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Related Experiment Video

Updated: May 8, 2026

A Method to Study the Correlation Between Local Collagen Structure and Mechanical Properties of Atherosclerotic Plaque Fibrous Tissue
13:45

A Method to Study the Correlation Between Local Collagen Structure and Mechanical Properties of Atherosclerotic Plaque Fibrous Tissue

Published on: November 11, 2022

Mouse models of plaque rupture.

Tetsuya Matoba1, Kei Sato, Kensuke Egashira

  • 1Department of Cardiovascular Medicine, Kyushu University Hospital, Fukuoka, Japan.

Current Opinion in Lipidology
|August 15, 2013
PubMed
Summary

Mouse models help study atherosclerotic plaque rupture, a key cause of heart attacks. The brachiocephalic artery model in ApoE-deficient mice shows promise for analyzing plaque destabilization and rupture mechanisms.

Area of Science:

  • Cardiovascular Research
  • Pathology
  • Translational Medicine

Background:

  • Atherosclerotic plaque rupture is a major cause of acute myocardial infarction (heart attack).
  • Understanding plaque rupture mechanisms is crucial for developing effective treatments.
  • Existing research highlights the need for reliable animal models to study this process.

Purpose of the Study:

  • To analyze the mechanisms underlying atherosclerotic plaque destabilization and rupture.
  • To evaluate the efficacy of novel therapeutic approaches using animal models.
  • To assess the suitability of specific mouse models for studying plaque rupture.

Main Methods:

  • Utilizing apolipoprotein E (ApoE)-deficient mice fed a high-fat diet.
  • Inducing plaque rupture in brachiocephalic arteries.

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  • Employing Angiotensin II infusion to accelerate plaque destabilization and rupture.
  • Comparing histological features with human ruptured plaques.

    • Main Results:

    • Atherosclerotic plaques in ApoE-deficient mice share histological similarities with human ruptured plaques.
    • Angiotensin II infusion accelerates plaque destabilization and rupture in this model.
    • The model allows for the analysis of pathophysiological and genetic factors influencing plaque rupture.
    • Discrepancies exist regarding thrombotic occlusion and mechanical stress compared to human plaques.

    Conclusions:

    • The brachiocephalic artery model in ApoE-deficient mice is a practical and feasible model for studying plaque rupture.
    • While not a perfect simulation, this model aids in analyzing plaque destabilization and rupture mechanisms.
    • Further research can refine this model to better mimic human plaque rupture conditions.