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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-1-24
pubmed:abstractText
Oxidative stress plays an important role in the development of cardiac remodeling after myocardial infarction (MI), but the sources of oxidative stress remain unclear. We investigated the role of Nox2-containing reduced nicotinamide-adenine dinucleotide phosphate oxidase in the development of cardiac remodeling after MI. Adult Nox2(-/-) and matched wild-type (WT) mice were subjected to coronary artery ligation and studied 4 weeks later. Infarct size after MI was similar in Nox2(-/-) and WT mice. Nox2(-/-) mice exhibited significantly less left ventricular (LV) cavity dilatation and dysfunction after MI than WT mice (eg, echocardiographic LV end-diastolic volume: 75.7+/-5.8 versus 112.4+/-12.3 microL; ejection fraction: 41.6+/-3.7 versus 32.9+/-3.2%; both P<0.05). Similarly, in vivo LV systolic and diastolic functions were better preserved in Nox2(-/-) than WT mice (eg, LV dP/dt(max): 7969+/-385 versus 5746+/-234 mm Hg/s; LV end-diastolic pressure: 12.2+/-1.3 versus 18.0+/-1.8 mm Hg; both P<0.05). Nox2(-/-) mice exhibited less cardiomyocyte hypertrophy, apoptosis, and interstitial fibrosis; reduced increases in expression of connective tissue growth factor and procollagen 1 mRNA; and smaller increases in myocardial matrix metalloproteinase-2 activity than WT mice. These data suggest that the Nox2-containing reduced nicotinamide-adenine dinucleotide phosphate oxidase contributes significantly to the processes underlying adverse cardiac remodeling and contractile dysfunction post-MI.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
319-25
pubmed:meshHeading
pubmed-meshheading:18180403-Animals, pubmed-meshheading:18180403-Apoptosis, pubmed-meshheading:18180403-Cardiomegaly, pubmed-meshheading:18180403-Echocardiography, pubmed-meshheading:18180403-Fibrosis, pubmed-meshheading:18180403-Heart Catheterization, pubmed-meshheading:18180403-Matrix Metalloproteinase 2, pubmed-meshheading:18180403-Membrane Glycoproteins, pubmed-meshheading:18180403-Mice, pubmed-meshheading:18180403-Mice, Knockout, pubmed-meshheading:18180403-Myocardial Infarction, pubmed-meshheading:18180403-Myocardium, pubmed-meshheading:18180403-NADPH Oxidase, pubmed-meshheading:18180403-RNA, Messenger, pubmed-meshheading:18180403-Staining and Labeling, pubmed-meshheading:18180403-Survival Analysis, pubmed-meshheading:18180403-Tyrosine, pubmed-meshheading:18180403-Ventricular Remodeling
pubmed:year
2008
pubmed:articleTitle
Involvement of Nox2 NADPH oxidase in adverse cardiac remodeling after myocardial infarction.
pubmed:affiliation
Department of Cardiology, King's College London School of Medicine, James Black Centre, 125 Coldharbour Ln, London SE5 9NU, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't