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Protective action on the renal system Acute kidney injury (AKI) manifests itself as an independent cause of mortality (Rewa and Bagshaw, 2014), and may also be seen as a co-morbidity in several diseases (Pereira et al., 2012)

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Evidently, intracellular cyst(e)ine contribute to ferroptosis suppression via at least two additional pathways in different contexts: in a mouse lung adenocarcinoma model, NFS1 cysteine desulfurase utilizes cysteine to synthesize ironsulfur clusters, which are necessary for preventing activation of the iron-starvation response, subsequent iron influx and ferroptosis 14 (Fig