Angiogenesis or neovascularization describes the formation of new blood vessels. It is critically associated with not only physiological phenomena such as ovulation and wound healing but also pathological ones such as tumor, inflammation and immune reaction. The process of neovascularization consists of sequential steps e.g. chemotaxis, tube formation and proliferation of vascular endothelial cells (ECs) .Various biological substances such as heparin-binding EC growth factors (acidic and basic fibroblast growth factors), transforming growth factor-α & β, angiogenin and platelet-derived EC growth factor were reported to enhance in vitro neovascularization. Inflammatory prostaglandins, prostacyclin and cytokines also enhanced neovascularization when examined by corneal micropocket technique. In contrast, some cartilage components and protamine inhibit angiogenic factor-induced neovascularization. It is, therefore, suggested that the above mentiond biological substances uniquely regulate both physiological and pathological angiogenesis. In therapeutic relevance, cortisone inhibits in vivo neovascularization in the presence of heparin. Disease-modifying antirheumatic drugs such as gold salts, D-penicillamine, bucillamine, lobenzarit disodium and methotrexate suppress both EC proliferation and corneal neovascularization.These drugs may, therefore, suppress disease activity through inhibition of local neovascularization. Deeper understanding of the regulation of angiogenesis will shed light on the therapeutic approaches to so-called angiogenic diseases such as tumor and inflammation.