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Updated: Aug 2, 2026
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Induction of Accelerated Atherosclerosis in Mice: The "Wire-Injury" Model
Published on: August 25, 2020
Mice lacking inducible nitric oxide synthase develop spontaneous hypercholesterolaemia and aortic atheromas
M Ihrig1, C A Dangler, J G Fox
1Division of Comparative Medicine, Massachusetts Institute of Technology, Building 16-825, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.
Atherosclerosis
|May 23, 2001
Summary
Inducible nitric oxide synthase (iNOS) plays a protective role in atherogenesis. iNOS-deficient mice exhibit higher blood pressure, elevated cholesterol, and increased atherosclerotic plaques, suggesting iNOS
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Immunology
Background:
- Nitric oxide (NO) has complex roles in atherogenesis, with both protective and cytotoxic effects.
- Increased inducible nitric oxide synthase (iNOS) expression is observed in atherosclerotic lesions, but its significance remains debated.
Purpose of the Study:
- To investigate the role of iNOS in the atherogenic process.
- To determine the impact of iNOS deficiency on blood pressure, cholesterol homeostasis, and atherosclerosis development.
Main Methods:
- Longitudinal study using iNOS-deficient and wild-type mice.
- Measurement of indirect systolic blood pressure via photoplethysmography.
- Monitoring of serum cholesterol levels and incidence of atherosclerotic plaques.
Main Results:
- iNOS-deficient mice showed significantly higher systolic blood pressure on both basal and high-salt diets.
- Elevated serum cholesterol levels were observed in iNOS-deficient mice at multiple time points.
- A significantly higher incidence of atherosclerotic plaques was found in iNOS-deficient mice compared to controls.
Conclusions:
- iNOS plays a crucial protective role in the atherogenic process.
- iNOS deficiency leads to adverse cardiovascular risk factors, including hypertension and hypercholesterolemia.
- iNOS-deficient mice represent a valuable model for studying cholesterol homeostasis and atherogenesis.
