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Under pro-inflammatory conditions, as evidenced by interventions with LPS or IFN-, microglia are insensitive to ferroptosis, yet susceptible to iron overload ( in vitro data showed that genetic depletion of iNOS renders Raw264.7 cells and EOC 20 cells vulnerable to ferroptosis, whereas NO donors (SNAP, DPTA-NONOate) empower the ferroptotic resistance of M2 microglia ( The sophisticated interplay between neuroinflammation, instigated by microglia in response to inflammatory stimuli, and ferroptosis in microglia has been documented

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Further demonstrating the Gpr183/oxysterol axis in regulating microglial activation, Song et al

[DOI] [PubMed] [Google Scholar] 95.Liew Z, Bach CC, Asarnow RF, Ritz B, Olsen J