Similarly, ALKBH5 overexpression alleviates cardiac function post-MI and promotes CM proliferation via the m6A-YTHDF1-YAP axis.313 Furthermore, METTL3-m6A-HNRNPA2B1 promotes the biogenesis of extracellular vesicle (EV)-encapsulated miR-503 derived from ECs in AMI, which promotes CM apoptosis and cardiac dysfunction.314 Ischemia-reperfusion (I/R) injury is a severe cardiac ischemia complication resulting in CHD deterioration. Here, METTL3 is linked to myocardial infarction.