BID links ferroptosis to mitochondrial cell death pathways

Ferroptosis has been defined as an oxidative and iron-dependent pathway of regulated cell death that is distinct from caspase-dependent apoptosis and established pathways of death receptor-mediated regulated necrosis. While emerging evidence linked features of ferroptosis induced e.g. by erastin-med...

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Bibliographic Details
Main Authors: Neitemeier, Sandra (Author) , Oppermann, Sina (Author)
Format: Article (Journal)
Language:English
Published: August 2017
In: Redox Biology
Year: 2017, Volume: 12, Pages: 558-570
ISSN:2213-2317
DOI:10.1016/j.redox.2017.03.007
Online Access:Resolving-System, Volltext: http://dx.doi.org/10.1016/j.redox.2017.03.007
Verlag, Volltext: https://www.sciencedirect.com/science/article/pii/S2213231717300654
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Author Notes:Sandra Neitemeier, Anja Jelinek, Vincenzo Laino, Lena Hoffmann, Ina Eisenbach, Roman Eying, Goutham K. Ganjam, Amalia M. Dolga, Sina Oppermann, Carsten Culmsee
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Summary:Ferroptosis has been defined as an oxidative and iron-dependent pathway of regulated cell death that is distinct from caspase-dependent apoptosis and established pathways of death receptor-mediated regulated necrosis. While emerging evidence linked features of ferroptosis induced e.g. by erastin-mediated inhibition of the Xc- system or inhibition of glutathione peroxidase 4 (Gpx4) to an increasing number of oxidative cell death paradigms in cancer cells, neurons or kidney cells, the biochemical pathways of oxidative cell death remained largely unclear. In particular, the role of mitochondrial damage in paradigms of ferroptosis needs further investigation.
Item Description:Available online 9 March 2017
Gesehen am 22.10.2018
Physical Description:Online Resource
ISSN:2213-2317
DOI:10.1016/j.redox.2017.03.007