Open Access
Article
PAI-1 and kidney fibrosis
Li-Jun Ma1,Agnes B Fogo1
1
Vanderbilt University Medical Center, Department of Pathology, Nashville, Tennessee, USA
DOI: 10.2741/3361 Volume 14 Issue 6, pp.2028-2041
Published: 01 January 2009
(This article belongs to the Special Issue New insights into the pathogenesis and therapeutics of renal fibrosis)
Abstract

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.

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Li-Jun Ma, Agnes B Fogo. PAI-1 and kidney fibrosis. Frontiers in Bioscience-Landmark. 2009. 14(6); 2028-2041.