PAI-1 and kidney fibrosis.

Ma LJ, Fogo AB
Front Biosci (Landmark Ed). 2009 14: 2028-41

PMID: 19273183 · PMCID: PMC4848749 · 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.

MeSH Terms (14)

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

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