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[DOI] [PubMed] [Google Scholar] 74.Bardaweel S.K., Gul M., Alzweiri M., Ishaqat A., ALSalamat H.A., Bashatwah R.M

We identified the causal gene through whole-genome resequencing-based polymorphism analysis and reverse-genetic approaches using mutants and NILs in the Enrei genetic background

On one hand, gut dysbiosis facilitates ferroptosis by affecting iron metabolic pathways, like blocking the synthesis and release of hepatic hepcidin and expression of the iron transporter FPN1 to inhibit iron efflux and causing systemic and local iron overload in joints, thus leading to ferroptosis in OA chondrocytes

Pediatr Res 38 , 585591 (1995)

Although astrocytes are known to supply cysteine and GSH precursors to neurons, thereby maintaining redox balance [58-60], our findings suggest that the neuroprotective effects of NAC in this model are primarily mediated through microglial and oxidative pathways rather than astrocytic modulation