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Keywords {🔍}

cell, ferroptosis, cells, acsl, death, pubmed, necroptosis, fig, mlkl, article, mice, google, scholar, cas, niht, expression, time, material, kidney, regulated, supplementary, protein, central, data, pathways, mlklknockout, necrosis, ferroptotic, germany, acute, lipid, studies, human, injury, iri, antibody, membrane, damage, vivo, renal, parental, reperfusion, wildtype, erastin, gpx, shown, observed, murine, ripk, analysis,

Topics {✒️}

crispr/cas9-based genome-editing technology px330-u6-chimeric_bb-cbh-hspcas9 ice-cold 10 mm tris–hcl 100 ng/ml tnfα + 25 µm zvad oncogenic-ras-harboring cancer cells pan-caspase inhibitor zvad-fmk inter-pathway cross-talk contributes necroptosis-insensitive mlkl-knockout mice article download pdf annexin v-fitc positivity atypical hemolytic-uremic syndrome vehicle-treated mlkl-knockout mice receptor-interacting protein kinase mlkl tris–edta buffer related subjects olympus u-do3 microscope gibco/thermo fisher scientific cystine-glutamate antiporter system clear time-dependent increases single-stranded sgrna oligos ferroptotic-mediated cell death jessica schmitz pharmacologically-induced reduction—albeit monoclonal rat mlkl annexin v-fitc antibody jan hinrich bräsen university hospital schleswig–holstein mlkl-knockout mice correlates full size image mlkl-knockout nih3t3 cells iron-dependent lipid peroxidation 0 mg/kg body weight crispr/cas9 technology ripk1 kinase-dependent apoptosis mlkl-edited nih3t3 cells mlkl-knockout mice compared hrp polymer system rsl3-induced cell death mlkl-driven membrane permeabilization increased time-dependent sensitivity acute tubular injury wildtype counterparts post-reperfusion ischemia-reperfusion injury acute renal failure acsl4-knockout nih3t3 cells dixon sj constitutive acsl4-knockout mice fluorescence-activated cell sorting anti-ferroptosis compounds acsl4-edited nih3t3 cells

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         headline:Necroptosis and ferroptosis are alternative cell death pathways that operate in acute kidney failure
         description:Ferroptosis is a recently recognized caspase-independent form of regulated cell death that is characterized by the accumulation of lethal lipid ROS produced through iron-dependent lipid peroxidation. Considering that regulation of fatty acid metabolism is responsible for the membrane-resident pool of oxidizable fatty acids that undergo lipid peroxidation in ferroptotic processes, we examined the contribution of the key fatty acid metabolism enzyme, acyl-CoA synthetase long-chain family member 4 (ACSL4), in regulating ferroptosis. By using CRISPR/Cas9 technology, we found that knockout of Acsl4 in ferroptosis-sensitive murine and human cells conferred protection from erastin- and RSL3-induced cell death. In the same cell types, deletion of mixed lineage kinase domain-like (Mlkl) blocked susceptibility to necroptosis, as expected. Surprisingly, these studies also revealed ferroptosis and necroptosis are alternative, in that resistance to one pathway sensitized cells to death via the other pathway. These data suggest a mechanism by which one regulated necrosis pathway compensates for another when either ferroptosis or necroptosis is compromised. We verified the synergistic contributions of ferroptosis and necroptosis to tissue damage during acute organ failure in vivo. Interestingly, in the course of pathophysiological acute ischemic kidney injury, ACSL4 was initially upregulated and its expression level correlated with the severity of tissue damage. Together, our findings reveal ACSL4 to be a reliable biomarker of the emerging cell death modality of ferroptosis, which may also serve as a novel therapeutic target in preventing pathological cell death processes.
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      headline:Necroptosis and ferroptosis are alternative cell death pathways that operate in acute kidney failure
      description:Ferroptosis is a recently recognized caspase-independent form of regulated cell death that is characterized by the accumulation of lethal lipid ROS produced through iron-dependent lipid peroxidation. Considering that regulation of fatty acid metabolism is responsible for the membrane-resident pool of oxidizable fatty acids that undergo lipid peroxidation in ferroptotic processes, we examined the contribution of the key fatty acid metabolism enzyme, acyl-CoA synthetase long-chain family member 4 (ACSL4), in regulating ferroptosis. By using CRISPR/Cas9 technology, we found that knockout of Acsl4 in ferroptosis-sensitive murine and human cells conferred protection from erastin- and RSL3-induced cell death. In the same cell types, deletion of mixed lineage kinase domain-like (Mlkl) blocked susceptibility to necroptosis, as expected. Surprisingly, these studies also revealed ferroptosis and necroptosis are alternative, in that resistance to one pathway sensitized cells to death via the other pathway. These data suggest a mechanism by which one regulated necrosis pathway compensates for another when either ferroptosis or necroptosis is compromised. We verified the synergistic contributions of ferroptosis and necroptosis to tissue damage during acute organ failure in vivo. Interestingly, in the course of pathophysiological acute ischemic kidney injury, ACSL4 was initially upregulated and its expression level correlated with the severity of tissue damage. Together, our findings reveal ACSL4 to be a reliable biomarker of the emerging cell death modality of ferroptosis, which may also serve as a novel therapeutic target in preventing pathological cell death processes.
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         ACSL4
         Necroptosis
         MLKL
         Ischemia-reperfusion injury
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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      name:Department of Pathology, University of Hannover, Hannover, Germany
      name:Department of Nephrology and Hypertension, University Hospital Schleswig–Holstein, Kiel, Germany
      name:Department of Pathology, University of Hannover, Hannover, Germany
      name:Department of Biological Sciences and Department of Chemistry, Columbia University of New York, New York, USA
      name:The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia
      name:Department of Medical Biology, University of Melbourne, Parkville, Australia
      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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