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Atherosclerosis and transit of HDL through the lymphatic vasculature
Catherine Martel1, Gwendalyn J Randolph
1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. cmartel@path.wustl.edu
Insights
Cholesterol removal from macrophages is key to halting atherosclerosis. Lymphatic vessels are crucial for clearing cholesterol from tissues, and impaired lymphatic function may drive plaque progression.
Area of Science:
- Cardiovascular Biology
- Atherosclerosis Research
- Lymphatic Physiology
Background:
- Macrophages and cholesterol are central to atherosclerotic plaque development.
- Cholesterol efflux from macrophage foam cells is understood to inhibit disease progression.
- High-density lipoprotein (HDL) plays a role in transporting cholesterol away from plaques.
Purpose of the Study:
- To highlight the critical role of lymphatic vasculature in cholesterol removal from tissues.
- To explore the connection between lymphatic function and atherosclerosis progression.
- To discuss how impaired cholesterol removal by lymphatics may contribute to arterial plaque buildup.
Main Methods:
- Review of recent evidence on lymphatic cholesterol transport.
- Analysis of the relationship between tissue cholesterol efflux and lymphatic function.
- Discussion of potential mechanisms linking lymphatic impairment to atherosclerosis.
Main Results:
- Recent evidence implicates lymphatic vasculature in removing cholesterol from tissues, including the artery wall.
- Cholesterol is likely transported via HDL within the lymphatic system.
- Sluggish lymphatic removal of cholesterol may be a factor in atherosclerosis progression.
Conclusions:
- The lymphatic system is essential for clearing cholesterol from the artery wall.
- Dysfunctional lymphatic vasculature could contribute to the development and progression of atherosclerosis.
- Targeting lymphatic cholesterol removal may offer new therapeutic strategies for cardiovascular disease.
Abstract:
Key components of atherosclerotic plaque known to drive disease progression are macrophages and cholesterol. It has been widely understood, and bolstered by recent evidence, that the efflux of cholesterol from macrophage foam cells quells disease progression or even to promote regression. Following macrophage cholesterol efflux, cholesterol loaded onto HDL must be removed from the plaque environment. Here, we focus on recent evidence that the lymphatic vasculature is critical for the removal of cholesterol, likely as a component of HDL, from tissues including skin and the artery wall. We discuss the possibility that progression of atherosclerosis might in part be linked to sluggish removal of cholesterol from the plaque.
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