Hypoxia-preconditioned cardiomyocyte-derived extracellular vesicles alleviate myocardial ischemic injury by reprogramming macrophage polarization via the Fgl2/NF-κB pathway

Cardiomyocyte-derived hypoxia/reoxygenation-EVs deliver miR-199b-3p to restrain Fgl2-dependent inflammatory signaling and post-infarction injury, highlighting the EV/miR-199b-3p/Fgl2 axis as a potential therapeutic target for improving outcomes after MI.