Publication: Angiogenesis in rheumatoid arthritis
Authors
Maruotti, Nicola ; Cantatore, F.P. ; Crivellato, E. ; Vacca, A. ; Ribatti, Doménico
item.page.secondaryauthor
item.page.director
Publisher
Murcia : F. Hernández
publication.page.editor
publication.page.department
Description
Abstract
There is much evidence that rheumatoid
arthritis is closely linked to angiogenesis. Important
angiogenic mediators have been demonstrated in
synovium and tenosynovium of rheumatoid joints.
VEGF (Vascular Endothelial Growth Factor), expressed
in response to soluble mediators such as cytokines and
growth factors and its receptors are the best
characterized system in the angiogenesis regulation of
rheumatoid joints. Moreover, other angiogenic mediators
such as platelet-derived growth factor (PDGF),
fibroblast growth factor-2 (FGF-2), epidermal growth
factor (EGF), insulin-like growth factor (IGF),
hepatocyte growth factor (HGF), transforming growth
factor beta (TGF-ß), tumor necrosis factor alpha (TNF-
a), interleukin-1 (IL-1), IL-6, IL-8, IL-13, IL-15, IL-18,
angiogenin, platelet activating factor (PAF),
angiopoietin, soluble adhesion molecules, endothelial
mediator (endoglin) play an important role in
angiogenesis in rheumatoid arthritis. On the other hand,
endostatin, thrombospondin-1 and -2 are angiogenic
inhibitors in rheumatoid arthritis. The persistence of
inflammation in rheumatoid joints is a consequence of
an imbalance between these inducers and inhibitors of
angiogenesis.
publication.page.subject
Citation
item.page.embargo
Ir a Estadísticas
Sin licencia Creative Commons.