Nephrol Dial Transplant (2004) 19: 759-761
Nephrol Dial Transplant Vol. 19 No. 4 © ERA-EDTA 2004; all rights reserved
Editorial Comment
Are there endogenous molecules that protect kidneys from injury? The case for bone morphogenic protein-7 (BMP-7)
1Center for Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, USA and 2Department of Nephrology and Rheumatology, Georg-August University Medical Center, Göttingen, Germany
Correspondence and offprint requests to: Dr Raghu Kalluri, Harvard Medical School, Center for Matrix Biology, DANA 514, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215, USA. Email: rkalluri@bidmc.harvard.edu
Keywords: chronic renal fibrosis; epithelial-to-mesenchymal transition (EMT); TGF-beta1; therapy; type 1 collagen
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Introduction |
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Injury to the kidney can be initiated via diverse mechanisms, such as genetic defects, autoimmune reactions, environmental insults and metabolic defects [1,2]. Based on the kinetics of disease progression, renal injury is traditionally grouped as either being an acute or chronic effect [3,4]. While the kidney displays an enormous potential to regenerate after acute renal injury, chronic renal disease is generally irreversible [1,5,6]. The switch from the normal potential to repair after acute injury, to an irreversible chronic disease phase, is not yet well understood. It has been
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Transforming growth factor-ß1 (TGF-ß1) |
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Bone morphogenic protein-7 (BMP-7) |
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Conclusion |
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