title: Cellular recruitment in myocardial ischaemia/reperfusion injury.
abstract: BACKGROUND
  Myocardial infarction (MI) is strictly linked to atherosclerosis. Beyond the mechanical narrowing of coronary vessels lumen, during MI a great burden of inflammation is carried out. One of the crucial events is represented by the ischaemia/reperfusion injury, a complex event involving inflammatory cells (such as neutrophils, platelets, monocytes/macrophages, lymphocytes and mast cells) and key activating signals (such as cytokines, chemokines and growth factors). Cardiac repair following myocardial infarction is dependent on a finely regulated response involving a sequential recruitment and the clearance of different subsets of inflammatory cells.
  
  
  METHODS
  This narrative review was based on the works detected on PubMed and MEDLINE up to November 2015.
  
  
  RESULTS
  Infarct healing classically follows three overlapping phases: the inflammatory phase, in which the innate immune pathways are activated and inflammatory leucocytes are recruited in order to clear the wound from dead cells; the proliferative phase, characterized by the suppression of pro-inflammatory signalling and infiltration of 'repairing' cells secreting matrix proteins in the injured area; and the maturation phase, which is associated with the quiescence and the elimination of the reparative cells together with cross-linking of the matrix. All these phases are timely regulated by the production of soluble mediators, such as cytokines, chemokines and growth factors.
  
  
  CONCLUSIONS
  Targeting inflammatory cell recruitment early during reperfusion and healing might be promising to selectively inhibit injury and favour repair. This approach might substantially improve adverse postischaemic left ventricle remodelling, characterized by dilation, hypertrophy of viable segments and progressive dysfunction.
authors.affiliation: First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, Genoa, Italy.|IRCCS AOU San Martino - IST Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy.
authors.forename: Aldo
authors.initials: A
authors.lastname: Bonaventura
authors.affiliation: First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, Genoa, Italy.|IRCCS AOU San Martino - IST Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy.
authors.forename: Fabrizio
authors.initials: F
authors.lastname: Montecucco
authors.affiliation: First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, Genoa, Italy.|IRCCS AOU San Martino - IST Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy.
authors.forename: Franco
authors.initials: F
authors.lastname: Dallegri
mesh_terms: D001792:Blood Platelets / Q000276:immunology; D049109:Cell Proliferation / Q000502:physiology; D018925:Chemokines / Q000276:immunology; D016207:Cytokines / Q000276:immunology*; D005109:Extracellular Matrix / Q000378:metabolism; D016326:Extracellular Matrix Proteins / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D036341:Intercellular Signaling Peptides and Proteins / Q000276:immunology*; D008264:Macrophages / Q000276:immunology; D008407:Mast Cells / Q000276:immunology; D009000:Monocytes / Q000276:immunology; D017202:Myocardial Ischemia / Q000276:immunology*; D015428:Myocardial Reperfusion Injury / Q000276:immunology*; D032383:Myocytes, Cardiac / Q000502:physiology*; D020556:Neutrophil Infiltration / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D012038:Regeneration
chemical_list: D018925:Chemokines; D016207:Cytokines; D016326:Extracellular Matrix Proteins; D036341:Intercellular Signaling Peptides and Proteins
keywords: Inflammation; ischaemia/reperfusion injury; macrophages; myocardial infarction; neutrophils