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Rheumatology 2006 45(Supplement 3):iii26-iii27; doi:10.1093/rheumatology/kel295
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Angiogenesis and vasculogenesis in systemic sclerosis

J. H. W. Distler, S. Gay1 and O. Distler1,

Department of Internal Medicine III, University of Erlangen-Nuremberg, Germany and 1Center of Experimental Rheumatology, University Hospital Zurich, Switzerland.

Correspondence to: Oliver Distler, MD, Center of Experimental Rheumatology, Department of Rheumatology, University Hospital Zurich, CH-8091 Zurich, Switzerland. E-mail: Oliver.Distler{at}usz.ch

In addition to inflammatory infiltrates and an accumulation of extracellular matrix proteins, vascular changes are a hallmark in the pathogenesis of systemic sclerosis (SSc). Consistent with the ongoing endothelial cell apoptosis, several markers of EC damage are up-regulated in the serum of SSc patients. Surprizingly, vascular endothelial growth factor (VEGF), a very potent angiogenic molecule, is overexpressed in SSc patients despite the insufficient angiogenesis. VEGF can protect patients from fingertip ulcers, but a prolonged overexpression of VEGF might have paradoxical effects leading to the formation of irregular vessels similar to that observed in SSc. Besides defective angiogenesis, recent studies suggest that vasculogenesis is also impaired in SSc patients with reduced numbers and functional defects of endothelial progenitor cells.


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