Angiogenesis is a dynamic, hypoxia-stimulated and growth factor-dependent process, eventually leading to the formation of new vessels from pre-existing blood vessels. In the last decade experimental and clinical studies have described the occurrence of hepatic angiogenesis in a number of different pathophysiological conditions, including those involving inflammatory, fibrotic and ischemic features. In particular, the literature evidence indicates that hepatic angiogenesis is strictly associated with, and may even favour fibrogenic progression of chronic inflammatory liver diseases of different aetiology. In this review, current "in vivo" and "in vitro" evidence supporting the potential pathogenetic role of angiogenesis in chronic liver diseases will be reviewed in an attempt to outline cellular and molecular mechanisms involved, with a specific emphasis on the crucial role of hypoxic conditions and hepatic stellate cells (HSCs), particularly when activated to the myofibroblast-like pro-fibrogenic phenotype.