Extracellular Vesicles in Myocardial Infarction: Dual Role in Ferroptosis Regulation and In Vivo Imaging

Acute myocardial infarction (AMI), a life-threatening event caused by cardiomyocyte death due to oxygen deprivation, drives cardiac dysfunction through ferroptosis—an iron-dependent cell death mechanism involving lipid peroxidation. By delivering multifunctional cargoes with low immunogenicity, extracellular vesicles (EVs) hold the therapeutic potential to inhibit cardiomyocyte ferroptosis through the regulation of iron metabolism and the mitigation of oxidative damage. Their dual role as targeted drug carriers and natural imaging probes enhances precision in AMI management. EVs enable the non-invasive tracking of biodistribution and therapeutic responses in real time when integrated with molecular imaging technology, offering insights into cardiac repair mechanisms. This synergy between EV-based therapy and advanced imaging presents a novel strategy for AMI diagnosis and targeted intervention.