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From these results, it could be inferred that CaOx-induced ferroptosis, as observed in the previous series of biochemical reactions, reduced the ability of cells to resist oxidation, thereby resulting in Fe2+ overload, mitochondrial damage and an increase in lipid peroxidation, which then induced an intracellular ROS outbreak, eventually causing severe cell injury

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It produces apoptosis through a mitochondrial membrane potential change and caspase 3 activation [23, 24]

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The UPR is activated only after three transmembrane proteins, namely, inositol-requiring protein 1 (IRE1), dsRNA-activated protein kinase (PKR)-like ER kinase (PERK), and activating transcription factor 6 (ATF6), dissociate from BiP/GRP78, which serves as an inhibitory binding chaperone