Journal
NATURE MEDICINE
Volume 19, Issue 9, Pages 1166-1172Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.3258
Keywords
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Funding
- US National Institutes of Health [1R01HL095612, HHSN 268201000044C, P01-A154904, U24-CA092782, P50-CA086355]
- Heart and Stroke Richard Lewar Centre of Excellence in Cardiovascular Research
- Department of Laboratory Medicine and Pathobiology, University of Toronto
- Massachusetts General Hospital Executive Committee on Research (ECOR) Postdoctoral Award
- German Research Foundation
- Max Kade Foundation
- Boehringer Ingelheim Funds
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During the inflammatory response that drives atherogenesis, macrophages accumulate progressively in the expanding arterial wall(1,2). The observation that circulating monocytes give rise to lesional macrophages(3-9) has reinforced the concept that monocyte infiltration dictates macrophage buildup. Recent work has indicated, however, that macrophage accumulation does not depend on monocyte recruitment in some inflammatory contexts(10). We therefore revisited the mechanism underlying macrophage accumulation in atherosclerosis. In murine atherosclerotic lesions, we found that macrophages turn over rapidly, after 4 weeks. Replenishment of macrophages in these experimental atheromata depends predominantly on local macrophage proliferation rather than monocyte influx. The microenvironment orchestrates macrophage proliferation through the involvement of scavenger receptor A (SR-A). Our study reveals macrophage proliferation as a key event in atherosclerosis and identifies macrophage self-renewal as a therapeutic target for cardiovascular disease.
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