IMR Press / FBL / Volume 14 / Issue 6 / DOI: 10.2741/3361

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

PAI-1 and kidney fibrosis
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1 Vanderbilt University Medical Center, Department of Pathology, Nashville, Tennessee, USA
Front. Biosci. (Landmark Ed) 2009, 14(6), 2028–2041;
Published: 1 January 2009

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-β), and novel molecules identified by proteomic analysis, such as thymosin- β4. 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.

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