Regressing Atherosclerosis by Resolving Plaque Inflammation
Abstract
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 regression.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2017
- Accession Number
- AD1050357
Entities
People
- Edward A Fisher
Organizations
- New York University