IL4I1 attenuates myocardial infarction by inhibiting macrophage ferroptosis via the I3P/AHR/NRF2 signaling pathway

We identify a novel cardioprotective axis wherein macrophage-derived IL4I1 catalyzes the production of I3P, activating AHR-NRF2 signaling to suppress ferroptosis, thereby mitigating post-MI inflammation, adverse remodeling, and cardiac dysfunction. Targeting IL4I1 and I3P represents a promising therapeutic strategy for ischemic heart disease.