Exploring the connection between chronic renal fibrosis and bone morphogenic protein-7.
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-beta1 (TGF-beta1) 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-beta 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.
Kalluri
R
R
Harvard Medical School, Program in Matrix Biology, Department of Medicine, Dana 514, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215, USA. rkalluri@caregroup.harvard.edu
Zeisberg
M
M
D000818:Animals; D055419:Bone Morphogenetic Protein 7; D019485:Bone Morphogenetic Proteins / Q000502:physiology*; D005355:Fibrosis / Q000209:etiology / Q000473:pathology*; D006801:Humans; D007668:Kidney / Q000473:pathology*; D007674:Kidney Diseases / Q000209:etiology / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000503:physiopathology; D051379:Mice; D016212:Transforming Growth Factor beta
C525819:BMP7 protein, human; D055419:Bone Morphogenetic Protein 7; D019485:Bone Morphogenetic Proteins; D016212:Transforming Growth Factor beta