Skip Navigation


NDT Advance Access originally published online on April 5, 2008
Nephrology Dialysis Transplantation 2008 23(8):2477-2479; doi:10.1093/ndt/gfn171
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
23/8/2477    most recent
gfn171v1
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 Strutz, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Strutz, F.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


The great escape—myofibroblasts in fibrosis and the immune system*

Frank Strutz

Department of Nephrology and Rheumatology, Georg-August-University Medical Center, Göttingen, Germany

Correspondence and offprint requests to: Frank Strutz, Department of Nephrology and Rheumatology, Georg-August-University Medical Center, Robert-Koch Str 40, 37099 Goettingen, Germany. Tel: +49-551-396981; Fax: +49-551-398906; E-mail: fstrutz@gwdg.de

Keywords: apoptosis; chronic renal failure; fas; fibroblast; fibrosis

The first 10% of the full text of this article appears below.



   Fibrosis and myofibroblasts
 
The extent of renal interstitial fibrosis is one of the most important prognostic factors in kidney biopsies and is a key component of almost every form of progressive renal failure [1]. Similarly, fibrosis is also a morphological correlate of progressive organ failure in liver, lung and heart. In all organs, fibrosis is the result of a process called fibrogenesis in which myofibroblasts (the name is due to the de novo expression of {alpha}-smooth muscle actin in these cells whose expression is normally restricted to vascular smooth muscle cells) are the key effector cells [2]. Myofibroblasts are formed via an intermediate form entitled the ‘protomyofibroblast’ characterized by the acquisition of contractile stress fibres [3]. In the kidney, myofibroblasts are derived mainly from activation of resident interstitial fibroblasts, albeit differentiation . . . [Full Text of this Article]



   Myofibroblasts and the immune system
 


   Clinical implications
 


   Conclusions
 

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