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Updated: Jul 4, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
Published on: September 26, 2018
Control of atherosclerotic plaque vulnerability: insights from transgenic mice
Sylvia Heeneman1, Esther Lutgens, Kitty B Schapira
1Department of Pathology, Maastricht University, Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands. s.heeneman@path.unimaas.nl
Abstract:
Atherosclerosis is a complex, progressive disease of the large systemic arteries. This multi-factorial disease is characterized by accumulation of lipids, cells and extracellular matrix in the vessel wall. The quest to unravel the molecular mechanisms leading to progression of human atherosclerotic plaques has lead to the development of a variety of animal models. Mice are easily amendable to transgenesis and multiple mutant and inbred strains have been generated in which potential regulators are manipulated and subsequently studied for effects on the development and progression of atherosclerosis. The scope of this review is to discuss the relevance, advantages and disadvantages of genetically-engineered mice to investigate mechanisms of plaque vulnerability. Features of human vulnerable lesions, such as large lipid-rich necrotic cores, active inflammation, matrix remodeling and signs of intraplaque hemorrhage are represented in mouse lesions. Here, we will discuss how atherosclerosis is modified by manipulations in apoptosis, lesional lipid metabolism, inflammatory pathways, matrix remodeling and thrombotic pathways in genetically-engineered mice, emphasizing the insights that have been gained from these studies for the control of plaque vulnerability.
Insights
Genetically-engineered mouse models are crucial for understanding atherosclerosis progression and plaque vulnerability. These models help researchers investigate molecular mechanisms and develop strategies to control vulnerable atherosclerotic plaques.
Area of Science:
- Cardiovascular Biology
- Translational Medicine
- Genetics
Background:
- Atherosclerosis is a complex, progressive arterial disease involving lipid and cellular accumulation.
- Understanding the molecular mechanisms of atherosclerotic plaque progression is critical.
- Genetically-engineered mouse models offer valuable tools for studying this disease.
Purpose of the Study:
- To review the relevance, advantages, and disadvantages of genetically-engineered mice for investigating plaque vulnerability mechanisms.
- To highlight insights gained from these models for controlling plaque vulnerability.
Main Methods:
- Review of existing literature on genetically-engineered mouse models in atherosclerosis research.
- Analysis of how genetic manipulations in mice affect key aspects of plaque development and vulnerability.
- Comparison of features in mouse lesions to human vulnerable plaques.
Main Results:
- Genetically-engineered mice replicate key features of human vulnerable atherosclerotic lesions.
- Manipulations in apoptosis, lipid metabolism, inflammation, matrix remodeling, and thrombosis pathways are effectively studied in mice.
- These models provide insights into the control of plaque vulnerability.
Conclusions:
- Genetically-engineered mouse models are indispensable for dissecting the molecular underpinnings of atherosclerosis and plaque vulnerability.
- These models facilitate the identification of therapeutic targets for managing vulnerable atherosclerotic plaques.
- Further utilization of these models will advance strategies for controlling atherosclerosis progression.
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