We are analyzing https://link.springer.com/article/10.1007/s00018-022-04416-w.

Title:
Vitamin K1 inhibits ferroptosis and counteracts a detrimental effect of phenprocoumon in experimental acute kidney injury | Cellular and Molecular Life Sciences
Description:
Ferroptosis, a type of iron-dependent programmed cell death distinct from apoptosis, necroptosis, and other types of cell death, is characterized by lipid peroxidation, reactive oxygen species production, and mitochondrial dysfunction. Accumulating evidence has highlighted vital roles for ferroptosis in multiple diseases, including acute kidney injury. Therefore, ferroptosis has become a major focus for translational research. However, despite its involvement in pathological conditions, there are no pharmacologic inhibitors of ferroptosis in clinical use. In the context of drug repurposing, a strategy for identifying new uses for approved drugs outside the original medical application, we discovered that vitamin K1 is an efficient inhibitor of ferroptosis. Our findings are strengthened by the fact that the vitamin K antagonist phenprocoumon significantly exacerbated ferroptotic cell death in vitro and also massively worsened the course of acute kidney injury in vivo, which is of utmost clinical importance. We therefore assign vitamin K1 a novel role in preventing ferroptotic cell death in acute tubular necrosis during acute kidney injury. Since the safety, tolerability, pharmacokinetics, and pharmacodynamics of vitamin K1 formulations are well documented, this drug is primed for clinical application, and provides a new strategy for pharmacological control of ferroptosis and diseases associated with this mode of cell death.
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Keywords {🔍}

ferroptosis, vitamin, pubmed, article, cell, google, scholar, cas, death, cells, kidney, phenprocoumon, fig, renal, aki, central, lipid, effect, germany, acute, injury, acsl, tubular, inhibitor, plasma, min, peroxidation, vitro, membrane, rsl, httpsdoiorgs, mice, ferrostatin, iri, cancer, biol, analysis, clinical, ferroptotic, role, expression, function, conditions, gpx, murine, animals, induced, patients, protective, nature,

Topics {✒️}

oncogenic-ras-harboring cancer cells renal ischemia–reperfusion injury worse safety profile jessica schmitz jan hinrich bräsen olympus u-do3 microscope called radical-trapping antioxidants acute kidney injury ir + phenprocoumon group compared university hospital schleswig–holstein university hospital schleswig-holstein acute tubular injury von samson-himmelstjerna article download pdf chronic kidney disease inhibit glutathione depletion-mediated anti-ferroptotic defense mechanism friedmann angeli jp vitamin k-dependent processes vitamin k-dependent biosynthesis warfarin-related nephropathy modeled cell death-aggravating impact preventing oxidative injury central animal facility free-radical-scavenging action acute kidney failure glutathione-independent ferroptosis suppressor k1/kg body weight christian-albrechts-university kiel benedikt kolbrink periodic acid-schiff staining article kolbrink original author dhodh-mediated ferroptosis defence view anti-β-actin antibody warfarin-related nephropathy occurs acute tubular necrosis full access anti-acsl4 antibody ab155282 cellular cystine import iron-dependent form privacy choices/manage cookies iron overload syndromes preserves kidney function renal disease—insights anti-ferroptotic properties cell death mediated ferroptotic cell death highlighted vital roles

Schema {🗺️}

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         description:Ferroptosis, a type of iron-dependent programmed cell death distinct from apoptosis, necroptosis, and other types of cell death, is characterized by lipid peroxidation, reactive oxygen species production, and mitochondrial dysfunction. Accumulating evidence has highlighted vital roles for ferroptosis in multiple diseases, including acute kidney injury. Therefore, ferroptosis has become a major focus for translational research. However, despite its involvement in pathological conditions, there are no pharmacologic inhibitors of ferroptosis in clinical use. In the context of drug repurposing, a strategy for identifying new uses for approved drugs outside the original medical application, we discovered that vitamin K1 is an efficient inhibitor of ferroptosis. Our findings are strengthened by the fact that the vitamin K antagonist phenprocoumon significantly exacerbated ferroptotic cell death in vitro and also massively worsened the course of acute kidney injury in vivo, which is of utmost clinical importance. We therefore assign vitamin K1 a novel role in preventing ferroptotic cell death in acute tubular necrosis during acute kidney injury. Since the safety, tolerability, pharmacokinetics, and pharmacodynamics of vitamin K1 formulations are well documented, this drug is primed for clinical application, and provides a new strategy for pharmacological control of ferroptosis and diseases associated with this mode of cell death.
         datePublished:2022-06-28T00:00:00Z
         dateModified:2022-06-28T00:00:00Z
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      headline:Vitamin K1 inhibits ferroptosis and counteracts a detrimental effect of phenprocoumon in experimental acute kidney injury
      description:Ferroptosis, a type of iron-dependent programmed cell death distinct from apoptosis, necroptosis, and other types of cell death, is characterized by lipid peroxidation, reactive oxygen species production, and mitochondrial dysfunction. Accumulating evidence has highlighted vital roles for ferroptosis in multiple diseases, including acute kidney injury. Therefore, ferroptosis has become a major focus for translational research. However, despite its involvement in pathological conditions, there are no pharmacologic inhibitors of ferroptosis in clinical use. In the context of drug repurposing, a strategy for identifying new uses for approved drugs outside the original medical application, we discovered that vitamin K1 is an efficient inhibitor of ferroptosis. Our findings are strengthened by the fact that the vitamin K antagonist phenprocoumon significantly exacerbated ferroptotic cell death in vitro and also massively worsened the course of acute kidney injury in vivo, which is of utmost clinical importance. We therefore assign vitamin K1 a novel role in preventing ferroptotic cell death in acute tubular necrosis during acute kidney injury. Since the safety, tolerability, pharmacokinetics, and pharmacodynamics of vitamin K1 formulations are well documented, this drug is primed for clinical application, and provides a new strategy for pharmacological control of ferroptosis and diseases associated with this mode of cell death.
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         Acute kidney injury
         Ischemia–reperfusion injury
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         Life Sciences
         Biochemistry
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      name:Department of Nephrology and Hypertension, University Hospital Schleswig-Holstein, Kiel, Germany
      name:Department of Nephrology and Hypertension, University Hospital Schleswig-Holstein, Kiel, Germany
      name:Department of Nephrology and Hypertension, University Hospital Schleswig-Holstein, Kiel, Germany
      name:Department of Nephrology and Hypertension, University Hospital Schleswig-Holstein, Kiel, Germany
      name:Nephropathology Unit, Institute of Pathology, University of Hannover, Hannover, Germany
      name:Nephropathology Unit, Institute of Pathology, University of Hannover, Hannover, Germany
      name:Department of Nephrology and Hypertension, University Hospital Schleswig-Holstein, Kiel, Germany
      name:Department of Nephrology and Hypertension, University Hospital Schleswig-Holstein, Kiel, Germany

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