Abstract
Renal fibrosis is the common end point of virtually all progressive kidney diseases. Renal fibrosis should not be viewed as a simple and uniform 'scar', but rather as a dynamic system that involves extracellular matrix components and many, if not all, renal and infiltrating cell types. The involved cells exhibit enormous plasticity or phenotypic variability—a fact that we are only beginning to appreciate. Only a detailed understanding of the underlying mechanisms of renal fibrosis can facilitate the development of effective treatments. In this Review, we discuss the most recent advances in renal, or more specifically, tubulointerstitial fibrosis. Novel mechanisms as well as potential treatment _targets based on different cell types are described. Problems that continue to plague the field are also discussed, including specific therapeutic _targeting of the kidney, the development of improved diagnostic methods to assess renal fibrosis and the shortcomings of available animal models.
Key Points
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Renal fibrosis is the common end point for all progressive renal diseases
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This entity involves virtually all intrinsic and infiltrating cells and is characterized by alterations in their phenotype
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Whether these alterations are part of a regenerative program or are largely pathological is still not clear
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Many potential treatment _targets for renal fibrosis have been identified in animal models
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The lack of noninvasive diagnostic tools for renal fibrosis hinders efficient translation of these _targets into clinical practice
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Change history
23 September 2010
In the version of this article initially published online, there was a mistake in Figure 4. The errors have been corrected in all electronic versions of the text.
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Acknowledgements
We apologize to all authors whose important work could not be cited owing to space limitations. We wish to thank Dr B. Hintz and members of J. Floege's laboratory for valuable discussions. Our work described in this Review was supported by grants from the Deutsche Forschungsgemeinschaft (SFB/TRR 57), projects P14, P17 and P19 (to T. Ostendorf, J. Floege).
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P. Boor wrote the manuscript; P. Boor, T. Ostendorf and J. Floege contributed equally to discussing content, and reviewing/editing the manuscript before submission.
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J. Floege has received speaker honoraria and grant support from Amgen. P. Boor and T. Ostendorf declare no competing interests.
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Boor, P., Ostendorf, T. & Floege, J. Renal fibrosis: novel insights into mechanisms and therapeutic _targets. Nat Rev Nephrol 6, 643–656 (2010). https://doi.org/10.1038/nrneph.2010.120
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DOI: https://doi.org/10.1038/nrneph.2010.120
