Moreover, neutrophils released the prestored PTX3 in the early phase of acute myocardial infarction that bind to activated circulating platelets and dampen their proinflammatory response [34], whereas PTX3 also aggregated with histones and protected from histone-mediated endothelial cytotoxicity in sepsis [35, 36]. This evidence concerns the gene PTX3 and myocardial infarction.