The role of angiogenesis in rheumatoid arthritis: recent developments
Alisa Erika KochNorthwestern
University Medical School and Veteran's Administration Chicago
Healthcare System, Lakeside Division, Ward Building 3-315, 303 E
Chicago Avenue, Chicago, IL 60611, USA
Correspondence to: Dr Koch (ae-koch@northwestern.edu)
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Introduction |
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Rheumatoid arthritis (RA) is characterised by synovial tissue leucocyte ingress and angiogenesis, or new blood vessel growth.1-8 The disease is thought to occur as an immunological response to an as yet unidentified antigen. Even in early RA, some of the earliest histological observations are blood vessels.9 A mononuclear infiltrate characterises the synovial tissue along with a luxuriant vasculature. Angiogenesis is integral to formation of the inflammatory pannus and without angiogenesis, leucocyte ingress could not occur.
Angiogenesis is regulated by a complex set of inducers and inhibitors. In this paper we will present representative examples of both angiogenesis inducers and inhibitors that may regulate RA neovascularisation (fig 1). In inflammatory states like RA, angiogenesis inducers outweigh angiogenesis inhibitors.
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Angiogenesis inducers |
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ENDOGLIN AS AN ANGIOGENIC MEDIATOR
There are a number of angiogenesis inducers that may play a part
in RA. Among these are endoglin, an endothelial glycoprotein, which
contains an arginine-glycine-aspartic acid (RGD)
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