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J Am Coll Cardiol. 2018 Oct 30;72(18):2181-2197. doi: 10.1016/j.jacc.2018.08.2147.

Macrophage Trafficking, Inflammatory Resolution, and Genomics in Atherosclerosis: JACC Macrophage in CVD Series (Part 2).

Author information

1
Department of Medicine, Leon H. Charney Division of Cardiology, Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine, New York, New York.
2
Department of Genetics & Genomic Sciences, Institute of Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, New York.
3
Department of Medicine, Columbia University, New York, New York; Department of Pathology and Cell Biology, Columbia University, New York, New York; Department of Physiology, Columbia University, New York, New York.
4
Department of Genetics & Genomic Sciences, Institute of Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, New York; Integrated Cardio Metabolic Centre, Department of Medicine, Karolinska Institutet, Karolinska Universitetssjukhuset, Huddinge, Sweden.
5
Department of Medicine, Columbia University, New York, New York.
6
The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: jason.kovacic@mountsinai.org.

Abstract

Atherosclerosis is characterized by the retention of modified lipoproteins in the arterial wall. These modified lipoproteins activate resident macrophages and the recruitment of monocyte-derived cells, which differentiate into mononuclear phagocytes that ingest the deposited lipoproteins to become "foam cells": a hallmark of this disease. In this Part 2 of a 4-part review series covering the macrophage in cardiovascular disease, we critically review the contributions and relevant pathobiology of monocytes, macrophages, and foam cells as relevant to atherosclerosis. We also review evidence that via various pathways, a failure of the resolution of inflammation is an additional key aspect of this disease process. Finally, we consider the likely role played by genomics and biological networks in controlling the macrophage phenotype in atherosclerosis. Collectively, these data provide substantial insights on the atherosclerotic process, while concurrently offering numerous molecular and genomic candidates that appear to hold great promise for selective targeting as clinical therapies.

KEYWORDS:

atherosclerosis; cardiovascular; inflammation; macrophage; resolution

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