“…By administering PEGylate-indoleamine 2,3-dioxygenase 1, they showed protection against IRI by reprogramming tryptophan immunometabolism. 14 Ferroptosis was shown to be a further promising target for IRI modulation by Rokop et al 15 Indeed, in a mouse model of in situ IRI, ferroptosis was upregulated in the fatty liver group together with lipid peroxidation. Mitochondrial damage is closely related to ferroptosis, inflammation, and lipid peroxidation, whereas the degree of mitochondrial damage was related to liver survival after reperfusion in grafts subjected to machine perfusion.…”