Liver fibrosis is a wound-healing response to liver injury, which can progress to cirrhosis and potentially lead to liver cancer and failure. The central event in liver fibrosis is the activation of hepatic stellate cells (HSCs), but other cell types such as bone marrow-derived cells and myofibroblasts also contribute. Liver fibrosis is a complex process involving various molecular and cellular events. This review focuses on the major events during liver fibrogenesis, including the activation of HSCs, the role of growth factors, chemokines, adipokines, neurotrophic factors, and inflammatory pathways. The review also discusses the reversibility of liver fibrosis, senescence in HSCs, autophagy, angiogenesis, and epithelial-to-mesenchymal transition (EMT). Additionally, it covers experimental models of liver fibrosis, both in vivo and in vitro, and highlights promising antifibrotic therapeutic approaches, such as targeting TGF-β1, cannabinoid receptors, and macrophage recruitment.Liver fibrosis is a wound-healing response to liver injury, which can progress to cirrhosis and potentially lead to liver cancer and failure. The central event in liver fibrosis is the activation of hepatic stellate cells (HSCs), but other cell types such as bone marrow-derived cells and myofibroblasts also contribute. Liver fibrosis is a complex process involving various molecular and cellular events. This review focuses on the major events during liver fibrogenesis, including the activation of HSCs, the role of growth factors, chemokines, adipokines, neurotrophic factors, and inflammatory pathways. The review also discusses the reversibility of liver fibrosis, senescence in HSCs, autophagy, angiogenesis, and epithelial-to-mesenchymal transition (EMT). Additionally, it covers experimental models of liver fibrosis, both in vivo and in vitro, and highlights promising antifibrotic therapeutic approaches, such as targeting TGF-β1, cannabinoid receptors, and macrophage recruitment.