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Because Fe-S clusters function as essential cofactors for components of the electron transport chain, TCA cycle enzymes, and genome maintenance machinery, their stability depends on a reducing intracellular environment that is maintained, in part, by GSH 203,208

(99) showed that triptolide could improve RA by down-regulating the inflammatory function of neutrophils (inhibiting the expression of pro-inflammatory cytokines, inhibiting migration, NETosis and autophagy, and promoting apoptosis)

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Additionally, the gut microbiota-derived metabolite capsiate relieves ferroptosis-related osteoarthritis through the regulation of solute carrier family 2 member 1 and HIF-1 [99]

Heat stress induced apoptosis is triggered by transcription-independent p53, Ca2+ dyshomeostasis and the subsequent Bax mitochondrial translocation