fibrosis characterizes a series of liver diseases, such as chronic hepatitis, alcoholism-induced liver damage, and hepatic autoimmune disorders . During this pathological process, hepatic stellate cells (HSCs) are the main executor of fibrogenesis. HSC activation increases the expression and secretion of collagen and other ECM components. It also stimulates hepatic microenvironment cells, such as macrophages, endothelial cells, and inflammatory cells, resulting in the promotion of fibrogenesis in an autocrine or paracrine manner [3, 4]. Therefore, understanding the molecular mechanism based on HSC activation is essential for diagnosis and treatment of hepatic fibrosis.