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Potential Approaches to Reverse or Repair Renal Fibrosis

Overview
Journal Nat Rev Nephrol
Specialty Nephrology
Date 2014 Feb 12
PMID 24514753
Citations 90
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Abstract

The concept of reversing chronic kidney disease (CKD) has been intensively researched over the past decade. Indeed, as the prevalence of end-stage renal disease is constantly on the rise, the lack of established antifibrotic therapies is a considerable unmet need in clinical practice. Now, the possibility of effective antifibrotic treatment has been established in experimental models of CKD and multiple antifibrotic compounds-in kidney disease, as well as in fibrotic diseases of the skin, liver and lung-are being assessed in clinical trials. These strategies target various components of the fibrotic pathway, from signalling molecules that include transforming growth factor-β, phosphatidylinositide 3-kinase and chemokines to microRNAs. Here, we discuss therapeutic concepts to inhibit or even reverse chronic kidney injury and review the leading candidate antifibrotic drugs to be introduced to clinical use.

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References
1.
LeBleu V, Sugimoto H, Miller C, Gattone 2nd V, Kalluri R . Lymphocytes are dispensable for glomerulonephritis but required for renal interstitial fibrosis in matrix defect-induced Alport renal disease. Lab Invest. 2008; 88(3):284-92. DOI: 10.1038/labinvest.3700715. View

2.
Boffa J, Tharaux P, Dussaule J, Chatziantoniou C . Regression of renal vascular fibrosis by endothelin receptor antagonism. Hypertension. 2001; 37(2 Pt 2):490-6. DOI: 10.1161/01.hyp.37.2.490. View

3.
Barry-Hamilton V, Spangler R, Marshall D, McCauley S, Rodriguez H, Oyasu M . Allosteric inhibition of lysyl oxidase-like-2 impedes the development of a pathologic microenvironment. Nat Med. 2010; 16(9):1009-17. DOI: 10.1038/nm.2208. View

4.
Harris R, Neilson E . Toward a unified theory of renal progression. Annu Rev Med. 2006; 57:365-80. DOI: 10.1146/annurev.med.57.121304.131342. View

5.
Bechtel W, McGoohan S, Zeisberg E, Muller G, Kalbacher H, Salant D . Methylation determines fibroblast activation and fibrogenesis in the kidney. Nat Med. 2010; 16(5):544-50. PMC: 3106179. DOI: 10.1038/nm.2135. View