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Genetic Mouse Models for Atherosclerosis
Take advantage of numerous genetic mouse models, including the ApoE or LDLr KO, to accelerate or tailor your atherosclerosis model of cardiovascular disease. Altered lipid metabolism, with or without high fat diets, leads to repeatable models of plaque buildup to evaluate your drug candidate.
The ApoE and LDLr knock out (KO) mice are two of the more widely used genetic models to evaluate atherosclerosis. The ApoE mouse develops hypercholesterolemia and plaque even when fed normal diets. While the LDLr mouse requires HFD for robust disease progression, this mouse is a model of familial hypercholesterolemia. Both models display several aspects of human disease such as inflammation, fibrous plaques, and a necrotic core to the lesions.
Why choose ApoE-/- Mice?
- HFD not required
- Atherosclerosis already develops by 2-3 months old
- Plaque develops at the aortic route, arch, and carotid arteries similar to large animal models and humans
Why choose LDLr -/- Mice?
- Lipid profile is more similar to humans
- Plaque can develop from the aortic arch to the distal aorta
- Models familial hypercholesterolemia
Numerous and robust endpoints
Utilize histology to evaluate cardiac and aorta remodeling. With the ability to evaluate even the most specific part of the heart or vasculature, we can test the effect of treatment at a granular level.