NDT Advance Access published online on April 5, 2008
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfn171
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© 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*
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
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Fibrosis and myofibroblasts |
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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
-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 |
Myofibroblasts and the immune system |
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Clinical implications |
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Conclusions |
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