title: Induction of a monocyte/macrophage phenotype switch by mesenchymal stem cells might contribute to improved infarct healing postacute myocardial infarction.
abstract: Inadequate healing following acute myocardial infarction (AMI) can lead to the development of heart failure. The ischemic myocardium triggers an inflammatory response that clears cell debris and initiates the onset of scar tissue formation. The duration and intensity of this inflammatory response have been linked to the cardiac functioning post-AMI. In order to diminish scar tissue formation and stimulate regeneration of cardiac tissue, mesenchymal stem cell (MSC) have been applied post-AMI and showed beneficial effects on cardiac function. However, other than the expected regeneration of cardiac tissue, modulation of the inflammatory response post-AMI, especially related to an effect on monocytes/macrophages, was recently found to be an important aspect of MSC therapy. In healing post-AMI, monocytes and macrophages are key players that can either stimulate or repress inflammation using different phenotypes. Increased levels of the proinflammatory phenotype have clinically been associated with poor cardiac functional outcome post-AMI. MSC have been suggested to switch the monocytes/macrophages phenotype into a more anti-inflammatory state and might therefore beneficially influence the duration and intensity of the inflammatory response and subsequent cardiac function post-AMI. To gain more insight into this effect of MSC, this review provides an overview of the most relevant studies regarding this modulatory effect of MSC on monocytes/macrophages including its mechanisms to improve cardiac functioning post-AMI.
authors.affiliation: Department of Pathology, VU University Medical Centre, Amsterdam the Netherlands 2 Department of Cardiology, Academic Medical Centre, University of Amsterdam, Amsterdam, the Netherlands - e.terhorst@vumc.nl.
authors.forename: E N
authors.initials: EN
authors.lastname: Ter Horst
authors.forename: B A
authors.initials: BA
authors.lastname: Naaijkens
authors.forename: P A
authors.initials: PA
authors.lastname: Krijnen
authors.forename: A M
authors.initials: AM
authors.lastname: Van Der Laan
authors.forename: J J
authors.initials: JJ
authors.lastname: Piek
authors.forename: H W
authors.initials: HW
authors.lastname: Niessen
mesh_terms: D000818:Animals; D002921:Cicatrix; D006333:Heart Failure / Q000209:etiology / Q000517:prevention & control; D006801:Humans; D007249:Inflammation / Q000503:physiopathology / Q000628:therapy*; D008264:Macrophages / Q000378:metabolism; D045164:Mesenchymal Stem Cell Transplantation / Q000379:methods*; D059630:Mesenchymal Stem Cells / Q000378:metabolism; D009000:Monocytes / Q000378:metabolism; D009203:Myocardial Infarction / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D010641:Phenotype; D013997:Time Factors