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2013;22:13e275

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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Rather, a growing body of evidence suggests that the systemic and local actions of incretins and metabolic hormones modulate multiple pathways that can promote inflammatory and fibrotic injury