| Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure. | |
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MedLine Citation:
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PMID: 10502816 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Cardiac rupture is a fatal complication of acute myocardial infarction lacking treatment. Here, acute myocardial infarction resulted in rupture in wild-type mice and in mice lacking tissue-type plasminogen activator, urokinase receptor, matrix metalloproteinase stromelysin-1 or metalloelastase. Instead, deficiency of urokinase-type plasminogen activator (u-PA-/-) completely protected against rupture, whereas lack of gelatinase-B partially protected against rupture. However, u-PA-/- mice showed impaired scar formation and infarct revascularization, even after treatment with vascular endothelial growth factor, and died of cardiac failure due to depressed contractility, arrhythmias and ischemia. Temporary administration of PA inhibitor-1 or the matrix metalloproteinase-inhibitor TIMP-1 completely protected wild-type mice against rupture but did not abort infarct healing, thus constituting a new approach to prevent cardiac rupture after acute myocardial infarction. |
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Authors:
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S Heymans; A Luttun; D Nuyens; G Theilmeier; E Creemers; L Moons; G D Dyspersin; J P Cleutjens; M Shipley; A Angellilo; M Levi; O Nübe; A Baker; E Keshet; F Lupu; J M Herbert; J F Smits; S D Shapiro; M Baes; M Borgers; D Collen; M J Daemen; P Carmeliet |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Nature medicine Volume: 5 ISSN: 1078-8956 ISO Abbreviation: Nat. Med. Publication Date: 1999 Oct |
Date Detail:
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Created Date: 1999-10-21 Completed Date: 1999-10-21 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9502015 Medline TA: Nat Med Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1135-42 Citation Subset: IM |
Affiliation:
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Center for Transgene Technology, Flanders Interuniversity, Leuven, Belgium. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arrhythmias, Cardiac Bone Marrow Transplantation Cardiac Output, Low / etiology* Cell Movement Collagenases / metabolism Gene Transfer Techniques Heart Rupture / etiology* Leukocytes / cytology, metabolism Matrix Metalloproteinase 3 / genetics Matrix Metalloproteinase 9 Metalloendopeptidases / antagonists & inhibitors* Mice Mice, Mutant Strains Myocardial Infarction / complications*, drug therapy* Neovascularization, Physiologic / drug effects Plasminogen Activator Inhibitor 1 / genetics, metabolism Plasminogen Activators / genetics Plasminogen Inactivators / therapeutic use* Protease Inhibitors / therapeutic use* Tissue Inhibitor of Metalloproteinase-1 / genetics, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Plasminogen Activator Inhibitor 1; 0/Plasminogen Inactivators; 0/Protease Inhibitors; 0/Tissue Inhibitor of Metalloproteinase-1; EC 3.4.21.-/Plasminogen Activators; EC 3.4.24.-/Collagenases; EC 3.4.24.-/Metalloendopeptidases; EC 3.4.24.17/Matrix Metalloproteinase 3; EC 3.4.24.35/Matrix Metalloproteinase 9 |
| Comments/Corrections | |
Comment In:
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Nat Med. 1999 Oct;5(10):1122-3
[PMID:
10502807
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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