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Regressing Atherosclerosis by Resolving Plaque Inflammation

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New York University School of Medicine New York United States

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Macrophages play key roles in progression of atherosclerosis. Our goal is to understand the mechanisms by which atherosclerosis can be clinically regressed by altering the macrophage state in the plaques to resolve the inflammation, as well as to develop new therapeutic strategies to promote atherosclerosis regression by altering the macrophage activation state. We have found that successful atherosclerosis regression requires the alteration of macrophages in the plaques to a tissue repair alternatively activated state. This switch in activation state requires the action of TH2 cytokines interleukin IL-4 or IL-13. To accomplish our goals, we are testing if these molecules, or derivative of these molecules, will be able to accelerate atherosclerosis regression in mouse models. Additionally, we will develop nanomedicines that can favorably and rapidly affect the content and inflammatory state of macrophages in atherosclerotic plaques to promote regression. Concurrently, we will characterize the macrophages to understand the mechanisms that promote atherosclerosis

Descriptive Note:

Technical Report,01 Jul 2017,30 Jun 2018



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Approved For Public Release;

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