Critical Role of the NAD(P)H Oxidase Subunit p47 phox for Left Ventricular Remodeling/Dysfunction and Survival After Myocardial Infarction
Abstract
Accumulating evidence suggests a critical role of increased reactive oxygen species production for left ventricular (LV) remodeling and dysfunction after myocardial infarction (MI). An increased myocardial activity of the NAD(P)H oxidase, a major oxidant enzyme system, has been observed in human heart failure; however, the role of the NAD(P)H oxidase for LV remodeling and dysfunction after MI remains to be determined. MI was induced in wild-type (WT) mice (n=46) and mice lacking the cytosolic NAD(P)H oxidase component p47 phox (p47 phox −/− mice) (n=32). Infarct size was similar among the groups. NAD(P)H oxidase activity was markedly increased in remote LV myocardium of WT mice after MI as compared with sham-operated mice (83±8 versus 16.7±3.5 nmol of O 2 − · μg −1 ·min −1 ; P <0.01) but not in p47 phox −/− mice after MI (13.5±3.6 versus 15.5±3.5 nmol of O 2 − · μg −1 ·min −1 ), as assessed by electron-spin resonance spectroscopy using the spin probe CP-H. Furthermore, increased myocardial xanthine oxidase activity was observed in WT, but not in p47 phox −/− mice after MI, suggesting NAD(P)H oxidase–dependent xanthine oxidase activation. Myocardial reactive oxygen species production was increased in WT mice, but not in p47 phox −/− mice, after MI. LV cavity dilatation and dysfunction 4 weeks after MI were markedly attenuated in p47 phox −/− mice as compared with WT mice, as assessed by echocardiography (LV end-diastolic diameter: 4.5±0.2 versus 6.3±0.3 mm, P <0.01; LV ejection fraction, 35.8±2.5 versus 22.6±4.4%, P <0.05). Furthermore, cardiomyocyte hypertrophy, apoptosis, and interstitial fibrosis were substantially reduced in p47 phox −/− mice as compared with WT mice. Importantly, the survival rate was markedly higher in p47 phox −/− mice as compared with WT mice after MI (72% versus 48%; P <0.05). These results suggest a pivotal role of NAD(P)H oxidase activation and its subunit p47 phox for LV remodeling/dysfunction and survival after MI. The NAD(P)H oxidase system represents therefore a potential novel therapeutic target to prevent cardiac failure after MI.
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Deletion of the organizer subunit p47phox ameliorates the hypertensive response to angiotensin II, decreases endothelial superoxide formation and eNOS uncoupling, and improves survival after MI.
“The deletion of the organizer subunit p47phox ameliorates the hypertensive response to angiotensin II, decreases endothelial superoxide formation and eNOS uncoupling, and improves survival after MI (238, 549, 550).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [238]
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- Authors
- Doerries, C., Grote, K., Hilfiker-Kleiner, D., Luchtefeld, M., Schaefer, A., Holland, S. M., Sorrentino, S., Manes, C., Schieffer, B., Drexler, H., & Landmesser, U.
- Affiliations
- National Institutes of Health (US)
- From the Abteilung Kardiologie und Angiologie (C.D., K.G., D.H.-K., M.L., A.S., S.S., C.M., B.S., H.D., U.L.), Medizinische Hochschule Hannover, Germany; and Laboratory of Clinical Infectious Diseases (S.H.), National Institutes of Health, Bethesda, Md.
- Venue
- Circulation Research
- Published
- 2007-03-30
- Volume
- 100
- Issue
- 6
- Pages
- 894-903
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W1983889201
- Cited by
- 206
- References
- 61
- Citations by year
- 2025: 4 · 2024: 6 · 2023: 3 · 2022: 7 · 2021: 5 · 2020: 8 · 2019: 6 · 2018: 12 · 2017: 8 · 2016: 9 · 2015: 12 · 2014: 15 · 2013: 15 · 2012: 24
- FWCI
- 11.47
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- p47phox, NADPH oxidase, left ventricular remodeling, myocardial infarction, reactive oxygen species, xanthine oxidase, cardiomyocyte apoptosis, interstitial fibrosis, cardiomyocyte hypertrophy, infarct size, survival after myocardial infarction, heart failure, oxidative stress, cardiomyocyte death
- MeSH terms
- Animals, Disease Models, Animal, Electron Spin Resonance Spectroscopy, Enzyme Activation, Enzyme Inhibitors, Heart Function Tests, Myocardial Infarction, Myocardium, Nitric Oxide, Superoxides, Xanthine Oxidase, Survival Rate, Apoptosis, Mice, Knockout, Disease Progression, Ventricular Dysfunction, Left, NADPH Oxidases, Ventricular Remodeling, Matrix Metalloproteinase 2, Mice
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