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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-18973

Beyer, C; Schett, G; Gay, S; Distler, O; Distler, J H W (2009). Hypoxia. Hypoxia in the pathogenesis of systemic sclerosis. Arthritis Research & Therapy, 11(2):220.

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Abstract

Autoimmunity, microangiopathy and tissue fibrosis are hallmarks of systemic sclerosis (SSc). Vascular alterations and reduced capillary density decrease blood flow and impair tissue oxygenation in SSc. Oxygen supply is further reduced by accumulation of extracellular matrix (ECM), which increases diffusion distances from blood vessels to cells. Therefore, severe hypoxia is a characteristic feature of SSc and might contribute directly to the progression of the disease. Hypoxia stimulates the production of ECM proteins by SSc fibroblasts in a transforming growth factor-beta-dependent manner. The induction of ECM proteins by hypoxia is mediated via hypoxia-inducible factor-1alpha-dependent and -independent pathways. Hypoxia may also aggravate vascular disease in SSc by perturbing vascular endothelial growth factor (VEGF) receptor signalling. Hypoxia is a potent inducer of VEGF and may cause chronic VEGF over-expression in SSc. Uncontrolled over-expression of VEGF has been shown to have deleterious effects on angiogenesis because it leads to the formation of chaotic vessels with decreased blood flow. Altogether, hypoxia might play a central role in pathogenesis of SSc by augmenting vascular disease and tissue fibrosis.

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28 citations in Web of Science®
33 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Center for Integrative Human Physiology
04 Faculty of Medicine > University Hospital Zurich > Rheumatology Clinic and Institute of Physical Medicine
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:21 April 2009
Deposited On:03 Jun 2009 10:11
Last Modified:27 Nov 2013 19:43
Publisher:BioMed Central
ISSN:1478-6354
Free access at:Related URL. An embargo period may apply.
Publisher DOI:10.1186/ar2598
Related URLs:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688169/
PubMed ID:19473554

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