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We are analyzing https://www.nature.com/articles/s41418-018-0173-9.

Title:
Ferroptosis and necroinflammation, a yet poorly explored link | Cell Death & Differentiation
Description:
Ferroptosis is a non-apoptotic form of cell death characterized by overwhelming iron-dependent lipid peroxidation, which contributes to a number of pathologies, most notably tissue ischemia/reperfusion injury, neurodegeneration and cancer. Cysteine availability, glutathione biosynthesis, polyunsaturated fatty acid metabolism and modulation of the phospholipidome are the key events of this necrotic cell death pathway. Non-enzymatic and enzymatic lipoxygenase (LOX)-mediated lipid peroxidation of lipid bilayers is efficiently counteracted by the glutathione (GSH)/glutathione peroxidase 4 (GPX4) axis. Preliminary studies suggest that bursting ferroptotic cells release pro-inflammatory damage-associated molecular patterns (DAMPs) that trigger the innate immune system as exemplified by diseased kidney and brain tissues where ferroptosis contributes to organ demise in a predominant manner. The GSH/GPX4 node is known to control the activities of LOX and prostaglandin-endoperoxide synthase (PTGS) via the so-called peroxide tone. Since LOX and PTGS products do have pro- and anti-inflammatory effects, one may speculate that these enzymes contribute to the ferroptotic process on several levels in cell-autonomous and non-autonomous ways. Hence, this review provides the reader with an outline on what is currently known about the link between ferroptosis and necroinflammation and discusses critical events that may alert the innate immune system in early phases when cells become sensitized towards ferroptosis.
Website Age:
30 years and 10 months (reg. 1994-08-11).

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🌆 Monumental Traffic: 20M - 50M visitors per month


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Keywords {🔍}

pubmed, ferroptosis, cell, google, scholar, cells, cas, death, gpx, central, lox, glutathione, ferroptotic, lipid, cancer, peroxidase, immune, biol, system, nature, ptgs, acid, mice, chem, tissue, gsh, necroinflammation, conrad, kidney, shown, lipoxygenase, enzymes, tumor, depletion, peroxidation, innate, peroxide, role, vivo, knockout, iron, process, mouse, activation, cellular, inhibitors, activity, article, pathway, levels,

Topics {✒️}

nature portfolio permissions reprints privacy policy oncogenic-ras-harboring cancer cells advertising tamoxifen-induced gpx4fl/fl_rosacreert2 mice open questions research performed reproducible research full access social media smaller extend α-tocopherol research nature author information authors iron-dependent cell death poorly explored link protein-coupled receptor e1 bis-allylic h-atoms iron-dependent lipid peroxidation cd8 positive t-cells author correspondence acute renal failure 3-hydroxy-3-methyl-glutaryl-coenzyme aif-mediated cell death potential pharmacodynamic marker/biomarker nutrient-deprived cancer cells oxidative stress-dependent small-molecule probes friedmann angeli jp initial data suggest rsl3-induced cell death massive cell death erastin-induced cell death melanoma cell lines prevent hydroperoxide-induced ferroptosis central nervous system ptgs2-derived prostaglandin d2 extracellular cysteine/cystine pool permissions cysteinyl-trna synthetase ncoa4-mediated autophagic degradation express mutant ras ferroptosis-related genes participate translates oxidative stress exchanging extracellular cysteine/cystathionine hmg-coa reductase crystal-induced mouse model kidney tubular cells pro-inflammatory markers

Questions {❓}

  • Are cancer cells undergoing ferroptosis immunogenic?
  • Does an impaired glutathione (GSH)/GPX4 axis prior to ferroptosis contribute to an activation of the innate immune system via increased LOX/PTGS signaling?
  • Glutathione peroxidase 4: a new player in neurodegeneration?
  • Is there a role of ferroptosis in physiological contexts?
  • Lipoxygenases—killers against their will?
  • What is the nature of DAMPs released by ferroptotic cells?
  • What is the sequence of events causing a full-blown immune cell activation?

Schema {🗺️}

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      description:Ferroptosis is a non-apoptotic form of cell death characterized by overwhelming iron-dependent lipid peroxidation, which contributes to a number of pathologies, most notably tissue ischemia/reperfusion injury, neurodegeneration and cancer. Cysteine availability, glutathione biosynthesis, polyunsaturated fatty acid metabolism and modulation of the phospholipidome are the key events of this necrotic cell death pathway. Non-enzymatic and enzymatic lipoxygenase (LOX)-mediated lipid peroxidation of lipid bilayers is efficiently counteracted by the glutathione (GSH)/glutathione peroxidase 4 (GPX4) axis. Preliminary studies suggest that bursting ferroptotic cells release pro-inflammatory damage-associated molecular patterns (DAMPs) that trigger the innate immune system as exemplified by diseased kidney and brain tissues where ferroptosis contributes to organ demise in a predominant manner. The GSH/GPX4 node is known to control the activities of LOX and prostaglandin-endoperoxide synthase (PTGS) via the so-called peroxide tone. Since LOX and PTGS products do have pro- and anti-inflammatory effects, one may speculate that these enzymes contribute to the ferroptotic process on several levels in cell-autonomous and non-autonomous ways. Hence, this review provides the reader with an outline on what is currently known about the link between ferroptosis and necroinflammation and discusses critical events that may alert the innate immune system in early phases when cells become sensitized towards ferroptosis.
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