WNT1 and myocardial infarction: Collectively, in MI model, ferroptosis leads to a decrease in the content of exosomal miR-106b-3p released by cardiomyocytes, resulting in the activation of Wnt1, which ultimately promotes M1 polarization in macrophages, whereas Fer-1 can block ferroptosis and restore the content of exosomal miR-106b-3p in cardiomyocyte thereby Fer-1 has a therapeutic effect.