J Korean Rheum Assoc.
2001 Dec;8(4):215-226.
Angiogenesis in Rheumatoid Arthritis
- Affiliations
-
- 1Department of Internal Medicine, Chonnam National University Medical School, Kwangju, Korea. chocs@cmc.cuk.ac.kr
- 2Department of Internal Medicine, Center for Rheumatic Diseases in Kangnam St. Mary's hospital, The Catholic University of Korea, Seoul, Korea.
Abstract
- Rheumatoid arthritis (RA)is characterized by synovial cell hyperplasia and the overgrowth of a fibrovascular granulation tissue,known as pannus,which proliferates like tumor cells and destroys cartilage and bone within the joint. Since neovascularization is necessary for the continual proliferation of synovial tissue,it is believed to play an important role in the development and progression of RA.Angiogenesis in the inflamed joints represents the net balance between the effects of angiogenic and anti-angiogenic factors.A number of angiogenic factors have been described in RA,of which vascular endothelial growth factor (VEGF)and basic fibroblast growth factor are the most potent. In RA,high levels of VEGF are present in synovial fluid and synovial tissue, which is produced by cells near endothelial cells and acts on endothelial cells via interaction with its receptors.VEGF is induced by hypoxia,which may occur in the inflamed joint.Not only do cytokines like interleukin (IL)-1beta,IL-6,and T G F-beta induce fibroblast expression of VEGF,but so does engagement of CD40 ligand.Recently,specific inhibition of VEGF by soluble receptor,sflt-1,and by anti-VEGF monoclonal antibody has been shown to attenuate collagen-induced arthritis in mice,supporting the major role of VEGF in promoting angiogenesis. Efforts are currently targeted at inhibiting angiogenic factors in RA.