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March 1, 2007Circulation Research

Critical Role of the NAD(P)H Oxidase Subunit p47 phox for Left Ventricular Remodeling/Dysfunction and Survival After Myocardial Infarction

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Why the study?

Does genetic deletion of p47(phox) improve left ventricular remodeling, dysfunction, and survival after myocardial infarction in mice?

Population

Wild-type mice and mice lacking the cytosolic NADH oxidase component p47 (p47-/- mice) with induced…

Comparison

Genetic deletion of p47(phox) (p47(phox)-/- mice) vs Wild-type (WT) mice

Design

Preclinical

Follow-up

4 weeks

Authors

CDCarola DoerriesKGKarsten GroteDHDenise Hilfiker‐Kleiner

Discussion

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Overview

Supports p47(phox) targeting in post-MI remodeling; hypothesis-generating in mice and untested clinically.

Structured PICO

Does genetic deletion of p47(phox) improve left ventricular remodeling, dysfunction, and survival after myocardial infarction in mice?

P
Population
Wild-type (WT) mice (n=46) and mice lacking the cytosolic NAD(P)H oxidase component p47(phox) (p47(phox)-/- mice) (n=32) with induced myocardial infarction.
I
Intervention
Genetic deletion of p47(phox) (p47(phox)-/- mice)
C
Comparator
Wild-type (WT) mice
O
Outcome
Left ventricular remodeling/dysfunction (LV end-diastolic diameter, LV ejection fraction) at 4 weeks and survival ratesurrogate

Genetic deletion of the NAD(P)H oxidase subunit p47(phox) attenuates left ventricular remodeling and dysfunction and improves survival after myocardial infarction in mice, suggesting it as a potential therapeutic target.

Cite This Study

Doerries et al. (2007) studied this question.

synapsesocial.com/papers/6a712d6ae5469ee92be1c838https://doi.org/10.1161/01.res.0000261657.76299.ff
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