Abstract
Endothelial cells lining the lumina of blood vessels are involved in leukocyte extravasation underlying inflammatory states, such as rheumatoid arthritis (RA). New vessel formation, termed angiogenesis, is also crucial for leukocyte extravasation during inflammatory synovitis. The outcome of neovascularization in the RA synovium is highly dependent on the balance or imbalance between angiogenic mediators and inhibitors. There have been several attempts to therapeutically interfere with the cellular and molecular mechanisms underlying RA-associated neovascularization. Most studies have been performed using animal models of arthritis. In addition, a limited number of human clinical trials gave promising results. In this review, authors summarize some relevant information on those angiogenic and angiostatic agents, which have also been studied in context with RA. In addition, further perspectives of anti-angiogenic therapy in arthritis are also discussed. Specific targeting of angiogenesis may be useful in the future management of various inflammatory, as well as malignant, diseases.
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