Evidence map›Paper›PMID 31740834›Full record

ReviewNature chemical biology2019

The chemical basis of ferroptosis.

Marcus Conrad, Derek A Pratt

Erratum issuedAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature chemical biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 529 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
529citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

529 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
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  3. Pooled it
  4. Review
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  7. Ferroptosis in health and disease.Molecular biomedicine · 2026
    Review
  8. Article
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  11. Ferroptosis as a target mechanism in heart and kidney disease.The Journal of clinical investigation · 2026
    Review
  12. Ferroptosis in depression: mechanisms, association, and therapeutic strategies.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  13. Article
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469 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Marcus Conrad *Helmholtz Zentrum München, Institute of Developmental Genetics, Neuherberg, Germany. marcus.conrad@helmholtz-muenchen.de.ORCID http://orcid.org/0000-0003-1140-5612
Derek A Pratt *Department of Chemistry and Biomolecular Science, University of Ottawa, Ottawa, Canada. dpratt@uottawa.ca.ORCID http://orcid.org/0000-0002-7305-745X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipid peroxidation underlies the mechanism of oxidative cell death now known as ferroptosis. This modality, distinct from other forms of cell death, has been intensely researched in recent years owing to its relevance in both degenerative disease and cancer. The demonstration that it can be modulated by small molecules in multiple pathophysiological contexts offers exciting opportunities for novel pharmacological interventions. Herein, we introduce the salient features of lipid peroxidation, how it can be modulated by small molecules and what principal aspects require urgent investigation by researchers in the field. The central role of non-enzymatic reactions in the execution of ferroptosis will be emphasized, as these processes have hitherto not been generally considered 'druggable'. Moreover, we provide a critical perspective on the biochemical mechanisms that contribute to cell vulnerability to ferroptosis and discuss how they can be exploited in the design of novel therapeutics.

Indexed as

FerroptosisHumansLipid PeroxidationOxidative StressReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

What OpenQuestion holds

Textmetadata
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.