PAI-1 and kidney fibrosis
Copyright policy )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.
- Vanderbilt University Medical Center United States
Angiotensins, Fibrosis, Renin-Angiotensin System, Thymosin, Transforming Growth Factor beta1, Disease Models, Animal, Mice, Organ Specificity, Chronic Disease, Plasminogen Activator Inhibitor 1, Animals, Humans, Kidney Diseases, Oligopeptides
Angiotensins, Fibrosis, Renin-Angiotensin System, Thymosin, Transforming Growth Factor beta1, Disease Models, Animal, Mice, Organ Specificity, Chronic Disease, Plasminogen Activator Inhibitor 1, Animals, Humans, Kidney Diseases, Oligopeptides
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