We are analyzing https://link.springer.com/article/10.1007/s00018-016-2194-1.

Title:
Mechanisms of ferroptosis | Cellular and Molecular Life Sciences
Description:
Ferroptosis is a non-apoptotic form of cell death that can be triggered by small molecules or conditions that inhibit glutathione biosynthesis or the glutathione-dependent antioxidant enzyme glutathione peroxidase 4 (GPX4). This lethal process is defined by the iron-dependent accumulation of lipid reactive oxygen species and depletion of plasma membrane polyunsaturated fatty acids. Cancer cells with high level RAS-RAF-MEK pathway activity or p53 expression may be sensitized to this process. Conversely, a number of small molecule inhibitors of ferroptosis have been identified, including ferrostatin-1 and liproxstatin-1, which can block pathological cell death events in brain, kidney and other tissues. Recent work has identified a number of genes required for ferroptosis, including those involved in lipid and amino acid metabolism. Outstanding questions include the relationship between ferroptosis and other forms of cell death, and whether activation or inhibition of ferroptosis can be exploited to achieve desirable therapeutic ends.
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Keywords {🔍}

cell, ferroptosis, pubmed, death, google, scholar, article, cas, cells, iron, gsh, gpx, erastin, cancer, glutathione, central, lipid, depletion, apoptosis, oxidative, cys, system, essential, form, inhibition, xtextc, chem, biol, small, lethal, pathway, activity, human, role, lros, ras, rsl, accumulation, table, required, studies, model, damage, function, membrane, mechanism, fig, trigger, antioxidant, levels,

Topics {✒️}

gpna l-g-glutamyl-p-nitroanilide broader ras-raf-mek pathway beta-unsaturated aldehyde 4-hydroxy-2-nonenal s-n-butyl homocysteine sulfoximine raf-mek-erk pathway activity oncogenic-ras-harboring cancer cells γ-l-glutamyl-l-cysteinylglycine ras-raf-mek pathway raf/mek/erk pathway polyunsaturated fatty acids p53-mediated cell-cycle arrest l-ros-mediated cellular collapse article download pdf acute oxalate-induced damage reactive oxygen species reactive oxygen species p53-inducible cell line p53-regulated transcription identifies acute renal failure iron-dependent l-ros accumulation synthetic antioxidant ferrostatin-1 poly adp-ribose polymerase transactivation-defective p53 mutants aif-dependent cell death glutamate-induced oxidative stress aif-mediated cell death bid-mediated mitochondrial damage free-radical-mediated damage caspase inhibitor zvad-fmk lipid ros-mediated damage specific iron-dependent enzyme ros-dependent ferroptotic phenotype iron-dependent cell death iron-mediated lipid peroxidation p53-mediated tumour suppression p53-dependent metabolic modulation gsh-dependent enzyme gpx4 slc7a11-mediated cys2 import pro-death enzymatic program express mutant ras induces caspase-independent apoptosis lipophilic antioxidant α-tocopherol α-kg alpha-ketoglutarate rsl3-induced cell death erastin-induced cell death erastin-treated cancer cells l-ros-mediated destruction major issue remaining genotype-selective antitumor agents aa-derived lipid fragments

Questions {❓}

Green DR, Victor B (2012) The pantheon of the fallen: why are there so many forms of cell death?
Why does GSH depletion and GPX4 inactivation not simply trigger apoptosis?

Schema {🗺️}

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         description:Ferroptosis is a non-apoptotic form of cell death that can be triggered by small molecules or conditions that inhibit glutathione biosynthesis or the glutathione-dependent antioxidant enzyme glutathione peroxidase 4 (GPX4). This lethal process is defined by the iron-dependent accumulation of lipid reactive oxygen species and depletion of plasma membrane polyunsaturated fatty acids. Cancer cells with high level RAS-RAF-MEK pathway activity or p53 expression may be sensitized to this process. Conversely, a number of small molecule inhibitors of ferroptosis have been identified, including ferrostatin-1 and liproxstatin-1, which can block pathological cell death events in brain, kidney and other tissues. Recent work has identified a number of genes required for ferroptosis, including those involved in lipid and amino acid metabolism. Outstanding questions include the relationship between ferroptosis and other forms of cell death, and whether activation or inhibition of ferroptosis can be exploited to achieve desirable therapeutic ends.
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      headline:Mechanisms of ferroptosis
      description:Ferroptosis is a non-apoptotic form of cell death that can be triggered by small molecules or conditions that inhibit glutathione biosynthesis or the glutathione-dependent antioxidant enzyme glutathione peroxidase 4 (GPX4). This lethal process is defined by the iron-dependent accumulation of lipid reactive oxygen species and depletion of plasma membrane polyunsaturated fatty acids. Cancer cells with high level RAS-RAF-MEK pathway activity or p53 expression may be sensitized to this process. Conversely, a number of small molecule inhibitors of ferroptosis have been identified, including ferrostatin-1 and liproxstatin-1, which can block pathological cell death events in brain, kidney and other tissues. Recent work has identified a number of genes required for ferroptosis, including those involved in lipid and amino acid metabolism. Outstanding questions include the relationship between ferroptosis and other forms of cell death, and whether activation or inhibition of ferroptosis can be exploited to achieve desirable therapeutic ends.
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         Iron
         Reactive oxygen species
         Glutathione
         Cancer
         RAS
         Glutathione peroxidase 4
         Erastin
         Sorafenib
         Ferrostatin-1
         Polyunsaturated fatty acid
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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