Angiogenesis is de novo capillary outgrowth from pre-existing blood vessels. This process not only is crucial for normal development, but also has an important role in supplying oxygen and nutrients to inflamed tissues, as well as in facilitating the migration of inflammatory cells to the synovium in rheumatoid arthritis, spondyloarthritis, and other tissues in systemic autoimmune diseases. Neovascularization is dependent on the balance of proangiogenic and antiangiogenic mediators, including growth factors, cytokines, chemokines, cell adhesion molecules and matrix metalloproteinases. In this lecture I will provide an overview of the various pathways that govern these angiogenic processes and discusses potential approaches to interfere with pathological angiogenesis, and thereby ameliorate inflammatory disease, by targeting these pathways specifically in endothelial cells.
In chronic inflammatory diseases, angiogenesis enables increased delivery of oxygen and nutrients to immune cell populations accumulating in inflamed tissues, and contributes to further immune cell infiltration
Angiogenesis is driven not only by hypoxia, but also by proinflammatory mediators produced by immune and stromal cells
Many pathways downstream of these proinflammatory stimuli contribute to various cellular processes involved in angiogenesis
Targeting proangiogenic pathways to inhibit neovascularization has been successfully exploited in several cancers, and may also prove beneficial in the treatment of chronic inflammatory diseases
Disclosure of Interest None declared
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