期刊
AUTOIMMUNITY
卷 42, 期 7, 页码 563-573出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/08916930903143083
关键词
angiogenesis; rheumatoid arthritis; vascular endothelial growth factor; angiostasis therapy
类别
资金
- NIH [AR-048267]
- Veterans' Administration
- National Scientific Research Fund [T048541]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI040987] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR048267] Funding Source: NIH RePORTER
Angiogenesis is the formation of new capillaries from pre-existing vessels. A number of soluble and cell-bound factors may stimulate neovascularization. The perpetuation of angiogenesis involving numerous soluble and cell surface-bound mediators has been associated with rheumatoid arthritis (RA). These angiogenic mediators, among others, include growth factors, primarily vascular endothelial growth factor (VEGF) and hypoxia-inducible factors (HIFs), as well as pro-inflammatory cytokines, various chemokines, matrix components, cell adhesion molecules, proteases and others. Among the several potential angiogenesis inhibitors, targeting of VEGF, HIF-1, angiogenic chemokines, tumor necrosis factor- and the V3 integrin may attenuate the action of angiogenic mediators and thus synovial angiogenesis. In addition, some naturally produced or synthetic compounds including angiostatin, endostatin, paclitaxel, fumagillin analogues, 2-methoxyestradiol and thalidomide may be included in the management of RA.
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