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Updated: Mar 14, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
Published on: September 26, 2018
Live Observation of Atherosclerotic Plaque Disruption in Apolipoprotein E-Deficient Mouse
V Daeichin1, J C Sluimer2, K van der Heiden1
1Erasmus Medical Center, Thoraxcenter Biomedical Engineering, Rotterdam, Netherlands.
Aim:
The actual occurrence of spontaneous plaque rupture in mice has been a matter of debate. We report on an in vivo observation of the actual event of possible plaque disruption in a living ApoE(-/-) mouse.
Methods And Results:
During live contrast-enhanced ultrasonography of a 50-week-old ApoE(-/-) male mouse, symptoms suggesting plaque disruption in the brachiocephalic artery were observed. Histological analysis confirmed the presence of advanced atherosclerotic lesions with dissections and intraplaque hemorrhage in the affected brachiocephalic trunk, pointing towards plaque rupture as the cause of the observed event. However, we did not detect a luminal thrombus or cap rupture, which is a key criterion for plaque rupture in human atherosclerosis.
Conclusion:
This study reports the real-time occurrence of a possible plaque rupture in a living ApoE(-/-) mouse.
Insights
Researchers observed possible plaque rupture in a living mouse model (ApoE-/-). Histology confirmed advanced lesions, but key human criteria like cap rupture were absent, sparking debate on spontaneous plaque disruption.
Area of Science:
- Cardiovascular Research
- Animal Models in Atherosclerosis
Background:
- Spontaneous plaque rupture in mice is debated.
- Apolipoprotein E knockout (ApoE-/-) mice are a common model for atherosclerosis research.
Purpose of the Study:
- To report in vivo observation of possible plaque disruption in a living ApoE-/- mouse.
- To investigate the event of spontaneous plaque rupture in a mouse model.
Main Methods:
- Live contrast-enhanced ultrasonography was performed on a 50-week-old ApoE-/- male mouse.
- Histological analysis of the brachiocephalic trunk was conducted.
Main Results:
- Ultrasonography revealed symptoms suggestive of plaque disruption in the brachiocephalic artery.
- Histology confirmed advanced atherosclerotic lesions with dissections and intraplaque hemorrhage.
- Luminal thrombus and cap rupture, key human criteria, were not detected.
Conclusions:
- This study presents a real-time observation of a possible plaque rupture event in a living ApoE-/- mouse.
- The findings contribute to the ongoing debate regarding spontaneous plaque rupture in mouse models.

