A recent study also suggested that M1 macrophages secrete pro-inflammatory EVs post-MI, which exert anti-angiogenic effects by transferring EV-enriched miR-155 into cardiac ECs to inhibit the angiogenesis and further accelerate MI injury by targeting the Sirt1/AMPKα2-endothelial nitric oxide synthase and RAC1-PAK2 signaling pathways [117]. This evidence concerns the gene PRKAA2 and myocardial infarction.