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March 14, 2014Clinical Science

Loss of NOX2 prevented the increase in oxidative stress, cardiomyocyte hypertrophy, myocardial fibrosis, and protected against diastolic and systolic dysfunction in response to pressure overload.

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Why the study?

Does loss of NOX2 prevent oxidative stress and progression to advanced heart failure in a pressure-overload model?

Population

Human dilated cardiomyopathy samples and mice subjected to a pressure-overload model of advanced heart failure

Comparison

Loss of NOX2 (NOX2-deficient mice) vs Wild-type mice subjected to pressure overload

Design

Preclinical

Authors

NPNirmal ParajuliHenry Ford Health SystemVPVaibhav B. PatelUniversity of CalgaryWWWang WangNanchang University

Discussion

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Member takes

Overview

NOX2 merits further study as HF target; hypothesis-generating in animals and should not change practice.

Structured PICO

Does loss of NOX2 prevent oxidative stress and progression to advanced heart failure in a pressure-overload model?

P
Population
Human dilated cardiomyopathy samples and mice subjected to a pressure-overload model of advanced heart failure
I
Intervention
Loss of NOX2 (NOX2-deficient mice)
C
Comparator
Wild-type mice subjected to pressure overload
O
Outcome
Oxidative stress, cardiomyocyte hypertrophy, myocardial fibrosis, and cardiac dysfunction (diastolic and systolic)surrogate

Loss of NOX2 prevents oxidative stress and adverse remodeling in pressure-overload heart failure, highlighting NOX2 as a potential therapeutic target.

Cite This Study

Parajuli et al. (2014) studied this question.

synapsesocial.com/papers/6a7132edf44fa9f079defab6https://doi.org/10.1042/cs20130787
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Involvement of Nox2 NADPH Oxidase in Adverse Cardiac Remodeling After Myocardial Infarction2008 · 252 citations
  2. 2Cell-specific effects of Nox2 on the acute and chronic response to myocardial infarction2016 · 51 citations
  3. 3The Dual Role of NOX4 in Cardiovascular Diseases: Driver of Oxidative Stress and Mediator of Adaptive Remodeling2025 · 15 citations
  4. 4Loss of p47 <sup>phox</sup> Subunit Enhances Susceptibility to Biomechanical Stress and Heart Failure Because of Dysregulation of Cortactin and Actin Filaments2013 · 51 citations
  5. 5Ca 2+ -Dependent NOX5 (NADPH Oxidase 5) Exaggerates Cardiac Hypertrophy Through Reactive Oxygen Species Production2020 · 65 citations