Mini Review ARTICLE
(Re) solving repair after myocardial infarction
- 1Ludwig-Maximilians-Universität München, Germany
Cardiovascular diseases, including myocardial infarction and its complications such as heart failure, are the leading cause of death worldwide. To date, basic and translational research becomes necessary to unravel the mechanisms of cardiac repair post myocardial infarction. The local inflammatory tissue response after acute myocardial infarction determines the subsequent healing process. The diversity of leukocytes such as neutrophils, macrophages and lymphocytes contribute to the clearance of dead cells while activating reparative pathways necessary for myocardial healing. Cardiomyocyte death triggers wall thinning, ventricular dilatation, and fibrosis that can cause left ventricular dysfunction and heart failure. The ultimate goal of cardiac repair is to regenerate functionally viable myocardium after myocardial infarction to prevent cardiac death. Current therapies for heart failure after myocardial infarction are limited and non-curative. At the moment in clinic, conventional surgical interventions such as coronary artery bypass graft or percutaneous coronary interventions are only able to partially restore heart function, with a minor improvement in the left ventricular ejection fraction. The goal of this review is to provide an overview of endogenous myocardial repair mechanisms possibly transferable to future treatment strategies. Among the innovative factors identified as essential in cardiac healing, we highlight specialized pro-resolving mediators as the emerging factors that provide the key molecular signals for the activation of the reparative cells in the myocardium.
Keywords: Cardiac, Ischemia, Inflammation, Resolution, repair
Received: 12 Jul 2018;
Accepted: 31 Oct 2018.
Edited by:Mauro Perretti, Queen Mary University of London, United Kingdom
Reviewed by:Raffaele Marfella, Università degli Studi della Campania "Luigi Vanvitelli" Caserta, Italy
Asma Nusrat, University of Michigan, United States
Copyright: © 2018 Leoni and Soehnlein. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Giovanna Leoni, Ludwig-Maximilians-Universität München, Munich, Germany, Giovanna.Leoni@med.uni-muenchen.de