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Laboratory study demonstrates cholesterol-induced vascular smooth muscle cell transdifferentiation into macrophage-like cells, suggesting distinct contributions to plaque formation.
Cholesterol loading of VSMC converts them to a macrophage-appearing state by downregulating the miR-143/145-myocardin axis. Although these cells would be classified by immunohistochemistry as macrophages in human and mouse plaques, their transcriptome and functional properties imply that their contributions to atherogenesis would not be those of classical macrophages.
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Vengrenyuk et al. (2015) studied this question.
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