Knowledge gaps to understanding cardiac macrophage polarization following myocardial infarction

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

卷:1862

Article

Lindsey, Merry L.^1,2  Saucerman, Jeffrey J.³  DeLeon-Pennell, Kristine Y.¹ 

[1] Univ Mississippi, Med Ctr, Dept Physiol & Biophys, Mississippi Ctr Heart Res, 2500 North State St, Jackson, MS 39216 USA

[2] GV Sonny Montgomery Vet Affairs Med Ctr, Res Serv, Jackson, MS USA

[3] Univ Virginia, Dept Biomed Engn, Charlottesville, VA USA

关键词: Macrophage;    Myocardial infarction;    Matrix metalloproteinases;    Computational modeling;    Big data;   

DOI  :  10.1016/j.bbadis.2016.05.013

来源: Elsevier

【 摘 要 】

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. (C) 2016 Elsevier B.V. All rights reserved.

【 授权许可】

Free