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These findings emphasize KXS’s potential in regulating neuroinflammation and preventing neuronal apoptosis (Guo et al., 2019)
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Disrupting this homeostasis by blocking fission using CRISPR/Cas9-mediated genetic depletion of dynamin-related protein 1 (DRP1) confers resistance to ferroptosis, whereas the lack of optic atrophy 1 type (OPA1) protects against ferroptosis through cysteine deprivation, xCT inhibition, and GPx4 inhibition [83,84]
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