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This suggests that the three pathways cooperate to cause AKI in kidney IRI.54 In this regard, in cell culture experiments, deficiency of the necroptotic protein MLKL favored the occurrence of ferroptosis, and absence of the pro-ferroptotic protein ACSL4 favored the occurrence of necroptosis.53 Furthermore, in kidney IRI, MLKL deficiency accelerated the increase in ACSL4 expression, potentially suggesting accelerated ferroptosis when necroptosis is suppressed, but prophylactic 16–86 followed by additional doses every 3h was not protective.53,54 Despite the authors suggestion that increased ACSL4 represents increased ferroptosis when necroptosis is suppressed, the fact that 16–86 failed to prevent kidney dysfunction in MLKL deficient mice indeed argues against recruitment of ferroptosis in this model, and, consequently argues against a role for ACSL4 as a marker of ferroptosis in vivo
