Ferroptosis: bug or feature?
Abstract
Summary: Ferroptosis is an iron‐dependent, oxidative form of non‐apoptotic cell death. This form of cell death does not share morphological, biochemical, or genetic similarities with classic necrosis, necroptosis, parthanatos, or other forms of non‐apoptotic cell death. Ferroptosis can be triggered by depleting the cell of the amino acid cysteine, or by inhibiting the phospholipid hydroperoxidase glutathione peroxidase 4 (GPX 4). Why certain stimuli trigger ferroptosis instead of another form of cell death, and whether this process could be adaptive in vivo, are two major unanswered questions concerning this process. Emerging evidence and consideration of related non‐apoptotic pathways suggest that ferroptosis could be an adaptive process, albeit one regulated and executed in a manner very different from apoptosis and other forms of cell death.
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Ferroptosis is initiated by specific perturbations of the intracellular microenvironment, notably severe lipid peroxidation, and relies on ROS generation and iron availability.
“Ferroptosis is a form of RCD initiated by specific perturbations of the intracellular microenvironment, notably severe lipid peroxidation, which relies on ROS generation and iron availability [533–536].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [533]
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Flagged first, then by citations
Cited by
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Galluzzi, L., Vitale, I., Aaronson, S. A., Abrams, J. M., Adam, D., Agostinis, P., Alnemri, E. S., Altucci, L., Amelio, I., Andrews, D. W., et al. (2018) · Cell Death & Differentiation · doi:10.1038/s41418-017-0012-4 · Cited by 6,680 · see citing works
Self-citationThe multifaceted role of reactive oxygen species in tumorigenesis
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Iron Pathophysiology in Alzheimer’s Diseases
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- Authors
- Dixon, S. J.
- Affiliations
- Stanford University (US)
- Corresponding author
- Dixon, Scott J.
- ORCID
- Dixon, Scott J.
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2017-04-30
- Volume
- 277
- Issue
- 1
- Pages
- 150-157
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- OpenAlex
- W2611252724
- Cited by
- 314
- References
- 114
- Citations by year
- 2026: 11 · 2025: 38 · 2024: 50 · 2023: 53 · 2022: 54 · 2021: 40 · 2020: 27 · 2019: 20 · 2018: 12 · 2017: 9
- FWCI
- 3.39
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Immunological Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (4R00CA166517‐03)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › 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, GPX4, cysteine depletion, necroptosis, parthanatos, oxidative stress
- MeSH terms
- Phospholipid Hydroperoxide Glutathione Peroxidase, Animals, Cysteine, Glutathione Peroxidase, Humans, Iron, Necrosis, Oxidation-Reduction, Cell Death, Apoptosis, Reactive Oxygen Species
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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