Vitamin K is recycled in the liver in order to maintain sufficient levels for activating vitamin K-dependent proteins (VKDP), including certain coagulation factors. In this process, vitamin K1 (taken up from the diet) is converted to vitamin K hydroquinone (KH2), either by the dithiol-dependent vitamin K-epoxide reductase (VKOR) or by NAD(P)H dehydrogenase quinone 1. KH2 is in turn oxidized to vitamin K epoxide (KO) by the enzyme gamma-glutamyl carboxylase (GGCX). During this conversion, GGCX activates the VKDPs by converting glutamate (Glu) to gamma-carboxyglutamate (Gla). Lastly, KO is converted back into vitamin K quinone by VKOR. Warfarin, a drug commonly used as a anticoagulant, inhibits VKOR, thus reducing the levels of VKH2 in the bloodstream. A too high dosage of warfarin can lead to heavy bleeding, a life-threatening condition. Threatment of this condition is a high dosis of Vitamine K, which is reduced to VHK2 by FSP1, a warfarin resistant reductase. The influence of FSP1 on this process, as well as its potential to eliminate lipid perozyl radicals, has been recently described in [https://doi.org/10.1038/s41586-022-05022-3 Nature(2022)] by Mishima et al.: A non-canonical vitamin K cycle is a potent ferroptosis suppressor. [LINE:c2514] Curved connections are not supported. [CONVERSION:id4c639557] Curved connections are not supported. [LINE:c2514] Invalid interaction type. [LINE:b6b59] Invalid interaction type. [LINE:b932d] Invalid interaction type. [LINE:fc9ff] Invalid interaction type. [LINE:id7f177b7f] Invalid interaction type. [LINE:idf5ba4b4a] Invalid interaction type. [UnknownPositiveInfluenceReaction:id4c639557] Reaction should contain only one reactant and one product. [-:-] Miriam data (PUBMED: 35922516) for ddb05 already exists. Ignoring...