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The primary genetic targets for treating ferroptosis may include p53, Gpx4, ACSL4, and Nrf2

There is still scarce data about the signaling pathways and especially the physiological role of erythrocyte necroptosis

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et al., 2023), and supplementing cofactors essential for GPX4 enzymatic activity, such as selenium (Ingold et al., 2018

This position is supported by in vivo studies, which used genetically encoded redox sensors to investigate the spatial patterning of cellular redox potential in Caenorhabditis elegans [11]

NHE is also situated in the membrane of mitochondria, and mitochondrial sodium/calcium exchanger NCLX regulates mitochondrial sodium import and calcium export