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Updated: Jul 28, 2025
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
SR-B1-/-ApoE-R61h/h Mice Mimic Human Coronary Heart Disease
Andrea Staršíchová1,2,3
1Graduate School Cell Dynamics and Disease, University of Muenster, Muenster, Germany. starsichova.andrea@gmail.com.
Insights
Atherosclerosis, a major cause of cardiovascular disease, can be studied using the SR-B1-/-ApoE-R61h/h mouse model. This model mimics vulnerable plaques, rupture, and thrombosis, aiding drug and technology development.
Area of Science:
- Cardiovascular Medicine
- Atherosclerosis Research
- Animal Models
Background:
- Cardiovascular diseases (CVDs) are the leading global cause of mortality.
- Atherosclerosis, characterized by plaque buildup, underlies most CVDs and can lead to acute events like myocardial infarction and stroke.
- Vulnerable plaque rupture and subsequent thrombus formation are key triggers for these acute clinical events.
Purpose of the Study:
- To review the utility of the SR-B1-/-ApoE-R61h/h mouse model in studying atherosclerosis.
- To highlight the model's capacity to mimic key aspects of human coronary heart disease, including vulnerable plaque rupture and thrombosis.
- To discuss the application of this model in evaluating therapeutic interventions and novel technologies for cardiovascular medicine.
Main Methods:
- Utilizing the SR-B1-/-ApoE-R61h/h mouse model, which exhibits spontaneous coronary atherosclerosis.
- Observing plaque development, rupture, thrombus formation, and arterial occlusion.
- Analyzing experimental data and recent publications related to this specific mouse model.
Main Results:
- The SR-B1-/-ApoE-R61h/h mouse model accurately recapitulates the progression of coronary atherosclerosis seen in humans.
- This model demonstrates vulnerable plaque phenotypes, spontaneous rupture, and subsequent thrombus formation leading to arterial occlusion.
- The model effectively results in myocardial infarction and ischemic events, mirroring clinical manifestations of heart disease.
Conclusions:
- The SR-B1-/-ApoE-R61h/h mouse is a highly relevant preclinical model for investigating the mechanisms of vulnerable atherosclerotic plaques.
- This model serves as a valuable platform for testing novel anti-inflammatory drugs, anti-rupture therapies, and innovative cardiovascular technologies.
- Further research using this model can significantly advance the understanding and treatment of atherosclerosis and its life-threatening consequences.
Abstract:
Cardiovascular diseases are the leading cause of death in the modern world. Atherosclerosis underlies the majority of these pathologies and may result in sudden life-threatening events such as myocardial infarction or stroke. Current concepts consider a rupture (resp. erosion) of "unstable/vulnerable" atherosclerotic plaques as a primary cause leading to thrombus formation and subsequent occlusion of the artery lumen finally triggering an acute clinical event. We and others described SR-B1-/-ApoE-R61h/h mice mimicking clinical coronary heart disease in all major aspects: from coronary atherosclerosis through vulnerable plaque ruptures leading to thrombus formation/coronary artery occlusion, finally resulting in myocardial infarction/ischemia. SR-B1-/-ApoE-R61h/h mouse provides a valuable model to study vulnerable/occlusive plaques, to evaluate bioactive compounds as well as new anti-inflammatory and "anti-rupture" drugs, and to test new technologies in experimental cardiovascular medicine. This review summarizes and discuss our knowledge about SR-B1-/-ApoE-R61h/h mouse model based on recent publications and experimental observations from the lab.
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