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Regulation of macrophage immunometabolism in atherosclerosis

Regulation of macrophage immunometabolism in atherosclerosis After activation, cells of the myeloid lineage undergo robust metabolic transitions, as well as discrete epigenetic changes, that can dictate both ongoing and future inflammatory responses. In atherosclerosis, in which macrophages play central roles in the initiation, growth, and ultimately rupture of arterial plaques, altered metabolism is a key feature that dictates macrophage function and subsequent disease progression. This Review explores how factors central to the plaque microenvironment (for example, altered cholesterol metabolism, oxidative stress, hypoxia, apoptotic and necrotic cells, and hyperglycemia) shape the metabolic rewiring of macrophages in atherosclerosis as well as how these metabolic shifts in turn alter macrophage immune-effector and tissue-reparative functions. Finally, this overview offers insight into the challenges and opportunities of harnessing metabolism to modulate aberrant macrophage responses in disease. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Immunology Springer Journals

Regulation of macrophage immunometabolism in atherosclerosis

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References (122)

Publisher
Springer Journals
Copyright
Copyright © 2018 by The Publisher
Subject
Biomedicine; Biomedicine, general; Immunology; Infectious Diseases
ISSN
1529-2908
eISSN
1529-2916
DOI
10.1038/s41590-018-0113-3
Publisher site
See Article on Publisher Site

Abstract

After activation, cells of the myeloid lineage undergo robust metabolic transitions, as well as discrete epigenetic changes, that can dictate both ongoing and future inflammatory responses. In atherosclerosis, in which macrophages play central roles in the initiation, growth, and ultimately rupture of arterial plaques, altered metabolism is a key feature that dictates macrophage function and subsequent disease progression. This Review explores how factors central to the plaque microenvironment (for example, altered cholesterol metabolism, oxidative stress, hypoxia, apoptotic and necrotic cells, and hyperglycemia) shape the metabolic rewiring of macrophages in atherosclerosis as well as how these metabolic shifts in turn alter macrophage immune-effector and tissue-reparative functions. Finally, this overview offers insight into the challenges and opportunities of harnessing metabolism to modulate aberrant macrophage responses in disease.

Journal

Nature Immunology – Springer Journals

Published: May 18, 2018

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