Involvement of Nox2 NADPH Oxidase in Adverse Cardiac Remodeling After Myocardial Infarction

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 cardia...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2008-02, Vol.51 (2), p.319-325
Main Authors: Looi, Yee H, Grieve, David J, Siva, Anjana, Walker, Simon J, Anilkumar, Narayana, Cave, Alison C, Marber, Michael, Monaghan, Mark J, Shah, Ajay M
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Cardiac Catheterization
Cardiology. Vascular system
Cardiomegaly - etiology
Cardiomegaly - metabolism
Echocardiography
Fibrosis
Heart
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
Matrix Metalloproteinase 2 - genetics
Medical sciences
Membrane Glycoproteins - deficiency
Membrane Glycoproteins - genetics
Membrane Glycoproteins - metabolism
Mice
Mice, Knockout
Myocardial Infarction - complications
Myocardial Infarction - diagnosis
Myocardial Infarction - pathology
Myocardial Infarction - physiopathology
Myocardium - metabolism
Myocardium - pathology
NADPH Oxidase 2
NADPH Oxidase 4
NADPH Oxidases - deficiency
NADPH Oxidases - genetics
NADPH Oxidases - metabolism
RNA, Messenger - metabolism
Staining and Labeling
Survival Analysis
Tyrosine - analogs & derivatives
Tyrosine - metabolism
Ventricular Remodeling
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Summary: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 volume75.7±5.8 versus 112.4±12.3 μL; ejection fraction41.6±3.7 versus 32.9±3.2%; both P
ISSN:0194-911X
1524-4563
DOI:10.1161/HYPERTENSIONAHA.107.101980