Crosstalk Between Inflammatory Cells to Promote Cardioprotective Angiogenesis

Inflammation following myocardial infarction (MI) occurs in a tightly regulated series of events that can either positively or negatively influence the outcome and recovery of the heart (1). The classical hallmark of MI-induced inflammation is the rapid recruitment of neutrophils, the front-line cells of the innate immune system, followed by circulating monocytes. This coordinated infiltration aids in the clearance of debris; however, when dysregulated, can result in inflammation that exacerbates tissue injury(2).