Related Experiment Video
Updated: Jun 15, 2026
A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Inflammatory cell recruitment in cardiovascular disease: murine models and potential clinical applications
Eileen McNeill1, Keith M Channon, David R Greaves
1Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK.
Insights
Atherosclerosis, a key factor in cardiovascular disease, involves inflammatory monocyte recruitment and cholesterol-laden foam cell formation. Research in animal models reveals critical roles for chemokines and scavenger receptors in disease progression, guiding new therapeutic strategies.
Area of Science:
- Cardiovascular Biology
- Immunology
- Pathology
Background:
- Atherosclerosis is the primary pathological process behind cardiovascular disease, a major cause of death.
- Plaque development involves monocyte recruitment, macrophage differentiation, and foam cell formation.
- Hypercholesterolemia models, like ApoE-/- mice, aid in dissecting atherosclerotic disease mechanisms.
Purpose of the Study:
- To review novel therapeutic strategies for cardiovascular disease.
- To highlight insights gained from experimental animal models of atherogenesis.
- To discuss the role of inflammation and specific molecular pathways in atherosclerosis.
Main Methods:
- Utilizing murine models of hypercholesterolemia (e.g., ApoE-/- mice).
- Employing transgenic technologies to study cellular and molecular biology.
- Investigating chemokine-deficient mouse models to understand their role in plaque formation.
Main Results:
- Murine models underscore the central role of inflammation in atherogenesis.
- Identification of key adhesion molecules, scavenger receptors, and macrophage activation receptors.
- Chemokines and their receptors are critical in promoting atherosclerotic plaque formation.
Conclusions:
- Understanding atherogenesis through animal models provides a basis for new cardiovascular disease treatments.
- Targeting inflammatory pathways and molecular mediators identified in research holds therapeutic potential.
- Further research into chemokine signaling may yield novel interventions for atherosclerosis.
Abstract:
Atherosclerosis is the pathological process that underlies the development of cardiovascular disease, a leading cause of mortality. Atherosclerotic plaque formation is driven by the recruitment of inflammatory monocytes into the artery wall, their differentiation into macrophages and the subsequent transformation of macrophages into cholesterol-laden foam cells. Models of hypercholesterolaemia such as the ApoE (apolipoprotein E)-/- mouse and the application of transgenic technologies have allowed us to undertake a thorough dissection of the cellular and molecular biology of the atherosclerotic disease process. Murine models have emphasized the central role of inflammation in atherogenesis and have been instrumental in the identification of adhesion molecules that support monocyte recruitment, scavenger receptors that facilitate cholesterol uptake by macrophages and other macrophage activation receptors. The study of mice deficient in multiple members of the chemokine family, and their receptors, has shown that chemokines play a critical role in promoting atherosclerotic plaque formation. In the present review, we will discuss novel therapeutic avenues for the treatment of cardiovascular disease that derive directly from our current understanding of atherogenesis gained in experimental animal models.
