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

Histol Histopathol. 2003 Jan;18(1):217-24. doi: 10.14670/HH-18.217.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Bone Morphogenetic Protein 7
  • Bone Morphogenetic Proteins / physiology*
  • Fibrosis / etiology
  • Fibrosis / pathology*
  • Humans
  • Kidney / pathology*
  • Kidney Diseases / etiology
  • Kidney Diseases / physiopathology*
  • Kidney Failure, Chronic / physiopathology
  • Mice
  • Transforming Growth Factor beta*

Substances

  • BMP7 protein, human
  • Bone Morphogenetic Protein 7
  • Bone Morphogenetic Proteins
  • Transforming Growth Factor beta