Liver fibrosis is a wound-healing response to liver injury, which can progress to cirrhosis, liver cancer, and failure. The activation of hepatic stellate cells (HSCs) is central to fibrosis, with other cells like bone marrow-derived cells and myofibroblasts also contributing. The liver's complex nature makes fibrogenesis a multifaceted process. This review discusses major events in liver fibrogenesis, including the role of HSCs, myofibroblasts, and various signaling pathways. It also covers antifibrotic therapies and experimental models used to study liver fibrosis. Liver fibrosis is caused by chronic injury from factors such as alcohol, NASH, viral hepatitis, autoimmune hepatitis, NAFLD, and cholestatic diseases. These factors lead to chronic inflammation and abnormal wound healing, resulting in fibrous scar formation. The liver's architecture is disrupted, leading to hepatocyte loss and impaired liver function. Liver fibrosis is reversible unless it progresses to cirrhosis. The pathogenesis of liver fibrosis involves the activation of myofibroblasts, which produce extracellular matrix (ECM) components. HSCs, activated by inflammatory mediators, differentiate into myofibroblasts, initiating tissue remodeling. Other cell types, such as endogenous portal fibroblasts, fibrocytes, and bone marrow-derived cells, also contribute to myofibroblast formation. Growth factors like PDGF, TGF-β1, and VEGF play significant roles in fibrogenesis by promoting ECM remodeling and collagen formation. Liver fibrosis is influenced by various mechanisms, including chemokine signaling, adipokines, neurochemical factors, and inflammatory pathways. Leptin and adiponectin have roles in fibrogenesis, with leptin promoting fibrosis and adiponectin having antifibrotic effects. Neurotrophic factors like CB1 and CB2 signaling also influence fibrosis, with CB1 promoting and CB2 inhibiting fibrogenesis. Liver fibrosis can be modeled experimentally using chemical agents like CCl4, thioacetamide, and DMN/DEN, as well as diet-based models such as MCD and high-fat diets. Surgery-based models like bile duct ligation (BDL) and genetically modified models are also used. In vitro models, such as primary HSC cultures, are used to study fibrosis mechanisms. Antifibrotic therapies aim to target fibrogenic pathways, including TGF-β1, integrins, and chemokine receptors. Therapies targeting macrophage recruitment and reversing fibrosis through MMPs and other enzymes are also explored. Combination therapies are considered important for effective antifibrotic treatment, as targeting a single pathway may not be sufficient. Liver fibrosis is a dynamic process that can be reversed if the causative agent is removed. HoweverLiver fibrosis is a wound-healing response to liver injury, which can progress to cirrhosis, liver cancer, and failure. The activation of hepatic stellate cells (HSCs) is central to fibrosis, with other cells like bone marrow-derived cells and myofibroblasts also contributing. The liver's complex nature makes fibrogenesis a multifaceted process. This review discusses major events in liver fibrogenesis, including the role of HSCs, myofibroblasts, and various signaling pathways. It also covers antifibrotic therapies and experimental models used to study liver fibrosis. Liver fibrosis is caused by chronic injury from factors such as alcohol, NASH, viral hepatitis, autoimmune hepatitis, NAFLD, and cholestatic diseases. These factors lead to chronic inflammation and abnormal wound healing, resulting in fibrous scar formation. The liver's architecture is disrupted, leading to hepatocyte loss and impaired liver function. Liver fibrosis is reversible unless it progresses to cirrhosis. The pathogenesis of liver fibrosis involves the activation of myofibroblasts, which produce extracellular matrix (ECM) components. HSCs, activated by inflammatory mediators, differentiate into myofibroblasts, initiating tissue remodeling. Other cell types, such as endogenous portal fibroblasts, fibrocytes, and bone marrow-derived cells, also contribute to myofibroblast formation. Growth factors like PDGF, TGF-β1, and VEGF play significant roles in fibrogenesis by promoting ECM remodeling and collagen formation. Liver fibrosis is influenced by various mechanisms, including chemokine signaling, adipokines, neurochemical factors, and inflammatory pathways. Leptin and adiponectin have roles in fibrogenesis, with leptin promoting fibrosis and adiponectin having antifibrotic effects. Neurotrophic factors like CB1 and CB2 signaling also influence fibrosis, with CB1 promoting and CB2 inhibiting fibrogenesis. Liver fibrosis can be modeled experimentally using chemical agents like CCl4, thioacetamide, and DMN/DEN, as well as diet-based models such as MCD and high-fat diets. Surgery-based models like bile duct ligation (BDL) and genetically modified models are also used. In vitro models, such as primary HSC cultures, are used to study fibrosis mechanisms. Antifibrotic therapies aim to target fibrogenic pathways, including TGF-β1, integrins, and chemokine receptors. Therapies targeting macrophage recruitment and reversing fibrosis through MMPs and other enzymes are also explored. Combination therapies are considered important for effective antifibrotic treatment, as targeting a single pathway may not be sufficient. Liver fibrosis is a dynamic process that can be reversed if the causative agent is removed. However