Contribution of monocyte-derived macrophages and smooth muscle cells to arterial foam cell formation

Smooth muscle cells (SMCs) are the main cell type in intimal thickenings and some stages of human atherosclerosis. Like monocyte-derived macrophages, SMCs accumulate excess lipids and contribute to the total intimal foam cell population. In contrast, apolipoprotein (Apo)E-deficient and LDL receptor-...

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Bibliographic Details
Published in:Cardiovascular research 2012-07, Vol.95 (2), p.165-172
Main Authors: Allahverdian, Sima, Pannu, Parveer S, Francis, Gordon A
Format: Article
Language:English
Subjects:
Animals
Arteries - metabolism
Arteries - pathology
Atherosclerosis - metabolism
Atherosclerosis - pathology
Cholesterol - metabolism
Foam Cells - metabolism
Foam Cells - pathology
Humans
Macrophages - cytology
Mice
Myocytes, Smooth Muscle - metabolism
Myocytes, Smooth Muscle - pathology
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Summary:Smooth muscle cells (SMCs) are the main cell type in intimal thickenings and some stages of human atherosclerosis. Like monocyte-derived macrophages, SMCs accumulate excess lipids and contribute to the total intimal foam cell population. In contrast, apolipoprotein (Apo)E-deficient and LDL receptor-deficient mice develop atherosclerotic lesions that are macrophage- as opposed to SMC-rich. The lesser contribution of SMCs to lesion development in these mouse models has distracted attention away from the importance of SMC cholesterol homeostasis in the artery wall. Intimal SMCs accumulate excess amounts of cholesteryl esters when compared with medial layer SMCs, possibly explained by reduced ATP-binding cassette transporter A1 expression and ApoA-I binding to intimal-type SMCs. The aim of this review is to compare the relative contribution of monocyte-derived macrophages and SMCs to human vs. mouse atherosclerosis, and describe what is known about lipid uptake and removal mechanisms contributing to arterial macrophage and SMC foam cell formation. An increased understanding of the contribution of these cell types to lesion development will help to delineate their relative importance in atherogenesis and as potential therapeutic targets.
ISSN:0008-6363
1755-3245
DOI:10.1093/cvr/cvs094