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Trends Cell Biol. 2016 Mar;26(3):165-176. doi: 10.1016/j.tcb.2015.10.014. Epub 2015 Dec 2.

Ferroptosis: Death by Lipid Peroxidation.

Author information

1
Department of Biological Sciences, Howard Hughes Medical Institute, Columbia University, New York, NY, USA. Electronic address: yangw@stjohns.edu.
2
Department of Biological Sciences, Howard Hughes Medical Institute, Columbia University, New York, NY, USA; Department of Chemistry, Columbia University, New York, NY, USA; Department of Systems Biology, Columbia University, New York, NY, USA. Electronic address: bstockwell@columbia.edu.

Abstract

Ferroptosis is a regulated form of cell death driven by loss of activity of the lipid repair enzyme glutathione peroxidase 4 (GPX4) and subsequent accumulation of lipid-based reactive oxygen species (ROS), particularly lipid hydroperoxides. This form of iron-dependent cell death is genetically, biochemically, and morphologically distinct from other cell death modalities, including apoptosis, unregulated necrosis, and necroptosis. Ferroptosis is regulated by specific pathways and is involved in diverse biological contexts. Here we summarize the discovery of ferroptosis, the mechanism of ferroptosis regulation, and its increasingly appreciated relevance to both normal and pathological physiology.

KEYWORDS:

GPX4; ROS; cell death; ferroptosis; lipid peroxides; system x(c)(−)

PMID:
26653790
PMCID:
PMC4764384
[Available on 2017-03-01]
DOI:
10.1016/j.tcb.2015.10.014
[Indexed for MEDLINE]
Free PMC Article

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