PAI-1 and kidney fibrosis.
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.
Ma
Li-Jun
LJ
Vanderbilt University Medical Center, Department of Pathology, Nashville, Tennessee, USA.
Fogo
Agnes B
AB
D000809:Angiotensins / Q000502:physiology; D000818:Animals; D002908:Chronic Disease; D004195:Disease Models, Animal; D005355:Fibrosis; D006801:Humans; D007674:Kidney Diseases / Q000378:metabolism / Q000503:physiopathology*; D051379:Mice; D009842:Oligopeptides / Q000502:physiology; D009928:Organ Specificity; D017395:Plasminogen Activator Inhibitor 1 / Q000502:physiology*; D012084:Renin-Angiotensin System; D013947:Thymosin / Q000502:physiology; D053773:Transforming Growth Factor beta1 / Q000502:physiology; D000099201:Thymosin beta(4)
D000809:Angiotensins; D009842:Oligopeptides; D017395:Plasminogen Activator Inhibitor 1; D013947:Thymosin; D053773:Transforming Growth Factor beta1; D000099201:Thymosin beta(4); C058504:goralatide