Evidence map›Paper›PMID 38401540›Full record

ArticleCell reports methods2024

A tangible method to assess native ferroptosis suppressor activity.

Toshitaka Nakamura, Junya Ito, André Santos Dias Mourão, Adam Wahida, Kiyotaka Nakagawa, Eikan Mishima, Marcus Conrad

Abstract read
In one paragraph

Article in Cell reports methods, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–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

15 citing papers in PubMed.

  1. Review
  2. Review
  3. Ferroptosis and its role in immune modulation in breast cancer.Apoptosis : an international journal on programmed cell death · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. MALT1 inhibitor MI-2 induces ferroptosis by direct targeting of GPX4.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. In defence of ferroptosis.Signal transduction and targeted therapy · 2025
    Review
  11. Targeting ferroptosis for treating kidney disease.Clinical and experimental nephrology · 2024
    Review
  12. Review
  13. Review
  14. Review
  15. Risk of Atherosclerosis Due to HMGB1-dependent Platelet-derived Microparticles in Patients with Type 2 Diabetes Mellitus.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    Article
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

7 authors.

Toshitaka NakamuraInstitute of Metabolism and Cell Death, Molecular Targets & Therapeutics Center, Helmholtz Zentrum München, 85764 Neuherberg, Bavaria, Germany.
Junya ItoInstitute of Metabolism and Cell Death, Molecular Targets & Therapeutics Center, Helmholtz Zentrum München, 85764 Neuherberg, Bavaria, Germany; Laboratory of Food Function Analysis, Tohoku University Graduate School of Agricultural Science, Sendai, Miyagi 980-8572, Japan.
André Santos Dias MourãoInstitute of Structural Biology, Molecular Targets & Therapeutics Center, Helmholtz Zentrum München, 85764 Neuherberg, Bavaria, Germany.
Adam WahidaInstitute of Metabolism and Cell Death, Molecular Targets & Therapeutics Center, Helmholtz Zentrum München, 85764 Neuherberg, Bavaria, Germany.
Kiyotaka NakagawaLaboratory of Food Function Analysis, Tohoku University Graduate School of Agricultural Science, Sendai, Miyagi 980-8572, Japan.
Eikan MishimaInstitute of Metabolism and Cell Death, Molecular Targets & Therapeutics Center, Helmholtz Zentrum München, 85764 Neuherberg, Bavaria, Germany; Division of Nephrology, Rheumatology and Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Miyagi 980-8574, Japan. Electronic address: eikan@med.tohoku.ac.jp.
Marcus ConradInstitute of Metabolism and Cell Death, Molecular Targets & Therapeutics Center, Helmholtz Zentrum München, 85764 Neuherberg, Bavaria, Germany. Electronic address: marcus.conrad@helmholtz-munich.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis, a regulated cell death hallmarked by unrestrained lipid peroxidation, plays a pivotal role in the pathophysiology of various diseases, making it a promising therapeutic target. Glutathione peroxidase 4 (GPX4) prevents ferroptosis by reducing (phospho)lipid hydroperoxides, yet evaluation of its actual activity has remained arduous. Here, we present a tangible method using affinity-purified GPX4 to capture a snapshot of its native activity. Next to measuring GPX4 activity, this improved method allows for the investigation of mutational GPX4 activity, exemplified by the GPX4

Indexed as

FerroptosisRegulated Cell DeathLipid PeroxidationLipid PeroxidesPhospholipid Hydroperoxide Glutathione PeroxidaseLipid PeroxidesPhospholipid Hydroperoxide Glutathione Peroxidaseaffinity purificationbiochemistrycell deathCP: Molecular biologydrug discoveryenzyme assayFSP1GPX4LC-MS/MSlipid peroxidationpull-down assayRSL3selenocysteine

Identifiers

PMID38401540
PMCPMC10985226

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Registered trials

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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.