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Recapitulation of kidney development paradigms by BMP-7 reverses chronic renal injury

Recapitulation of kidney development paradigms by BMP-7 reverses chronic renal injury Clin Exp Nephrol (2005) 9:100–101 © Japanese Society of Nephrology 2005 DOI 10.1007/s10157-005-0360-0 REVIEW ARTICLE Hirokazu Okada · Raghu Kalluri Recapitulation of kidney development paradigms by BMP-7 reverses chronic renal injury Received: December 8, 2004 / Accepted: March 25, 2005 Key words Bone morphogenic protein-7 · Fibrogenesis · release of proinflammatory/fibrogenic cytokines from tubu- Epithelial-mesenchymal transition lar epithelial cells, reverses epithelial-mesenchymal transi- tion (EMT), and inhibits renal tubular cell apoptosis, to 3,12,17 restore or repair normal renal architecture. Molecular understanding and the control of chronic renal In relation to EMT, intracellular pathways are, as yet, disease progression still represent a major challenge for only partially identified. BMP-7 binds to the Alk3 and Alk6 scientists and clinicians. A number of recent experimental type I serine/threonine kinase receptors, which function via strategies suggest that improvement of renal function and the phosphorylation of Smad1, Smad5, and Smad8, leading 2–5 architectural integrity is potentially feasible. Chronic to an increase in E-cadherin expression in renal tubular renal diseases are characterized by interstitial fibrosis, 8,18 cells. On the other hand, TGF-b binds to Alk5 receptor which is a morphological and functional predictor tightly and activates Smad2 and Smad3, decreasing the expression linked to the survival http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical and Experimental Nephrology Springer Journals

Recapitulation of kidney development paradigms by BMP-7 reverses chronic renal injury

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References (21)

Publisher
Springer Journals
Copyright
Copyright © 2005 by Japanese Society of Nephrology
Subject
Medicine & Public Health; Nephrology; Urology
ISSN
1342-1751
eISSN
1437-7799
DOI
10.1007/s10157-005-0360-0
pmid
15980942
Publisher site
See Article on Publisher Site

Abstract

Clin Exp Nephrol (2005) 9:100–101 © Japanese Society of Nephrology 2005 DOI 10.1007/s10157-005-0360-0 REVIEW ARTICLE Hirokazu Okada · Raghu Kalluri Recapitulation of kidney development paradigms by BMP-7 reverses chronic renal injury Received: December 8, 2004 / Accepted: March 25, 2005 Key words Bone morphogenic protein-7 · Fibrogenesis · release of proinflammatory/fibrogenic cytokines from tubu- Epithelial-mesenchymal transition lar epithelial cells, reverses epithelial-mesenchymal transi- tion (EMT), and inhibits renal tubular cell apoptosis, to 3,12,17 restore or repair normal renal architecture. Molecular understanding and the control of chronic renal In relation to EMT, intracellular pathways are, as yet, disease progression still represent a major challenge for only partially identified. BMP-7 binds to the Alk3 and Alk6 scientists and clinicians. A number of recent experimental type I serine/threonine kinase receptors, which function via strategies suggest that improvement of renal function and the phosphorylation of Smad1, Smad5, and Smad8, leading 2–5 architectural integrity is potentially feasible. Chronic to an increase in E-cadherin expression in renal tubular renal diseases are characterized by interstitial fibrosis, 8,18 cells. On the other hand, TGF-b binds to Alk5 receptor which is a morphological and functional predictor tightly and activates Smad2 and Smad3, decreasing the expression linked to the survival

Journal

Clinical and Experimental NephrologySpringer Journals

Published: Jan 1, 2005

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