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Cardiovasc Res. 2019 Jul 1;115(9):1416-1424. doi: 10.1093/cvr/cvz107.

Immunometabolism orchestrates training of innate immunity in atherosclerosis.

Author information

1
Department of Internal Medicine, Radboud University Medical Center Nijmegen, Geert Grooteplein Zuid 8, GA, HB Nijmegen, The Netherlands.
2
Department of Medical Genetics, Iuliu Hatieganu University of Medicine and Pharmacy, Str. Pasteur 6, Cluj-Napoca, Romania.
3
Department for Genomics & Immunoregulation, Life and Sciences Institute (LIMES), University of Bonn, Carl-Troll-Straβe 31, Bonn, Germany.

Abstract

Atherosclerosis is characterized by a persistent, low-grade inflammation of the arterial wall. Monocytes and monocyte-derived macrophages play a pivotal role in the various stages of atherosclerosis. In the past few years, metabolic reprogramming has been identified as an important controller of myeloid cell activation status. In addition, metabolic and epigenetic reprogramming are key regulatory mechanisms of trained immunity, which denotes the non-specific innate immune memory that can develop after brief stimulation of monocytes with microbial or non-microbial stimuli. In this review, we build the case that metabolic reprogramming of monocytes and macrophages, and trained immunity in particular, contribute to the pathophysiology of atherosclerosis. We discuss the specific metabolic adaptations, including changes in glycolysis, oxidative phosphorylation, and cholesterol metabolism, that have been reported in atherogenic milieus in vitro and in vivo. In addition, we will focus on the role of these metabolic pathways in the development of trained immunity.

KEYWORDS:

Atherosclerosis; Immunometabolism; Macrophage; Monocyte; Trained immunity

PMID:
31050710
DOI:
10.1093/cvr/cvz107

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