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Biochim Biophys Acta. 2016 Dec;1862(12):2288-2292. doi: 10.1016/j.bbadis.2016.05.013. Epub 2016 May 27.

Knowledge gaps to understanding cardiac macrophage polarization following myocardial infarction.

Author information

1
Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA; Research Service, G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, MS, USA. Electronic address: mllindsey@umc.edu.
2
Department of Biomedical Engineering, University of Virginia, Charlottesville, VA, USA.
3
Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA. Electronic address: kdeleon@umc.edu.

Abstract

Following myocardial infarction (MI), macrophages coordinate both pro-inflammatory and reparative responses of the left ventricle (LV) by reacting to and secreting cytokines, chemokines, and growth factors and by stimulating endothelial cells and fibroblasts to modulate neovascularization and scar formation. Healing of the infarcted LV can be divided into three distinct, but overlapping phases: inflammatory, proliferative, and maturation. Macrophages are involved in all phases. Despite macrophages being a major leukocyte cell type in the post-MI LV, how this cell type regulates LV remodeling over the post-MI time continuum is not completely understood. In this review, we summarize the current literature as a foundation to discuss the major knowledge gaps that remain. Defining the post-MI temporal macrophage phenotypes to establish a classification system is the first step in exploring how macrophage phenotypes are regulated, how temporal stimulation and secretion profiles evolve, and how best to modify stimuli to yield predictable cell responses. This article is part of a Special Issue entitled: The role of post-translational protein modifications on heart and vascular metabolism edited by Jason R.B. Dyck & Jan F.C. Glatz.

KEYWORDS:

Big data; Computational modeling; Macrophage; Matrix metalloproteinases; Myocardial infarction

PMID:
27240543
PMCID:
PMC5124538
DOI:
10.1016/j.bbadis.2016.05.013
[Indexed for MEDLINE]
Free PMC Article

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