Cited by 3,727Ferroptosis and cancer prognosisIron Metabolism and DisordersCell death mechanisms and regulation

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Ferroptosis: process and function

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Xie, Y, Hou, W, Song, X, Yu, Y, Huang, J, Sun, X, Kang, R, Tang, D·2016·Cell Death & Differentiation

DOI 10.1038/cdd.2015.158PMC PMC5072448

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Abstract

Ferroptosis is a recently recognized form of regulated cell death. It is characterized morphologically by the presence of smaller than normal mitochondria with condensed mitochondrial membrane densities, reduction or vanishing of mitochondria crista, and outer mitochondrial membrane rupture. It can be induced by experimental compounds (e.g., erastin, Ras-selective lethal small molecule 3, and buthionine sulfoximine) or clinical drugs (e.g., sulfasalazine, sorafenib, and artesunate) in cancer cells and certain normal cells (e.g., kidney tubule cells, neurons, fibroblasts, and T cells). Activation of mitochondrial voltage-dependent anion channels and mitogen-activated protein kinases, upregulation of endoplasmic reticulum stress, and inhibition of cystine/glutamate antiporter is involved in the induction of ferroptosis. This process is characterized by the accumulation of lipid peroxidation products and lethal reactive oxygen species (ROS) derived from iron metabolism and can be pharmacologically inhibited by iron chelators (e.g., deferoxamine and desferrioxamine mesylate) and lipid peroxidation inhibitors (e.g., ferrostatin, liproxstatin, and zileuton). Glutathione peroxidase 4, heat shock protein beta-1, and nuclear factor erythroid 2-related factor 2 function as negative regulators of ferroptosis by limiting ROS production and reducing cellular iron uptake, respectively. In contrast, NADPH oxidase and p53 (especially acetylation-defective mutant p53) act as positive regulators of ferroptosis by promotion of ROS production and inhibition of expression of SLC7A11 (a specific light-chain subunit of the cystine/glutamate antiporter), respectively. Misregulated ferroptosis has been implicated in multiple physiological and pathological processes, including cancer cell death, neurotoxicity, neurodegenerative diseases, acute renal failure, drug-induced hepatotoxicity, hepatic and heart ischemia/reperfusion injury, and T-cell immunity. In this review, we summarize the regulation mechanisms and signaling pathways of ferroptosis and discuss the role of ferroptosis in disease.

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1 retracted

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Authors: Xie, Y., Hou, W., Song, X., Yu, Y., Huang, J., Sun, X., Kang, R., & Tang, D.
Affiliations: Central South University (CN)
University of Pittsburgh (US)
Third Affiliated Hospital of Guangzhou Medical University (CN)
Corresponding author: Kang, R
Tang, D
ORCID: Xie, Y
Song, X
Yu, Y
Huang, J
Kang, R
Tang, D
Venue: Cell Death & Differentiation
Publisher: Springer Science and Business Media LLC
Published: 2016-01-22
Volume: 23
Issue: 3
Pages: 369-379
ISSN: 1350-9047 (ISSN-L)
1476-5403
DOI: 10.1038/cdd.2015.158
PMC: PMC5072448
OpenAlex: W2265062179
Cited by: 3,727
References: 47
Citations by year: 2026: 295 · 2025: 482 · 2024: 644 · 2023: 618 · 2022: 588 · 2021: 470 · 2020: 284 · 2019: 157 · 2018: 94 · 2017: 60 · 2016: 30
FWCI: 19.74
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.springer.com/tdm (tdm)
Locations: Cell Death and Differentiation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: University of Pittsburgh
National Natural Science Foundation of China (201508020258, R01GM115366, 201400000003, R01CA160417, 31171229, U1132005)
National Institutes of Health
National Cancer Institute (R01CA160417)
National Institute of General Medical Sciences (R01GM115366)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Ferroptosis and cancer prognosis
Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords: ferroptosis, regulated cell death, lipid peroxidation, reactive oxygen species, iron metabolism, GPX4, NADPH oxidase, p53, NF-E2-related factor 2, mitochondrial membrane damage, mitochondrial voltage-dependent anion channel, endoplasmic reticulum stress, iron chelators, ferroptosis inhibitors, cancer cell death, neurodegenerative diseases, drug-induced liver injury, ischemia-reperfusion injury, T cell immunity
MeSH terms: Animals, Humans, Iron, Iron Chelating Agents, Mitochondria, Lipid Peroxidation, Signal Transduction, Cell Death, Reactive Oxygen Species, Oxidative Stress, Endoplasmic Reticulum Stress

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