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Related Experiment Video

Updated: Mar 31, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Atherosclerotic Plaque Destabilization in Mice: A Comparative Study.

Helene Hartwig¹, Carlos Silvestre-Roig², Jeffrey Hendrikse¹

¹Department of Pathology, Academic Medical Center, Amsterdam, The Netherlands.

|October 23, 2015

Summary

Researchers identified an optimal mouse model for studying vulnerable atherosclerotic plaques. This model, combining shear stress modification and hypercholesterolemia, closely mimics human atherosclerotic lesions, aiding research into plaque destabilization.

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Isolation and Analysis of Aortic Arch and Root Lesions in an Atherosclerotic Mouse Model

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Published on: February 14, 2025

Area of Science:

Cardiovascular Research
Translational Medicine
Animal Models in Atherosclerosis

Background:

Atherosclerosis is a leading cause of death, progressing to vulnerable plaques that trigger acute coronary syndromes.
Current hyperlipidemic mouse models inadequately replicate plaque destabilization, hindering research into its mechanisms.
A need exists for robust animal models to study the progression and vulnerability of atherosclerotic plaques.

Purpose of the Study:

To evaluate and compare plaque vulnerability in different mouse models of atherosclerosis.
To identify a superior animal model that accurately mimics human atherosclerotic plaque destabilization.
To advance the understanding of mechanisms underlying the transition to rupture-prone plaques.

Main Methods:

Comparison of plaque vulnerability features across distinct mouse models.
Induction of hypercholesterolemia in combination with shear stress modification.
Histological analysis of atherosclerotic lesions to assess human-like characteristics.

Main Results:

The mouse model combining shear stress modification and hypercholesterolemia demonstrated a high incidence of human-like atherosclerotic lesions.
This specific model showed greater plaque vulnerability features compared to other tested models.
The findings highlight the utility of this combined approach for studying advanced atherosclerotic disease.

Conclusions:

A mouse model integrating shear stress modification and hypercholesterolemia effectively recapitulates human atherosclerotic plaque vulnerability.
This model offers a valuable tool for investigating the mechanisms of plaque destabilization and rupture.
Further research using this model can improve strategies for preventing cardiovascular events associated with vulnerable plaques.