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. 2019 Nov 14;40(1):20–33. doi: 10.1161/ATVBAHA.119.312802

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© 2019 The Authors.

Arteriosclerosis, Thrombosis, and Vascular Biology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure. — Dynamics of macrophage plasticity and trafficking in atherosclerosis. Atherosclerotic lesions are characterized by proinflammatory macrophages which sustain lesion growth by contributing to local and systemic plaque inflammation. Atherosclerosis development and macrophage dysfunction is accelerated during hypercholesterolemia (high LDL-C [lowdensity lipoprotein-cholesterol), and hyperglycemia. Atherogenic lipid-lowering remodels lesions towards a stable phenotype, a process driven mainly by macrophages. Broad changes in the plaque macrophage transcriptome are characteristic of atherosclerosis regression, most commonly distinguished by enrichment of M2-associated transcripts. The dynamic change in plaque macrophage phenotype raises the possibility that inducing of macrophage polarization potential in vivo will represent a viable therapeutic option for atherosclerotic cardiovascular disease regression and suppress residual inflammatory risk.