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      The cellular immune system in the post-myocardial infarction repair process.

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          Abstract

          Growing evidence indicates that overactivation and prolongation of the inflammatory response after acute myocardial infarction (AMI) result in worse left ventricular remodelling, dysfunction and progression to heart failure. This post-AMI inflammatory response is characterised by the critical involvement of cells from both the innate and adaptive immune systems. In this review paper, we aim to summarise and discuss the emergence of immune cells in the bloodstream and myocardium after AMI in men and mice. Subset composition, phenotypes, and kinetics of immune cells are considered. In addition, the relation with post-MI cardiac remodelling, function and outcome is reported. Increased knowledge of immune components, the mechanisms and interactions by which these cells contribute to myocardial damage and repair following AMI may help to close the gaps that limit improvement of treatments of those who survive the acute infarction.

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          Author and article information

          Journal
          Int. J. Cardiol.
          International journal of cardiology
          Elsevier BV
          1874-1754
          0167-5273
          Jan 20 2015
          : 179
          Affiliations
          [1 ] Cardiovascular Diseases, Department of Translational Pathophysiological Research, University of Antwerp, Campus Drie Eiken, Universiteitsplein 1, 2610 Wilrijk, Belgium; Laboratory of Cellular and Molecular Cardiology, Department of Cardiology, Antwerp University Hospital, Wilrijkstraat 10, 2650 Edegem, Belgium. Electronic address: Sam.Latet@uantwerpen.be.
          [2 ] Cardiovascular Diseases, Department of Translational Pathophysiological Research, University of Antwerp, Campus Drie Eiken, Universiteitsplein 1, 2610 Wilrijk, Belgium; Laboratory of Cellular and Molecular Cardiology, Department of Cardiology, Antwerp University Hospital, Wilrijkstraat 10, 2650 Edegem, Belgium. Electronic address: Vicky.Hoymans@uza.be.
          [3 ] Cardiovascular Diseases, Department of Translational Pathophysiological Research, University of Antwerp, Campus Drie Eiken, Universiteitsplein 1, 2610 Wilrijk, Belgium; Laboratory of Cellular and Molecular Cardiology, Department of Cardiology, Antwerp University Hospital, Wilrijkstraat 10, 2650 Edegem, Belgium. Electronic address: Paul.VanHerck@uza.be.
          [4 ] Cardiovascular Diseases, Department of Translational Pathophysiological Research, University of Antwerp, Campus Drie Eiken, Universiteitsplein 1, 2610 Wilrijk, Belgium; Laboratory of Cellular and Molecular Cardiology, Department of Cardiology, Antwerp University Hospital, Wilrijkstraat 10, 2650 Edegem, Belgium. Electronic address: Chris.Vrints@uza.be.
          Article
          S0167-5273(14)02148-2
          10.1016/j.ijcard.2014.11.006
          25464457

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