Ferroptosis: molecular mechanisms and health implications

Cell death can be executed through different subroutines. Since the description of ferroptosis as an iron-dependent form of non-apoptotic cell death in 2012, there has been mounting interest in the process and function of ferroptosis. Ferroptosis can occur through two major pathways, the extrinsic o...

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Published in:Cell research Vol. 31; no. 2; pp. 107 - 125
Main Authors: Tang, Daolin, Chen, Xin, Kang, Rui, Kroemer, Guido
Format: Journal Article
Language:English
Published: Singapore Springer Singapore 01.02.2021
Nature Publishing Group
Subjects:
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631/80
Animals
Antioxidants
Antioxidants - metabolism
Apoptosis
Autophagy
Biochemistry, Molecular Biology
Biomedical and Life Sciences
Cancer
Cell Biology
Cell death
Cellular Biology
Epigenesis, Genetic
Epigenetics
Ferroptosis
Ferroptosis - genetics
Ferroptosis - immunology
Free radicals
Humans
Inflammation
Iron - metabolism
Life Sciences
Lipid Peroxidation
Lipids
Molecular machines
Molecular modelling
Mortality
Neoplasms - metabolism
Neurodegeneration
NF-E2-Related Factor 2
Oxidants
Oxidation
Oxidizing agents
Phagocytosis
Post-transcription
Reactive Oxygen Species - metabolism
Review
Review Article
Signal Transduction
ISSN:1001-0602, 1748-7838, 1748-7838
Online Access:Get full text
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Summary:Cell death can be executed through different subroutines. Since the description of ferroptosis as an iron-dependent form of non-apoptotic cell death in 2012, there has been mounting interest in the process and function of ferroptosis. Ferroptosis can occur through two major pathways, the extrinsic or transporter-dependent pathway and the intrinsic or enzyme-regulated pathway. Ferroptosis is caused by a redox imbalance between the production of oxidants and antioxidants, which is driven by the abnormal expression and activity of multiple redox-active enzymes that produce or detoxify free radicals and lipid oxidation products. Accordingly, ferroptosis is precisely regulated at multiple levels, including epigenetic, transcriptional, posttranscriptional and posttranslational layers. The transcription factor NFE2L2 plays a central role in upregulating anti-ferroptotic defense, whereas selective autophagy may promote ferroptotic death. Here, we review current knowledge on the integrated molecular machinery of ferroptosis and describe how dysregulated ferroptosis is involved in cancer, neurodegeneration, tissue injury, inflammation, and infection.
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ISSN:1001-0602
1748-7838
1748-7838
DOI:10.1038/s41422-020-00441-1