Cardiac resident macrophages: key regulatory mediators in the aftermath of myocardial infarction

Figures

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  Figure 1. Cardiac niche with respect to cMacs. The figure depicts the macroscopic structure of the heart, including cardiac valves, atrioventricular node, ventricular wall, and coronary arteries, presented alongside magnified images of distinct tissue sections. These panels highlight the specific interactions between cardiac resident macrophages and cardiomyocytes in those areas. AV, Atrioventricular; cMacs, Cardiac resident macrophages; CX43, Connexin 43; ECs, Endothelial cells; SMCs, Smooth muscle cells.

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  Figure 2. Schematic representation of the imbalance among different cMacs subpopulations within the myocardial tissue post-AMI. AMI, Acute myocardial infarction; cMacs, Cardiac resident macrophages; CCR2, C-C chemokine receptor type 2.

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  Figure 3. Electrochemical Interaction Between cMacs and Cardiomyocytes. (A) cMacs establish communication with cardiomyocytes via connexin 43 (CX43)-containing gap junctions, enabling the transfer of charges between cells; (B) In the resting membrane potential phase, macrophages possess a higher charge relative to cardiomyocytes’ resting membrane potential, leading to the migration of cations towards the cardiomyocytes, reducing their negative charge; (C) Upon cardiomyocyte depolarization, they become more positively charged than macrophages, instigating a transfer of cations back to the macrophages and supporting the rapid repolarization of the cardiomyocytes; (D) The electrocardiogram depicts a normal cardiac cycle (blue), contrasted with the ECG following macrophage depletion (red). The absence of cardiac macrophages prevents the propagation of the depolarization signal from atria to ventricles, resulting in an atrioventricular block. This condition, characterized by the decoupling of the atrial P waves and the infrequent ventricular QRS complexes. cMacs, Cardiac resident macrophages; CX43, Connexin 43.