Transforming growth factor-beta in human glomerular injury

Curr Opin Nephrol Hypertens. 1997 Jul;6(4):389-93. doi: 10.1097/00041552-199707000-00014.

Abstract

Overexpression of the cytokine transforming growth factor-beta has been identified as the key mediator of chronic progressive kidney fibrosis in experimental and human kidney diseases. The renoprotective effects of angiotensin II blockade and low-protein diets have recently been linked to downregulation of transforming growth factor-beta production. Neutralizing the actions of transforming growth factor-beta by decorin gene therapy appears to be a highly effective new approach in the treatment of renal fibrosis.

Publication types

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

MeSH terms

  • Angiotensin II / antagonists & inhibitors
  • Animals
  • Decorin
  • Extracellular Matrix Proteins
  • Genetic Therapy
  • Humans
  • Kidney Diseases / etiology
  • Kidney Diseases / physiopathology
  • Kidney Diseases / therapy
  • Kidney Glomerulus / injuries*
  • Proteoglycans / genetics
  • Proteoglycans / therapeutic use
  • Transforming Growth Factor beta / antagonists & inhibitors
  • Transforming Growth Factor beta / physiology*

Substances

  • DCN protein, human
  • Decorin
  • Extracellular Matrix Proteins
  • Proteoglycans
  • Transforming Growth Factor beta
  • Angiotensin II