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PMID: 19273183 Published · epublish English Journal Article Research Support, N.I.H., Extramural Review

PAI-1 and kidney fibrosis.

Frontiers in bioscience (Landmark edition) ·Vol. 14 ·2009-01-01 ·Pages 2028-41

Ma LJ, Fogo AB

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.

MeSH Terms
Angiotensins/physiology Animals Chronic Disease Disease Models, Animal Fibrosis Humans Kidney Diseases/metabolism,physiopathology Mice Oligopeptides/physiology Organ Specificity Plasminogen Activator Inhibitor 1/physiology Renin-Angiotensin System Thymosin/physiology Transforming Growth Factor beta1/physiology
Chemicals
Angiotensins Oligopeptides Plasminogen Activator Inhibitor 1 Transforming Growth Factor beta1 thymosin beta(4) Thymosin goralatide
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Ma Li-Jun
Vanderbilt University Medical Center, Department of Pathology, Nashville, Tennessee, USA.
Fogo Agnes B
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Article Info
Journal
Frontiers in bioscience (Landmark edition)
Abbr.
Front Biosci (Landmark Ed)
ISSN
2768-6698
Published
2009-01-01
Epub
2009-00-01
Pages
2028-41
Language
English
Region
Singapore
NLM ID
101612996
PMCID
PMC4848749
Subset
IM
Grants
NIDDK NIH HHS · P50 DK044757 · United States
NIDDK NIH HHS · R01 DK056942 · United States
NIDDK NIH HHS · DK44757 · United States
NIDDK NIH HHS · DK56942 · United States
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