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Seibt, T.M.* ; Proneth, B. ; Conrad, M.

Role of GPX4 in ferroptosis and its pharmacological implication.

Free Radical Biol. Med. 133, 144-152 (2019)
Verlagsversion DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Ferroptosis is a non-apoptotic form of cell death characterized by iron-dependent lipid peroxidation and metabolic constraints. Dependence on NADPH/H+, polyunsaturated fatty acid metabolism, and the mevalonate and glutaminolysis metabolic pathways have been implicated in this novel form of regulated necrotic cell death. Genetic studies performed in cells and mice established the selenoenzyme glutathione peroxidase (GPX4) as the key regulator of this form of cell death. Besides these genetic models, the identification of a series of small molecule ferroptosis-specific inhibitors and inducers have not only helped in the delineation of the molecular underpinnings of ferroptosis but they might also prove highly beneficial when tipping the balance between cell death inhibition and induction in the context of degenerative diseases and cancer, respectively. In the latter, the recent recognition that a subset of cancer cell lines including certain triple negative breast cancer cells and those of therapy-resistant high-mesenchymal cell state present a high dependence on this lipid make-up offers unprecedented opportunities to eradicate difficult to treat cancers. Due to the rapidly growing interest in this form of cell death, we provide an overview herein what we know about this field today and its future translational impact.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Regulated Necrosis ; Gpx4 ; Lipid Peroxidation ; Cysteine Metabolism ; Non-apoptotic Cell Death ; Ferritinophagy; Glutathione-peroxidase 4; Dependent Cell-death; Lipid-peroxidation; System X(c)(-); Cystine/glutamate Antiporter; Cystine Transporter; Parkinsons-disease; Therapeutic Target; Oxidative Stress; Cancer-cells
ISSN (print) / ISBN 0891-5849
e-ISSN 1873-4596
Quellenangaben Band: 133, Heft: , Seiten: 144-152 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort New York, NY
Begutachtungsstatus Peer reviewed