Chemokines in Myocardial Infarction
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REVIEW ARTICLE
Chemokines in Myocardial Infarction Bijun Chen 1 & Nikolaos G. Frangogiannis 1 Received: 13 January 2020 / Accepted: 15 April 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract In the infarcted myocardium, cardiomyocyte necrosis triggers an intense inflammatory reaction that not only is critical for cardiac repair, but also contributes to adverse remodeling and to the pathogenesis of heart failure. Both CC and CXC chemokines are markedly induced in the infarcted heart, bind to endothelial glycosaminoglycans, and regulate leukocyte trafficking and function. ELR+ CXC chemokines (such as CXCL8) control neutrophil infiltration, whereas CC chemokines (such as CCL2) mediate recruitment of mononuclear cells. Moreover, some members of the chemokine family (such as CXCL10 and CXCL12) may mediate leukocyte-independent actions, directly modulating fibroblast and vascular cell function. This review manuscript discusses our understanding of the role of the chemokines in regulation of injury, repair, and remodeling following myocardial infarction. Although several chemokines may be promising therapeutic targets in patients with myocardial infarction, clinical implementation of chemokine-based therapeutics is hampered by the broad effects of the chemokines in both injury and repair. Keywords Chemokine . Leukocyte . Myocardial infarction . Cardiac remodeling . CCL2 . CXCL12
Introduction Myocardial infarction (MI) is a leading cause of morbidity and mortality worldwide [1]. Sudden occlusion of a coronary artery results in complete loss of perfusion in the myocardial segments subserved by the vessel. Severe and sustained ischemia triggers a wavefront of cardiomyocyte death [2], leading to loss of large amounts of cardiac muscle. Because the adult mammalian heart has negligible regenerative capacity, repair of the infarcted heart is dependent on inflammation-driven formation of a scar. Over the last 40 years, new pharmacologic therapies [3, 4] and the successful implementation of early reperfusion [5] have significantly reduced mortality in patients presenting with acute MI. However, improved survival resulted in an expanding pool of MI patients who survive the acute event, but remain at a high risk for development of chronic heart failure. The pathobiology of post-infarction heart failure is Associate Editor Saskia de Jager oversaw the review of this article * Nikolaos G. Frangogiannis [email protected] 1
The Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, 1300 Morris Park Avenue Forchheimer G46B, Bronx, NY, USA
linked with “cardiac remodeling,” a complex process that involves both infarcted and non-infarcted myocardial segments and results in progressive functional deterioration and an increased incidence of arrhythmias, typically associated with chamber dilation. The severity of post-infarction remodeling is dependent not only on the size of the infarct, but also on the qualitative chara
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