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. 2020 Mar 1;41(9):989-994.
doi: 10.1093/eurheartj/ehz159.

Novel functions of macrophages in the heart: insights into electrical conduction, stress, and diastolic dysfunction

Affiliations

Novel functions of macrophages in the heart: insights into electrical conduction, stress, and diastolic dysfunction

Florian Leuschner et al. Eur Heart J. .

Abstract

Over a century ago, Élie Metchnikoff described the macrophages' ability to phagocytose. Propelled by advances in technology enabling phenotypic and functional analyses at unpreceded resolution, a recent renaissance in macrophage research has shed new light on these 'big eaters'. We here give an overview of cardiac macrophages' provenance in the contexts of cardiac homeostasis and stress. We highlight the recently identified mechanism by which these cells regulate electrical conduction in the atrioventricular node and discuss why we need a deeper understanding of monocytes and macrophages in systolic and diastolic dysfunctions.

Keywords: Conduction; Diastolic dysfunction; Macrophages; Monocytes; Myocardial infarction.

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Figures

Figure 1
Figure 1
Overview and comparison of monocyte subsets (top) and cardiac macrophages (bottom) defined in humans and mice with their respective surface markers.
Figure 2
Figure 2
Macrophage populations and functions in the healthy adult heart. Schematic depicting cardiac resident macrophages within the myocardium. Their developmental origin and proposed functions are illustrated during development and homeostasis (left). The interplay between cardiomyocytes and macrophages in the atrioventricular (AV) node in electrical conduction of the heart (right).
Figure 3
Figure 3
Cardiac macrophages in the context of stress conditions. Various stressors can activate macrophage subpopulations in heart (left). These stress conditions lead to an increase in macrophages by local proliferation and by recruitment of monocytes from bone marrow and spleen (right). Tissue-resident CCR2+ macrophages may further spur the recruitment of myeloid cells, remove tissue debris, and modulate the cardiac microenvironment by the release of matrix metalloproteinases (MMPs), proteases, and cytokines. The latter may exert beneficial or harmful effects—as illustrated for IL-10—depending on disease context and timing. DAMP, damage-associated molecular pattern.

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