Evidence map›Paper›PMID 32575749›Full record

ReviewCells2020

Ferroptosis and Cancer: Mitochondria Meet the "Iron Maiden" Cell Death.

Anna Martina Battaglia, Roberta Chirillo, Ilenia Aversa, Alessandro Sacco, Francesco Costanzo, Flavia Biamonte

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 335 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
335citing papers in PubMed, 1 pooled it
30.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

335 citing papers in PubMed, 1 synthesis or guideline pooled it, 530 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Ferroptosis in heatstroke: Mechanisms and therapeutic perspectives (Review).International journal of molecular medicine · 2026
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  8. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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275 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Anna Martina BattagliaDepartment of Experimental and Clinical Medicine, "Magna Graecia" University of Catanzaro, 88100 Catanzaro, Italy.
Roberta ChirilloDepartment of Experimental and Clinical Medicine, "Magna Graecia" University of Catanzaro, 88100 Catanzaro, Italy.
Ilenia AversaDepartment of Experimental and Clinical Medicine, "Magna Graecia" University of Catanzaro, 88100 Catanzaro, Italy.ORCID 0000-0003-4721-6792
Alessandro SaccoDepartment of Experimental and Clinical Medicine, "Magna Graecia" University of Catanzaro, 88100 Catanzaro, Italy.
Francesco CostanzoDepartment of Experimental and Clinical Medicine, "Magna Graecia" University of Catanzaro, 88100 Catanzaro, Italy.
Flavia BiamonteDepartment of Experimental and Clinical Medicine, "Magna Graecia" University of Catanzaro, 88100 Catanzaro, Italy.ORCID 0000-0003-3248-3863
Magna Graecia University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis is a new type of oxidative regulated cell death (RCD) driven by iron-dependent lipid peroxidation. As major sites of iron utilization and master regulators of oxidative metabolism, mitochondria are the main source of reactive oxygen species (ROS) and, thus, play a role in this type of RCD. Ferroptosis is, indeed, associated with severe damage in mitochondrial morphology, bioenergetics, and metabolism. Furthermore, dysregulation of mitochondrial metabolism is considered a biochemical feature of neurodegenerative diseases linked to ferroptosis. Whether mitochondrial dysfunction can, per se, initiate ferroptosis and whether mitochondrial function in ferroptosis is context-dependent are still under debate. Cancer cells accumulate high levels of iron and ROS to promote their metabolic activity and growth. Of note, cancer cell metabolic rewiring is often associated with acquired sensitivity to ferroptosis. This strongly suggests that ferroptosis may act as an adaptive response to metabolic imbalance and, thus, may constitute a new promising way to eradicate malignant cells. Here, we review the current literature on the role of mitochondria in ferroptosis, and we discuss opportunities to potentially use mitochondria-mediated ferroptosis as a new strategy for cancer therapy.

Indexed as

AnimalsCell DeathFerroptosisHumansIronMitochondriaNeoplasmsReactive Oxygen SpeciesIronReactive Oxygen Speciescancercell deathferroptosisironmitochondriaROS

Identifiers

PMID32575749
PMCPMC7349567
OpenAlexW3035851500

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.