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Friedmann Angeli, J.P.F. ; Proneth, B. ; Conrad, M.

Glutathione peroxidase 4 and ferroptosis.

In: Selenium: Its Molecular Biology and Role in Human Health. 2016. 511-521 ( ; 4)
DOI
Glutathione peroxidase 4 (Gpx4) is one of eight members of the mammalian glutathione peroxidase family of enzymes. Gpx4 is unique due to its capacity to efficiently reduce phospholipid hydroperoxides. Additionally, it has been recognized that Gpx4 governs a novel form of non-apoptotic cell death, named ferroptosis. Ferroptosis was initially described to be induced by small molecules in specific tumor types and in engineered cells overexpressing oncogenic RAS. Recently, its relevance in non-transformed cells and tissues was highlighted expanding the importance of this cell death pathway in several pathophysiological contexts, encompassing immunity, neurodegenerative diseases and tissue damage upon ischemia/reperfusion scenarios. Importantly, regulation of selenoprotein biosynthesis emerges as an important factor in control of ferroptosis. In this chapter, we present an updated view on the ferroptotic process as well as review the implications of how selenoprotein expression might impact on ferroptosis per se.
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Publikationstyp Artikel: Sammelbandbeitrag/Buchkapitel
Korrespondenzautor
Schlagwörter Ferroptotic Signaling ; Ischemia/reperfusion Injury ; Lipid Peroxidation ; Liproxstatin-1 ; Mevalonate Pathway ; Neurodegeneration ; Non-apoptotic Cell Death ; Phgpx ; Phospholipid Hydroperoxide Glutathione Peroxidase ; Regulated Necrosis
ISSN (print) / ISBN 978-3-319-41281-8
e-ISSN 978-3-319-41283-2
Bandtitel Selenium: Its Molecular Biology and Role in Human Health
Quellenangaben Band: 4, Heft: , Seiten: 511-521 Artikelnummer: , Supplement: ,
Nichtpatentliteratur Publikationen
Institut(e) Institute of Developmental Genetics (IDG)