The chapter discusses the development and progression of liver fibrosis, a dynamic process involving complex cellular and molecular mechanisms. Liver fibrogenesis is triggered by chronic tissue injury and inflammation, leading to the activation of tissue repair mechanisms. The process includes three phases: acute inflammation, synthesis of extracellular matrix (ECM) components, and tissue remodeling. In chronic liver diseases, the persistence of injury results in prolonged activation of repair mechanisms, leading to fibrosis rather than effective tissue repair. The ECM in fibrotic liver is dramatically increased in quantity and redistributed, contributing to a new biochemical environment that affects cell functions. In chronic hepatitis due to HBV or HCV infection, fibrosis initially develops at the edge of portal tracts, leading to portal tract enlargement and subsequent formation of cirrhotic nodules. This process is associated with rapid metabolic and hemodynamic changes, including portal hypertension and its complications. Within cirrhotic nodules, fibrosis progresses at the edge between the parenchyma and fibrous septa, and sinusoidal blood supply becomes primarily arterialized, with structural changes known as capillarization.The chapter discusses the development and progression of liver fibrosis, a dynamic process involving complex cellular and molecular mechanisms. Liver fibrogenesis is triggered by chronic tissue injury and inflammation, leading to the activation of tissue repair mechanisms. The process includes three phases: acute inflammation, synthesis of extracellular matrix (ECM) components, and tissue remodeling. In chronic liver diseases, the persistence of injury results in prolonged activation of repair mechanisms, leading to fibrosis rather than effective tissue repair. The ECM in fibrotic liver is dramatically increased in quantity and redistributed, contributing to a new biochemical environment that affects cell functions. In chronic hepatitis due to HBV or HCV infection, fibrosis initially develops at the edge of portal tracts, leading to portal tract enlargement and subsequent formation of cirrhotic nodules. This process is associated with rapid metabolic and hemodynamic changes, including portal hypertension and its complications. Within cirrhotic nodules, fibrosis progresses at the edge between the parenchyma and fibrous septa, and sinusoidal blood supply becomes primarily arterialized, with structural changes known as capillarization.