The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.
Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death
Open accessAbstract
Nonapoptotic forms of cell death may facilitate the selective elimination of some tumor cells or be activated in specific pathological states. The oncogenic RAS-selective lethal small molecule erastin triggers a unique iron-dependent form of nonapoptotic cell death that we term ferroptosis. Ferroptosis is dependent upon intracellular iron, but not other metals, and is morphologically, biochemically, and genetically distinct from apoptosis, necrosis, and autophagy. We identify the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes. Indeed, erastin, like glutamate, inhibits cystine uptake by the cystine/glutamate antiporter (system x(c)(-)), creating a void in the antioxidant defenses of the cell and ultimately leading to iron-dependent, oxidative death. Thus, activation of ferroptosis results in the nonapoptotic destruction of certain cancer cells, whereas inhibition of this process may protect organisms from neurodegeneration.
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In the citing paper
“At the same time, the loss of the lipid repair enzyme glutathione peroxidase 4 (GPX4) in invasive cancer cells with a mesenchymal and drug-resistant phenotype causes the accumulation of lipid hydroperoxides (lipid-ROS) triggering the iron-dependent cell death known as ferroptosis (7).”
From Secreted Apoe rewires melanoma cell state vulnerability to ferroptosis (2024) · cites this paper as [7]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Daily injection of ferrostatin—a lipid ROS scavenger [286]—markedly reduces oligodendrocyte death and 4-HNE accumulation at two days and two weeks of cuprizone consumption [101].”
From Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination (2022) · cites this paper as [286]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“eprenetapopt is the first compound to reach a phase 3 clinical trial where triggering ferroptosis is central to its anticancer efficacy.”
From Eprenetapopt triggers ferroptosis, inhibits NFS1 cysteine desulfurase, and synergizes with serine and glycine dietary restriction (2022) · cites this paper as [21]
Experimental — accuracy not yet measuredIn the citing paper
“erastin triggers ferroptosis by (indirectly) affecting the catalytic cycle of GPX4 via a mechanism that involves the inhibition of the cystine/glutamate antiporter system xc− and consequent decrease in intracellular cysteine (which derives from cystine reduction in the cytoplasm) and GSH (which is synthesized from cysteine) [539, 548, 549, 551].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [539]
In the citing paper
“Ferroptosis occurs independently of caspases, necrosome components and CYPD, and the molecular machinery for autophagy [539]”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [539]
In the citing paper
“the ferroptosis-inhibiting effect of iron depletion by either chelators [539, 543, 548] or phosphorylase kinase catalytic subunit gamma 2 (PHKG2) knockdown [566]”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [539]
In the citing paper
“oxidized PUFAs accumulate upon GPX4 inactivation and this can result in PUFA fragmentation and ferroptosis [539, 547].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [539]
In the citing paper
“Inhibitors of this transporter have been found to deplete intracellular glutathione in cancer cells, resulting in iron-dependent accumulation of ROS and a form of cell death termed ferroptosis (Dixon et al., 2012; Dixon et al., 2014; Yang et al., 2014).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Dixon et al., 2012
In the citing paper
“MEK-inhibition in PDAC increased both lysosome biosynthesis and ferritinophagy, necessary to support increased iron-sulfur cluster proteins for respiration217”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [217]
In the citing paper
“Ferroptosis is this non-apoptotic, peroxidation-driven form of regulated cell death that requires abundant and accessible cellular iron; the existence of this ancient form of cell death was unknown and only discovered recently using a pharmacological approach [10].”
From Ferroptosis: Death by Lipid Peroxidation (2016) · cites this paper as [10]
In the citing paper
“Indeed, analysis with dichlorofluorescein (DCF), a ROS-detecting dye, revealed that erastin causes the generation of ROS in sensitive cell lines [10, 13].”
From Ferroptosis: Death by Lipid Peroxidation (2016) · cites this paper as [10]
In the citing paper
“However, RSL3 treatment does not prevent the import of radiolabeled cystine, indicating that RSL3 does not inhibit system xc− [10].”
From Ferroptosis: Death by Lipid Peroxidation (2016) · cites this paper as [10]
In the citing paper
“Taken together, the mode of cell death induced by erastin, RSL3 and related compounds was proposed to be a previously unrecognized form of cell death termed ferroptosis (ferro = “ferrous ion (Fe2+)”, ptosis = “fall”), suggesting a critical role for cellular iron in this regulated form of oxidative cell death [10].”
From Ferroptosis: Death by Lipid Peroxidation (2016) · cites this paper as [10]
In the citing paper
“Although non-apoptotic, erastin-induced cell death proceeds normally upon knockdown of RIPK1/RIPK3, or pharmacological inhibition of RIPK1 [10, 15, our unpublished data], known components of necroptosis [16].”
From Ferroptosis: Death by Lipid Peroxidation (2016) · cites this paper as [10]
In the citing paper
“Indeed, erastin treatment abolished the import of radiolabeled cystine [10], a substrate for the system xc− antiporter, confirming that erastin inhibits system xc−.”
From Ferroptosis: Death by Lipid Peroxidation (2016) · cites this paper as [10]
In the citing paper
“In addition, modulatory profiles of erastin and sulfasalazine (SAS), an inhibitor of system xc−, were similar to each other, suggesting that erastin might act as a system xc− inhibitor to initiate ferroptosis [10].”
From Ferroptosis: Death by Lipid Peroxidation (2016) · cites this paper as [10]
In the citing paper
“Ferrostatin-1 acts as a lipid ROS scavenger and prevents ferroptosis induced by erastin and RSL3, but does not suppress cell death induced by staurosporine (an apoptosis inducer) or hydrogen peroxide (an oxidative necrosis inducer) [10].”
From Ferroptosis: Death by Lipid Peroxidation (2016) · cites this paper as [10]
In the citing paper
“In cell culture models, the addition of iron to culture media sensitizes cancer cells to ferroptosis”
From Ferroptosis: Death by Lipid Peroxidation (2016) · cites this paper as [10]
In the citing paper
“copper (Cu2+) and cobalt (Co2+) are known to catalyze Fenton chemistry, but these metals do not sensitize cells to ferroptosis, whereas iron does [10].”
From Ferroptosis: Death by Lipid Peroxidation (2016) · cites this paper as [10]
In the citing paper
“probably by lowering the threshold to initiate oxidative damage [10].”
From Ferroptosis: Death by Lipid Peroxidation (2016) · cites this paper as [10]
In the citing paper
“The term ferroptosis was introduced to describe cell death induced by the compound erastin, which causes glutathione depletion through the glutamate-cystine antiporter system Xc- inhibition and consequently glutathione peroxidase 4 (GPX4) inactivation leading to accumulation of lipid peroxides (Ursini et al., 1982; Dixon et al., 2012).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Dixon et al., 2012
In the citing paper
“Accumulation of iron-dependent lipid modifications promotes a specific form of cell death, known as ferroptosis [4].”
From Iron as a central player and promising target in cancer progression (2019) · cites this paper as [4]
In the citing paper
“However, when the capacity of red pulp macrophages (the iron-recycling macrophage population in the spleen, henceforward abbreviated as RPM) and KC is overwhelmed, the cells die, presumably by a specific form of cell death called ferroptosis that is induced by iron-mediated oxidative stress and lipid peroxidation [54].”
From “Pumping iron”—how macrophages handle iron at the systemic, microenvironmental, and cellular levels (2017) · cites this paper as [54]
In the citing paper
“It is characterized by iron-dependent radical formation via the Fenton reaction and subsequent membrane lipid peroxidation, and is morphologically, biochemically and genetically different from apoptosis, necroptosis and autophagy.”
From Iron in immune cell function and host defense (2021) · cites this paper as [104]
In the citing paper
“Ferroptosis describes a form of iron dependent cell death induced by the small molecule erastin”
From Iron in immune cell function and host defense (2021) · cites this paper as [104]
In the citing paper
“Neurodegeneration that results from iron toxicity can lead to apoptosis73 and ferroptosis, an iron-specific form of non-apoptotic cell death.74”
From The role of iron in brain ageing and neurodegenerative disorders (2014) · cites this paper as [74]
In the citing paper
“Cell death elicited by ferroptosis-inducing compounds (FINs) (e.g. erastin and RSL3) can also be mitigated through various iron chelators (Dfo, 2,2-bipyridile or compound 311) [62], [66], [81].”
From Iron accumulation in senescent cells is coupled with impaired ferritinophagy and inhibition of ferroptosis (2018) · cites this paper as [62]
In the citing paper
“Distinctly, ferroptosis can be initiated through repression of the p53 target, SLC7A11, which encodes a component of the cysteine/glutamate antiporter (system Xc-), resulting in iron-dependent accumulation of ROS and glutathione (antioxidant) depletion [62], [82].”
From Iron accumulation in senescent cells is coupled with impaired ferritinophagy and inhibition of ferroptosis (2018) · cites this paper as [62]
In the citing paper
“Cells are also desensitized to ferroptosis through genetic silencing of iron uptake (TfR1), metabolism (IRP2 and ISCU) and storage (ferritin) genes [62], [66], [82], or through depletion of transferrin in the extracellular environment [83].”
From Iron accumulation in senescent cells is coupled with impaired ferritinophagy and inhibition of ferroptosis (2018) · cites this paper as [62]
In the citing paper
“Ferroptosis, a unique cell death pathway distinct from apoptosis [62], [66], [80], is reliant on the availability of iron [62], [66], [81] liberated through ferritinophagy [63].”
From Iron accumulation in senescent cells is coupled with impaired ferritinophagy and inhibition of ferroptosis (2018) · cites this paper as [62]
In the citing paper
“an iron-dependent autophagic cell death program [62], [63], [64] that can be inhibited in MEFs by genetically inactivating autophagy or ferritinophagy [65].”
From Iron accumulation in senescent cells is coupled with impaired ferritinophagy and inhibition of ferroptosis (2018) · cites this paper as [62]
In the citing paper
“Ferroptosis is characterized by the accumulation of iron and malondialdehyde (MDA), and peroxidation of lipids; depletion of glutathione (GSH); and alteration in mitochondrial morphology, including decreased number of or diminished mitochondrial cristae and ruptured outer mitochondrial membranes (Dixon et al., 2012;Xie et al., 2016).”
From MiR-378a-3p/ SLC7A11 regulate ferroptosis in nerve injury induced by lead exposure (2022) · cites this paper as Dixon et al., 2012
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Metadata
- Authors
- Dixon, S. J., Lemberg, K. M., Lamprecht, M. R., Skouta, R., Zaitsev, E. M., Gleason, C. E., Patel, D. N., Bauer, A. J., Cantley, A. M., Yang, W. S., Morrison, B., & Stockwell, B. R.
- Affiliations
- Columbia University (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Stockwell, Brent R.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2012-05
- Volume
- 149
- Issue
- 5
- Pages
- 1060-1072
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3367386
- OpenAlex
- W1997183854
- Cited by
- 18,691
- References
- 48
- Citations by year
- 2026: 2902 · 2025: 3499 · 2024: 3393 · 2023: 2809 · 2022: 2342 · 2021: 1539 · 2020: 828 · 2019: 500 · 2018: 294 · 2017: 209 · 2016: 160 · 2015: 92 · 2014: 61 · 2013: 29 · 2012: 14
- FWCI
- 50.51
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5R01CA097061, 5R01GM085081, R01CA161061)
- Arnold and Mabel Beckman Foundation
- Columbia University
- Empire State Development's Division of Science, Technology and Innovation
- Canadian Institutes of Health Research
- National Science Foundation (CHE-0840451)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Ferroptosis and cancer prognosis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Keywords
- ferroptosis, non-apoptotic cell death, iron-dependent cell death, erastin, ferrostatin-1, SLC7A11, system xc-, cystine uptake, glutamate-induced cell death, neurodegeneration, cancer cell death, oxidative stress, antioxidant defense
- MeSH terms
- Animals, Cyclohexylamines, Fibroblasts, Hippocampus, Humans, Iron, Neoplasms, Phenylenediamines, Piperazines, Cell Death, Reactive Oxygen Species, Glutamic Acid, Lipid Metabolism, Rats, In Vitro Techniques
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