» Articles » PMID: 30360827

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

Overview
Date 2018 Oct 27
PMID 30360827
Citations 90
Authors
Affiliations
Soon will be listed here.
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.

Citing Articles

PIM1 instigates endothelial-to-mesenchymal transition to aggravate atherosclerosis.

Xue Z, Han M, Sun T, Wu Y, Xing W, Mu F Theranostics. 2025; 15(2):745-765.

PMID: 39744686 PMC: 11671384. DOI: 10.7150/thno.102597.


Apolipoprotein B-containing lipoproteins in atherogenesis.

Boren J, Packard C, Binder C Nat Rev Cardiol. 2025; .

PMID: 39743565 DOI: 10.1038/s41569-024-01111-0.


Macropinocytosis enhances foamy macrophage formation and cholesterol crystallization to activate NLRP3 inflammasome after spinal cord injury.

Zhang C, Zhao S, Huang Z, Xue A, Liu H, Dai S Redox Biol. 2024; 79():103469.

PMID: 39700693 PMC: 11723182. DOI: 10.1016/j.redox.2024.103469.


Management of Hypercholesterolemia in Patients with Coronary Artery Disease: A Glimpse into the Future.

Sciahbasi A, Russo P, Zuccanti M, Chiorazzo L, Castelli F, Granatelli A J Clin Med. 2024; 13(23).

PMID: 39685877 PMC: 11642370. DOI: 10.3390/jcm13237420.


Factors related to type 2 diabetic retinopathy and their clinical application value.

Lian X, Zhu M Front Endocrinol (Lausanne). 2024; 15:1484197.

PMID: 39634174 PMC: 11614660. DOI: 10.3389/fendo.2024.1484197.


References
1.
Qiu H, Gabrielsen A, Agardh H, Wan M, Wetterholm A, Wong C . Expression of 5-lipoxygenase and leukotriene A4 hydrolase in human atherosclerotic lesions correlates with symptoms of plaque instability. Proc Natl Acad Sci U S A. 2006; 103(21):8161-6. PMC: 1459628. DOI: 10.1073/pnas.0602414103. View

2.
Serhan C . Pro-resolving lipid mediators are leads for resolution physiology. Nature. 2014; 510(7503):92-101. PMC: 4263681. DOI: 10.1038/nature13479. View

3.
Hagg S, Skogsberg J, Lundstrom J, Noori P, Nilsson R, Zhong H . Multi-organ expression profiling uncovers a gene module in coronary artery disease involving transendothelial migration of leukocytes and LIM domain binding 2: the Stockholm Atherosclerosis Gene Expression (STAGE) study. PLoS Genet. 2009; 5(12):e1000754. PMC: 2780352. DOI: 10.1371/journal.pgen.1000754. View

4.
Babaev V, Gleaves L, Carter K, Suzuki H, Kodama T, Fazio S . Reduced atherosclerotic lesions in mice deficient for total or macrophage-specific expression of scavenger receptor-A. Arterioscler Thromb Vasc Biol. 2000; 20(12):2593-9. DOI: 10.1161/01.atv.20.12.2593. View

5.
Gerrity R, Naito H . Lipid clearance from fatty streak lesions by foam cell migration. Artery. 1980; 8(3):215-9. View