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Bioluminescence Imaging of NADPH Oxidase Activity in Different Animal Models
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Bioluminescence Imaging of NADPH Oxidase Activity in Different Animal Models

Published on: October 22, 2012

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NADPH oxidase 4 protects against development of endothelial dysfunction and atherosclerosis in LDL receptor deficient

Heike Langbein1, Coy Brunssen1, Anja Hofmann1

  • 1Division of Vascular Endothelium and Microcirculation, Department of Medicine III, University Hospital Carl Gustav Carus Dresden, Technische Universität Dresden, Fetscherstr. 74, 01307 Dresden, Germany.

European Heart Journal
|November 19, 2015
PubMed
Abstract

Insights

Genetic deletion of Nox4 worsens endothelial dysfunction and atherosclerosis. Loss of Nox4-derived hydrogen peroxide (H2O2) leads to severe endothelial dysfunction and increased plaque burden in mice.

Area of Science:

  • Cardiovascular Biology
  • Oxidative Stress
  • Atherosclerosis Research

Background:

  • Endothelial dysfunction is a key early event in atherosclerosis development.
  • NADPH oxidases (Nox) 1, 2, and 5 contribute to dysfunction by reducing nitric oxide.
  • Nox4, the main endothelial isoform, produces hydrogen peroxide (H2O2) with a vasoprotective role.

Purpose of the Study:

  • To investigate the impact of genetic Nox4 deletion on endothelial dysfunction.
  • To assess the role of Nox4 in the development of atherosclerosis in a mouse model.

Main Methods:

  • Utilized the low-density lipoprotein receptor (Ldlr) knockout mouse model.
  • Assessed ex vivo endothelial function using Mulvany myography.
  • Analyzed in vivo endothelial function via optical coherence tomography (OCT) for flow-mediated dilation.

Main Results:

  • Nox4(-/-)/Ldlr(-/-) mice exhibited impaired endothelial function and increased atherosclerotic plaque burden compared to Ldlr(-/-) controls.
  • High-fat diet exacerbated endothelial dysfunction and atherosclerosis in Nox4-deficient mice.
  • In vivo analysis revealed altered flow-mediated dilation in Nox4(-/-) mice, highlighting Nox4's role in peripheral arteries.

Conclusions:

  • Nox4 is crucial for maintaining endothelial function in both physiological and pathological states.
  • While nNOS upregulation can partially compensate for H2O2 loss, severe endothelial dysfunction and accelerated atherosclerosis occur without Nox4.
  • Genetic deletion of Nox4 significantly contributes to endothelial dysfunction and promotes atherosclerosis progression.
Keywords:
AtherosclerosisEndothelial dysfunctionFlow-mediated dilationLdlr−/− miceNADPH oxidase 4Nox4

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