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Updated: Jul 9, 2026
A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Inflammation and atherosclerosis
Göran K Hansson1, Anna-Karin L Robertson, Cecilia Söderberg-Nauclér
1Department of Medicine, Center for Molecular Medicine, Karolinska Institute, Stockholm SE-17176, Sweden. Goran.Hansson@ki.se
Insights
Atherosclerosis is an inflammatory disease driven by cholesterol buildup, leading to plaque formation and potentially heart attack or stroke. Understanding this inflammatory process is key to developing effective anti-inflammatory therapies.
Area of Science:
- Cardiovascular Biology
- Immunology
- Pathology
Background:
- Atherosclerosis is a major cause of myocardial infarction, stroke, and ischemic gangrene.
- The disease is characterized by inflammation within the arterial wall.
Purpose of the Study:
- To elucidate the inflammatory mechanisms underlying atherosclerosis.
- To highlight the role of lipoproteins, immune cells, and signaling pathways in disease progression.
Main Methods:
- Review of the molecular and cellular events initiating and perpetuating atherosclerotic plaque development.
- Focus on the roles of low-density lipoproteins, macrophages, and T cells.
Main Results:
- Low-density lipoprotein accumulation activates endothelial cells, promoting leukocyte recruitment.
- Monocytes differentiate into macrophages, internalizing lipids to form foam cells.
- Toll-like receptors and T helper-1 responses drive inflammation via cytokine release.
- Plaque rupture and thrombus formation result from intensified inflammatory activation.
Conclusions:
- Atherosclerosis is fundamentally an inflammatory disease.
- Inflammatory markers can monitor disease progression.
- Anti-inflammatory therapies show potential for managing atherosclerotic disease activity.
Abstract:
Atherosclerosis, the cause of myocardial infarction, stroke, and ischemic gangrene, is an inflammatory disease. The atherosclerotic process is initiated when cholesterol-containing low-density lipoproteins accumulate in the intima and activate the endothelium. Leukocyte adhesion molecules and chemokines promote recruitment of monocytes and T cells. Monocytes differentiate into macrophages and upregulate pattern recognition receptors, including scavenger receptors and toll-like receptors. Scavenger receptors mediate lipoprotein internalization, which leads to foam-cell formation. Toll-like receptors transmit activating signals that lead to the release of cytokines, proteases, and vasoactive molecules. T cells in lesions recognize local antigens and mount T helper-1 responses with secretion of pro-inflammatory cytokines that contribute to local inflammation and growth of the plaque. Intensified inflammatory activation may lead to local proteolysis, plaque rupture, and thrombus formation, which causes ischemia and infarction. Inflammatory markers are already used to monitor the disease process and anti-inflammatory therapy may be useful to control disease activity.
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