Aldosterone and PAI-1: Implications for renal injury

Nancy J. Brown*, Douglas E. Vaughan, Agnes B. Fogo

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

35 Scopus citations

Abstract

Aldosterone modulates cardiovascular and renal injury and fibrosis in animal models. This review explores the hypothesis that aldosterone causes injury and fibrosis, in part, through effects on plasminogen activator inhibitor-1, the major physiological inhibitor of plasminogen activators in vivo. Aldosterone interacts with angiotensin II to increase plasminogen activator inhibitor-1 expression in vitro and in vivo. Plasminogen activator inhibitor-1, by inhibiting the production of plasmin from plasminogen, tips the balance in favor of extracellular matrix accumulation and promotes fibrosis. Aldosterone receptor antagonism decreases both PAI-1 expression and fibrosis in animal models. These findings have implications for the clinical management of cardiovascular and renal disease.

Original languageEnglish (US)
Pages (from-to)230-235
Number of pages6
JournalJournal of Nephrology
Volume15
Issue number3
StatePublished - 2002

Keywords

  • Aldosterone
  • Angiotensin converting enzyme inhibitor
  • Fibrosis
  • Plasminogen activator inhibitor-1

ASJC Scopus subject areas

  • Nephrology

Fingerprint Dive into the research topics of 'Aldosterone and PAI-1: Implications for renal injury'. Together they form a unique fingerprint.

Cite this