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Front Biosci (Landmark Ed). 2009 Jan 1;14:2028-41.

PAI-1 and kidney fibrosis.

Author information

1
Vanderbilt University Medical Center, Department of Pathology, Nashville, Tennessee, USA.

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.

PMID:
19273183
PMCID:
PMC4848749
DOI:
10.2741/3361
[Indexed for MEDLINE]
Free PMC Article

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