| Title | Angiogenesis in rheumatoid arthritis. | | Author(s) | Szekanecz Z, Besenyei T, Paragh G, Koch AE | | Institution | Department of Rheumatology, Institute of Medicine, University of Debrecen Medical and Health Sciences Center, Debrecen, H-4032, Hungary. szekanecz.zoltan@med.unideb.hu | | Source | Autoimmunity 2009 Nov; 42(7):563-73. | | Abstract | 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-alpha and the alpha(V)beta(3) 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. | | Language | eng | | Pub Type(s) | Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
| | PubMed ID | 19863375 |
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