Exploring the connection between chronic renal fibrosis and bone morphogenic protein-7

R. Kalluri and M. Zeisberg

Program in Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, USA

Offprint requests to: Dr. Raghu Kalluri, Associate Professor of Medicine, Harvard Medical School, Program in Matrix Biology, Department of Medicine, Dana 514, Beth Israel Deaconess Medical Center, 330 Brookline Avenue. Boston, MA 02215, USA. Fax: 617-667-2562. e-mail: rkalluri@caregroup.harvard.edu

 

Summary. Tubulointerstitial fibrosis is a hallmark feature of chronic renal injury. Specific therapies to control the progression of renal fibrosis towards end-stage renal failure are still limited. Transforming growth factor-ß1 (TGF-ß1) has been identified as a major mediator of renal fibrosis. Recent reports have suggested that Bone Morphogenic Protein-7 (BMP-7), another member of the TGF-ß superfamily, accelerates repair of acute renal injury and ameliorates progression of chronic renal fibrosis in a variety of animal models. Interestingly, BMP-7, an endogenous molecule which is present in the normal kidney, vastly decreases its expression during renal injury. Although, the mechanism of BMP-7 action in the kidney is not yet fully understood, the idea of an endogenous molecule with reno-protective function is intriguing. Histol. Histopathol. Volume 18, 217-228 (2003)

Key words: Bone Morphogenic Protein-7 (BMP-7), Osteogenic Protein-1 (OP-1), Transforming Growth Factor-ß1 (TGF-ß1), Renal Fibrosis, Tubular Epithelial Cells (TECs)

DOI: 10.14670/HH-18.217