Blood vessels, a potential therapeutic target in rheumatoid arthritis?

被引:43
|
作者
Semerano, Luca [1 ,2 ]
Clavel, Gaelle [2 ,3 ]
Assier, Eric [2 ]
Denys, Anne [2 ]
Boissier, Marie-Christophe [1 ,2 ]
机构
[1] Avicenne Hosp, AP HP, Dept Rheumatol, Bobigny, France
[2] LI2P Paris 13 Univ, EA4222, Bobigny, France
[3] Fdn Ophtalmol Adolphe de Rothschild, Paris, France
关键词
Rheumatoid arthritis; Angiogenesis; Targeted treatments; Atherosclerosis; Cardiovascular disease; COLLAGEN-INDUCED ARTHRITIS; ENDOTHELIAL GROWTH-FACTOR; TUMOR-NECROSIS-FACTOR; PROGENITOR CELLS; INFLIXIMAB THERAPY; PSORIATIC SKIN; ANGIOGENESIS INHIBITION; GENE-TRANSFER; RECEPTOR; VEGF;
D O I
10.1016/j.jbspin.2010.06.004
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
New micro-vessels formation within synovium and macro-vesssels endothelial damage with atheroma are two major features of rheumatoid arthritis, the former related to the articular involvement of the disease, the latter to its main systemic complication. The similarities between pannus development and solid tumors growth, and the efficacy of anti-angiogenic treatments in oncology, opened the perspective of directly targeting angiogenesis in arthritis. Nevertheless, despite the success of different anti-angiogenic therapeutic strategies in many arthritis experimental models, the application in human disease is still lacking. Recent data suggest that synovial neoangiogenesis and macro-vessels endothelial damage might be two linked phenomena. While synovial angiogenesis seems to be detrimental to endothelial damage repair, even anti-angiogenic treatments might paradoxically aggravate macro-vascular disease, especially in the context of uncontrolled inflammation. These elements induce to further explore the interconnections between inflammation and angiogenesis on one side and between micro-and macro-vascular diseases on the other, in order to establish the proper way to therapeutically target blood vessels in rheumatoid arthritis. (C) 2010 Societe francaise de rhumatologie. Published by Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:118 / 123
页数:6
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