CD4 and myocardial infarction: Most exosomes from different sources can protect the damaged myocardium, but some experimental results show that some exosomes from cardiomyocytes can inhibit angiogenesis, promote inflammation and cardiomyocyte apoptosis (32, 37, 150, 151, 158); circulating exosomes also induce inflammation and ferroptosis, exacerbate MI/RI (142); M1 macrophages and CD4+ T-cell-derived exosomes can promote inflammation and ventricular remodeling (163).