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Updated: May 6, 2026

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
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Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

Published on: December 8, 2013

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p47phox is required for atherosclerotic lesion progression in ApoE(-/-) mice

P A Barry-Lane1, C Patterson, M van der Merwe

  • 1Sealy Center for Molecular Cardiology, University of Texas Medical Branch, Galveston, Texas, USA.

The Journal of Clinical Investigation
|November 21, 2001
PubMed

Insights

NADPH oxidase activity, a source of reactive oxygen species (ROS), drives smooth muscle cell proliferation and atherosclerotic lesion formation. Inhibiting this enzyme reduces lesion development in mice, highlighting its role in vascular disease.

Area of Science:

  • Biochemistry
  • Cardiovascular Biology
  • Immunology

Background:

  • NADPH oxidase (NOX) is upregulated in smooth muscle cells (SMCs) upon growth factor stimulation, increasing reactive oxygen species (ROS) production.
  • ROS generated by NOX play a role in SMC proliferation and vascular disease pathogenesis.

Purpose of the Study:

  • To investigate the role of ROS produced by NADPH oxidase in SMC responses to growth factors.
  • To determine the contribution of NADPH oxidase-derived ROS to atherosclerotic lesion formation in apolipoprotein E-deficient (ApoE(-/-)) mice.

Main Methods:

  • Compared growth factor responsiveness and ROS generation in SMCs from wild-type, p47phox(-/-), and gp91phox(-/-) mice.
  • Assessed atherosclerotic lesion formation in genetically modified mice (wild-type, p47phox(-/-), ApoE(-/-), and ApoE(-/-)/p47phox(-/-)) fed standard or high-fat diets.

Main Results:

  • p47phox(-/-) SMCs exhibited diminished superoxide production and reduced proliferative response to growth factors compared to wild-type SMCs.
  • ApoE(-/-)/p47phox(-/-) mice displayed significantly reduced atherosclerotic lesion areas compared to ApoE(-/-) mice.
  • gp91phox(-/-) SMC response was similar to wild-type, suggesting p47phox subunit is critical for NOX-driven SMC proliferation.

Conclusions:

  • Superoxide generation by NADPH oxidase is essential for atherosclerotic lesion development.
  • These findings support a critical role for NADPH oxidase activity in vascular lesion formation and suggest potential therapeutic targets.

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