PAI-1 and kidney fibrosis

Front Biosci (Landmark Ed). 2009 Jan 1;14(6):2028-41. doi: 10.2741/3361.


Substantial evidence demonstrates a link of increased plasminogen activator inhibitor-1 (PAI-1) and glomerulosclerosis and kidney fibrosis, providing a novel therapeutic option for prevention and treatment of chronic kidney diseases. Several mechanisms contributing to increased PAI-1 will be addressed, including classic key profibrotic factors such as the renin-angiotensin-system (RAS) and transforming growth factor-beta (TGF-b???and novel molecules identified by proteomic analysis, such as thymosin- b4. The fibrotic sequelae caused by increased PAI-1 in kidney depend not only on its classic inhibition of tissue-type and urokinase-type plasminogen activators (tPA and uPA), but also its influence on cell migration.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Angiotensins / physiology
  • Animals
  • Chronic Disease
  • Disease Models, Animal
  • Fibrosis
  • Humans
  • Kidney Diseases / metabolism
  • Kidney Diseases / physiopathology*
  • Mice
  • Oligopeptides / physiology
  • Organ Specificity
  • Plasminogen Activator Inhibitor 1 / physiology*
  • Renin-Angiotensin System
  • Thymosin / physiology
  • Transforming Growth Factor beta1 / physiology


  • Angiotensins
  • Oligopeptides
  • Plasminogen Activator Inhibitor 1
  • Transforming Growth Factor beta1
  • thymosin beta(4)
  • Thymosin
  • goralatide