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Additionally, the role of non-classical ferroptosis suppressors (e.g., FSP1, DHODH, and GCH1/BH4) in ADPKD is entirely unexploredwhether these pathways compensate for GPX4 downregulation in cystic kidneys or if their dysfunction exacerbates ferroptosis susceptibility remains unknown, limiting the development of multi-targeted interventions

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Following MP phagocytosis, immune cells obstructed cortical capillaries, producing neurological deficits that persisted for 4 weeks (Huang et al., 2025)