Skip Navigation

Rheumatology 2006 45(Supplement 3):iii39-iii41; doi:10.1093/rheumatology/kel277
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow An erratum has been published
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Neuhofer, W.
Right arrow Articles by Pittrow, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Neuhofer, W.
Right arrow Articles by Pittrow, D.
Related Collections
Right arrow Systemic Sclerosis
Right arrow Vasculitis
Right arrow Systemic Lupus Erythematosus and Autoimmunity
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 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

Endothelin in human autoimmune diseases with renal involvement

W. Neuhofer and D. Pittrow1

Department of Physiology and Medical Clinic Innenstadt, University of Munich, Munich and 1Institute for Clinical Pharmacology, Technical University of Dresden, Dresden, Germany.

Correspondence to: PD Dr Wolfgang Neuhofer, Department of Physiology, University of Munich, Pettenkoferstrasse 12, D-80336 Munich, Germany. E-mail: Wolfgang.Neuhofer{at}med.uni-muenchen.de

Endothelin (ET)-1 is a potent renal vasoconstrictor with pro-inflammatory, profibrotic and mitogenic potential. Animal studies support a pathogenetic contribution of ET-1 and its cognate receptors in several renal manifestations of autoimmune disorders. However, data in humans are limited. The present minireview thus summarizes the observations available in humans. Similar to animal models, ET-1 is overexpressed in glomerular and tubulointerstitial lesions, which is reflected by an increased urinary excretion of ET-1. Since antagonizing the ET system has beneficial effects in experimental models, this approach may be translated to the human kidney, thus counteracting vasoconstriction, inflammation and extracellular matrix deposition during the course of human autoimmune disease.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.