4.5 Review

PAI-1 and kidney fibrosis

Journal

FRONTIERS IN BIOSCIENCE-LANDMARK
Volume 14, Issue -, Pages 2028-2041

Publisher

BIOSCIENCE RESEARCH INST-BRI
DOI: 10.2741/3361

Keywords

PAI-1; kidney; EMT; angiotensin; aldosterone; thymosin beta-4; Review

Funding

  1. National Institutes of Health [DK56942, DK44757]
  2. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P50DK044757, R01DK056942] Funding Source: NIH RePORTER

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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-beta), and novel molecules identified by proteomic analysis, such as thymosin-beta 4. 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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