In this study, AMs-derived exosomes were typically saucer-like with a size from 40 to 160 nm, which could express specific markers CD9, CD63, and CD81 and successfully loaded with Fcn B. The transfection of si-Fcnb inhibited the occurrence of autophagy and ferroptosis in BLM-induced lung epithelial cells, but this effect was reversed by oe-Fcnb-transfected and BLM-treated AMs-derived exosomes, suggesting that BLM-induced AMs mediated lung epithelial cells ferroptosis through Fcn B transported by exosomes. Here, CD63 is linked to Bloom syndrome.