Role for Nox1 NADPH oxidase in atherosclerosis
Related Experiment Video
Updated: Jun 3, 2026

ROS Live Cell Imaging During Neuronal Development
Published on: February 9, 2021
Andrea L Sheehan1, Samuel Carrell, Bryon Johnson
1Department of Internal Medicine, The University of Iowa, Iowa City, IA 52242, United States.
Objective:
Examine the contribution of Nox1 NADPH oxidase to atherogenesis.
Methods And Results:
Male apolipoprotein E deficient mice (ApoE(-/-)) and male mice deficient in both apolipoprotein E and Nox1 (ApoE(-/-) Nox1(-/y)) received an atherogenic diet for 18 weeks. Mean blood pressures, body weights, and serum cholesterol levels were similar between the two groups of mice. Deficiency of Nox1 decreased superoxide levels and reduced lesion area in the aortic arch from 43% (ApoE(-/-)) to 28% (ApoE(-/-) Nox1(-/y)). The reduction in lesion size at the level of the aortic valve in ApoE(-/-)/Nox1(-/y) was accompanied by a decrease in macrophage infiltration as compared to ApoE(-/-) mice. Carotid artery ligation in ApoE(-/-) mice induced accelerated intimal hyperplasia with decreased cellular proliferation and increased collagen content in the neointima of vessels deficient in Nox1.
Conclusions:
Nox1-derived ROS modify lesion composition and contribute to lesion size in a murine model of atherosclerosis.
Insights
Nox1 NADPH oxidase contributes to atherosclerosis by increasing superoxide levels and lesion size. Its deficiency in mice reduced atherosclerotic lesions and macrophage infiltration, indicating its role in disease progression.
Area of Science:
- Cardiovascular Research
- Oxidative Stress Biology
- Molecular Medicine
Background:
- Atherosclerosis is a chronic inflammatory disease of arteries.
- NADPH oxidases (Nox) are implicated in oxidative stress and cardiovascular pathology.
- Nox1's specific role in atherogenesis requires further elucidation.
Purpose of the Study:
- To investigate the contribution of Nox1 NADPH oxidase to the development of atherosclerosis.
- To determine the impact of Nox1 deficiency on atherosclerotic lesion characteristics in a mouse model.
Main Methods:
- Apolipoprotein E-deficient mice (ApoE(-/-)) and dual-deficient ApoE(-/-) Nox1(-/y) mice were fed an atherogenic diet for 18 weeks.
- Superoxide levels, lesion area, macrophage infiltration, and intimal hyperplasia were assessed.
- Carotid artery ligation was performed to induce intimal hyperplasia.
Main Results:
- Nox1 deficiency significantly reduced aortic arch lesion area (43% to 28%) and superoxide levels.
- Reduced lesion size in Nox1-deficient mice was associated with decreased macrophage infiltration.
- Inhibition of Nox1 attenuated intimal hyperplasia, decreasing cellular proliferation and increasing collagen content.
Conclusions:
- Nox1-derived reactive oxygen species (ROS) are critical in modifying atherosclerotic lesion composition.
- Nox1 plays a significant role in promoting lesion size and progression in a murine model of atherosclerosis.
Related Concept Videos
Atherosclerosis I: Introduction
Nitric Oxide Signaling Pathway
Coronary Artery Disease II: Pathophysiology
Atherosclerosis III: Management
Inflammation
Coronary Artery Disease I: Introduction
