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Experimental cisplatin and folic acid nephropathy are frequently studied models which have a human counterpart.55 Folic acid-AKI is characterized by a tubular cell death and there is evidence that early injury is mediated by ferroptosis: whereas single prophylactic doses of either or both apoptosis or necroptosis inhibitors were not protective, a single prophylactic dose of ferrostatin-1 reduced renal injury and improved renal function.21 Moreover, ferrostatin-1 prevented the inflammatory response and the expression of necroptotic proteins, suggesting that ferroptosis may activate other pathways of cell death, including necroptosis, which was previously shown to depend on the proinflammatory cytokine TWEAK and its receptor Fn14 in this model.21,56 In this regard, folic acid nephropathy could represent an excellent model to study ferroptosis biomarkers, given the demonstrated role of ferroptosis, the high levels of kidney 4-HNE and oxygenated AA-PE species and the response of both markers to ferrostatin-1.21,29 Moreover, in folic acid nephropathy, ferroptosis is an early event that triggers an inflammatory response and a secondary wave of necroptotic cell death that amplifies and maintains kidney dysfunction56 (Fig

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Cellular cooperation: insights from microbes