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Updated: May 25, 2026
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
Cardiac and vascular phenotypes in the apolipoprotein E-deficient mouse
Elisardo C Vasquez1, Veronica A Peotta, Agata L Gava
1Department of Physiological Sciences, Health Sciences Center, Federal University of Espirito Santo, Vitoria, ES, Brazil. evasquez@pq.cnpq.br
Insights
Atherosclerosis mouse models are crucial for studying cardiovascular disease. This review details cardiac and vascular changes, focusing on factors like nitric oxide and aging in these models.
Area of Science:
- Cardiovascular Science
- Animal Models
- Atherosclerosis Research
Background:
- Atherosclerosis is a major cause of cardiovascular death worldwide.
- Genetically engineered mouse models are vital for understanding cardiovascular diseases.
- The apolipoprotein E-deficient mouse model rapidly develops hypercholesterolemia and atherosclerotic lesions.
Purpose of the Study:
- To review cardiac and vascular phenotypes in apolipoprotein E-deficient mice.
- To discuss the influence of nitric oxide, reactive oxygen species, aging, and diet on cardiovascular function.
- To highlight the utility of this model in atherosclerosis research.
Main Methods:
- Review of existing literature on apolipoprotein E-deficient mouse models.
- Analysis of cardiac and vascular phenotypes reported in studies.
- Discussion of molecular and environmental factors affecting cardiovascular outcomes.
Main Results:
- Apolipoprotein E-deficient mice exhibit significant hypercholesterolemia and atherosclerotic lesions.
- Impaired cardiovascular function is linked to alterations in nitric oxide and reactive oxygen species.
- Aging and dietary factors exacerbate cardiovascular dysfunction in this model.
Conclusions:
- The apolipoprotein E-deficient mouse is a valuable model for studying human atherosclerosis.
- Understanding the interplay of factors like aging and diet is key to mitigating cardiovascular disease.
- Further research using this model can elucidate mechanisms of cardiovascular impairment.
Abstract:
Cardiovascular death is frequently associated with atherosclerosis, a chronic multifactorial disease and a leading cause of death worldwide. Genetically engineered mouse models have proven useful for the study of the mechanisms underlying cardiovascular diseases. The apolipoprotein E-deficient mouse has been the most widely used animal model of atherosclerosis because it rapidly develops severe hypercholesterolemia and spontaneous atherosclerotic lesions similar to those observed in humans. In this review, we provide an overview of the cardiac and vascular phenotypes and discuss the interplay among nitric oxide, reactive oxygen species, aging and diet in the impairment of cardiovascular function in this mouse model.
