Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 하헌주 | * |
dc.date.accessioned | 2016-10-15T01:10:21Z | - |
dc.date.available | 2016-10-15T01:10:21Z | - |
dc.date.issued | 2009 | * |
dc.identifier.issn | 1759-5061 | * |
dc.identifier.other | OAK-5601 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/232411 | - |
dc.description.abstract | The 50 kDa glycoprotein plasminogen activator inhibitor 1 (PAI-1) is the major physiological inhibitor of tissue-type and urokinase-type plasminogen activator. These two molecules convert inactive plasminogen into its fibrin-degrading form, plasmin. Plasma and tissue concentrations of PAI-1 are extremely low under normal circumstances but increase under pathologic conditions. This increase is mediated by many factors, including reactive oxygen species. Increased PAI-1 activity is associated with an increased risk of ischemic cardiovascular events and tissue fibrosis. Whereas the antifibrinolytic property of PAI-1 derives mainly from its inhibition of serine proteases, its profibrotic actions seem to derive from a capacity to stimulate interstitial macrophage recruitment and increase transcription of profibrotic genes, as well as from inhibition of serine proteases. Despite studies in mice that lack or overexpress PAI-1, the biological effects of this molecule in humans remain incompletely understood because of the complexity of the PAI-1-plasminogen- activator-plasmin system. The cardioprotective and renoprotective properties of some currently available drugs might be attributable in part to inhibition of PAI-1. The development of an orally active, high-affinity PAI-1 inhibitor will provide a potentially important pharmacological tool for further investigation of the role of PAI-1 and might offer a novel therapeutic strategy in renal and cardiovascular diseases. © 2009 Macmillan Publishers Limited. All rights reserved. | * |
dc.language | English | * |
dc.title | The role of plasminogen activator inhibitor 1 in renal and cardiovascular diseases | * |
dc.type | Review | * |
dc.relation.issue | 4 | * |
dc.relation.volume | 5 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 203 | * |
dc.relation.lastpage | 211 | * |
dc.relation.journaltitle | Nature Reviews Nephrology | * |
dc.identifier.doi | 10.1038/nrneph.2009.15 | * |
dc.identifier.wosid | WOS:000265854400008 | * |
dc.identifier.scopusid | 2-s2.0-67049167761 | * |
dc.author.google | Ha H. | * |
dc.author.google | Oh E.Y. | * |
dc.author.google | Lee H.B. | * |
dc.contributor.scopusid | 하헌주(7202277106) | * |
dc.date.modifydate | 20240422113229 | * |