Angiogenesis: From chronic liver inflammation to hepatocellular carcinoma.

Chronic liver inflammation, irrespective of its underlying cause, promotes a sustained wound‑healing response that includes fibrosis, activation of hepatic stellate cells, and extensive angiogenesis. This article describes the cellular and molecular pathways through which inflammatory mediators, hypoxia, and extracellular matrix remodeling drive pathological neovascularization in the liver. Particular attention is given to the interplay between pro‑angiogenic cytokines, sinusoidal endothelial dysfunction, and the progression from chronic inflammatory injury to cirrhosis and hepatocellular carcinoma (HCC). Understanding these mechanisms helps explain how inflammation‑induced angiogenesis contributes to hepatocarcinogenesis and supports the rationale for anti‑angiogenic therapies in chronic liver disease.