Abstract
Endothelial cells are involved in leukocyte extravasation underlying inflammation. A number of adhesion molecules play a role in leukocyte-endothelial interactions. New vessel formation, termed angiogenesis, is also crucial for leukocyte extravasation. The outcome of neovascularization 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, such as leukocyte-endothelial cell adhesion and angiogenesis. Most studies have been performed using animal models of various types of inflammation, such as arthritis. In addition, a very limited number of human clinical trials gave promising results. In this review, authors summarize the most relevant information on adhesion molecules, as well as angiogenic and angiostatic agents. In addition, further perspectives of anti-adhesive and anti-angiogenic therapy are also discussed. Specific targeting of pathological endothelial function including adhesion and angiogenesis, may be useful for the future management of various inflammatory diseases.
Keywords: endothelial cells, angiogenesis, rheumatoid arthritis, inflammation
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