Fig. 1

Known function of organelles in ferroptosis. In the mitochondrion, glutamine is oxidatively phosphorylated, contributing to ROS production. The ER stress response is mediated by the PERK-eIF2α-ATF4 pathway involved in GPX4 degradation, ultimately, inhibiting oxidative injury. In the lysosome, STAT3-mediated cathepsin B expression is required for ferroptosis via the MEK-ERK pathway. Meanwhile, chaperone-mediated autophagy (CMA) regulated by HSP90, CDDO, HSC70 and Lamp-2a promotes the degradation of GPX4. In the Golgi apparatus, Golgi-disrupting compounds enable inhibition of ARF1, an inhibitor of GSH and ACSL4, and activator of SLC7A11, leading to increased ROS