Cellular recruitment in myocardial ischemia/reperfusion injury

BACKGROUND: Myocardial infarction 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 ischemia/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 sequential recruitment and clearance of different subsets of inflammatory cells. MATERIALS AND 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 leukocytes are recruited in order to clear the wound from dead cells; the proliferative phase, characterized by the suppression of pro-inflammatory signaling and infiltration of "repairing" cells secreting matrix proteins in the injured area; and the maturation phase, that is associated with quiescence and elimination of the reparative cells together with cross-linking of the matrix. All these phases are timely regulated by production soluble mediators, such as cytokines, chemokines, and growth factors. CONCLUSION: Targeting inflammatory cell recruitment early during reperfusion and healing might be promising to selectively abrogate injury and favoring repair. This approach might substantially improve adverse post-ischemic left ventricle remodeling, characterized by dilation, hypertrophy of viable segments, and progressive dysfunction.