Author:
Pluijmert Niek J.,Atsma Douwe E.,Quax Paul H. A.
Abstract
Following acute occlusion of a coronary artery causing myocardial ischemia and implementing first-line treatment involving rapid reperfusion, a dynamic and balanced inflammatory response is initiated to repair and remove damaged cells. Paradoxically, restoration of myocardial blood flow exacerbates cell damage as a result of myocardial ischemia–reperfusion (MI-R) injury, which eventually provokes accelerated apoptosis. In the end, the infarct size still corresponds to the subsequent risk of developing heart failure. Therefore, true understanding of the mechanisms regarding MI-R injury, and its contribution to cell damage and cell death, are of the utmost importance in the search for successful therapeutic interventions to finally prevent the onset of heart failure. This review focuses on the role of innate immunity, chemokines, cytokines, and inflammatory cells in all three overlapping phases following experimental, mainly murine, MI-R injury known as the inflammatory, reparative, and maturation phase. It provides a complete state-of-the-art overview including most current research of all post-ischemic processes and phases and additionally summarizes the use of immunomodulatory therapies translated into clinical practice.
Subject
Cardiology and Cardiovascular Medicine
Reference260 articles.
1. Phosphatidylcholine biosynthesis in myocardial ischaemia;Lochner;J Mol Cell Cardiol.,1989
2. Development of cell injury in sustained acute ischemia;Jennings;Circulation.,1990
3. Biomarkers of cardiac injury: an update;Rajappa;Angiology.,2005
4. Biomarkers and acute coronary syndromes: an update;Mueller;Eur Heart J.,2014
5. Regulation of the inflammatory response in cardiac repair;Frangogiannis;Circ Res.,2012
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