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Int J Mol Sci. 2019 May 19;20(10). pii: E2474. doi: 10.3390/ijms20102474.

Role of Macrophages in Cardioprotection.

Yap J1, Cabrera-Fuentes HA2,3,4,5,6, Irei J7, Hausenloy DJ8,9,10,11,12, Boisvert WA13,14.

Author information

1
Center for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96813, USA. jktyap@hawaii.edu.
2
Tecnologico de Monterrey, Centro de Biotecnologia-FEMSA, Monterrey, NL 264610, Mexico. hacafu@tec.mx.
3
National Heart Research Institute Singapore, National Heart Centre, Singapore 169609, Singapore. hacafu@tec.mx.
4
Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore 169857, Singapore. hacafu@tec.mx.
5
Institute of Biochemistry, Medical School, Justus-Liebig University, 35392 Giessen, Germany. hacafu@tec.mx.
6
Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. hacafu@tec.mx.
7
Center for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96813, USA. jasonsi@hawaii.edu.
8
National Heart Research Institute Singapore, National Heart Centre, Singapore 169609, Singapore. d.hausenloy@ucl.ac.uk.
9
Institute of Biochemistry, Medical School, Justus-Liebig University, 35392 Giessen, Germany. d.hausenloy@ucl.ac.uk.
10
Yong Loo Lin School of Medicine, National University Singapore, Singapore 117597, Singapore. d.hausenloy@ucl.ac.uk.
11
The Hatter Cardiovascular Institute, University College London, London WC1E 6HX, UK. d.hausenloy@ucl.ac.uk.
12
The National Institute of Health Research University College London Hospitals Biomedical Research Centre, Research & Development, London W1T 7DN, UK. d.hausenloy@ucl.ac.uk.
13
Center for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96813, USA. wab@hawaii.edu.
14
Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420008 Kazan, Russia. wab@hawaii.edu.

Abstract

Cardiovascular diseases are the leading cause of mortality worldwide. It is widely known that non-resolving inflammation results in atherosclerotic conditions, which are responsible for a host of downstream pathologies including thrombosis, myocardial infarction (MI), and neurovascular events. Macrophages, as part of the innate immune response, are among the most important cell types in every stage of atherosclerosis. In this review we discuss the principles governing macrophage function in the healthy and infarcted heart. More specifically, how cardiac macrophages participate in myocardial infarction as well as cardiac repair and remodeling. The intricate balance between phenotypically heterogeneous populations of macrophages in the heart have profound and highly orchestrated effects during different phases of myocardial infarction. In the early "inflammatory" stage of MI, resident cardiac macrophages are replaced by classically activated macrophages derived from the bone marrow and spleen. And while the macrophage population shifts towards an alternatively activated phenotype, the inflammatory response subsides giving way to the "reparative/proliferative" phase. Lastly, we describe the therapeutic potential of cardiac macrophages in the context of cell-mediated cardio-protection. Promising results demonstrate innovative concepts; one employing a subset of yolk sac-derived, cardiac macrophages that have complete restorative capacity in the injured myocardium of neonatal mice, and in another example, post-conditioning of cardiac macrophages with cardiosphere-derived cells significantly improved patient's post-MI diagnoses.

KEYWORDS:

cardiac repair; cardioprotection; innate immune response; macrophages; myocardial infarction; remodeling

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