Liver fibrosis is a dynamic process involving complex cellular and molecular mechanisms, resulting from the chronic activation of tissue repair mechanisms following repeated liver injury. Recent advances have led to a better understanding of liver fibrogenesis, including its relationships with portal hypertension, cholestasis, and hepatocellular carcinoma. The elucidation of mechanisms underlying liver fibrosis has provided a foundation for developing pharmacological strategies to modulate this process. Fibrogenesis is closely related to the extent and duration of parenchymal injury. The process of liver fibrosis, similar to normal wound healing, includes three phases: acute inflammation, synthesis of extracellular matrix (ECM) components, and tissue remodeling. While a single injury may lead to resolution, persistent injury leads to fibrosis. The ECM in fibrotic liver is similar to normal liver but in greater quantity and redistributed. This change contributes to a new biochemical environment, essential for multicellular functions. In chronic liver diseases, accumulation of fibrillar ECM is a common marker of damage and leads to cirrhosis. Fibrosis patterns vary depending on the cause and progression of liver damage. In chronic hepatitis, fibrosis initially occurs at the portal tract edge, leading to portal tract enlargement and eventually cirrhotic nodules. Fibrosis progresses at the interface between parenchyma and fibrous septa, with changes in sinusoidal blood supply and structural alterations in sinusoids. These changes have significant metabolic and hemodynamic consequences, including portal hypertension.Liver fibrosis is a dynamic process involving complex cellular and molecular mechanisms, resulting from the chronic activation of tissue repair mechanisms following repeated liver injury. Recent advances have led to a better understanding of liver fibrogenesis, including its relationships with portal hypertension, cholestasis, and hepatocellular carcinoma. The elucidation of mechanisms underlying liver fibrosis has provided a foundation for developing pharmacological strategies to modulate this process. Fibrogenesis is closely related to the extent and duration of parenchymal injury. The process of liver fibrosis, similar to normal wound healing, includes three phases: acute inflammation, synthesis of extracellular matrix (ECM) components, and tissue remodeling. While a single injury may lead to resolution, persistent injury leads to fibrosis. The ECM in fibrotic liver is similar to normal liver but in greater quantity and redistributed. This change contributes to a new biochemical environment, essential for multicellular functions. In chronic liver diseases, accumulation of fibrillar ECM is a common marker of damage and leads to cirrhosis. Fibrosis patterns vary depending on the cause and progression of liver damage. In chronic hepatitis, fibrosis initially occurs at the portal tract edge, leading to portal tract enlargement and eventually cirrhotic nodules. Fibrosis progresses at the interface between parenchyma and fibrous septa, with changes in sinusoidal blood supply and structural alterations in sinusoids. These changes have significant metabolic and hemodynamic consequences, including portal hypertension.