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Based on the current evidence, we propose that the iron-overloaded, ROS-prone milieu of EMS renders EESCs susceptible to Erastin-triggered, multi-pathway regulated cell death that integrates ferroptosis with necroptotic and pyroptotic signaling, while ferritin handling and mitophagy act as key modulators of susceptibility

We found the most evident maintenance of GPX4 in the Glu- or erastin-induced HT22 cell injury model after pretreatment with lapatinib