Evidence map›Paper›PMID 39218970›Full record

ArticleNature communications2024

Suppression of ferroptosis by vitamin A or radical-trapping antioxidants is essential for neuronal development.

Juliane Tschuck, Vidya Padmanabhan Nair, Ana Galhoz, Carole Zaratiegui, Hin-Man Tai, Gabriele Ciceri, Ina Rothenaigner, Jason Tchieu, Brent R Stockwell, Lorenz Studer and 4 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. PLA2G2F suppresses ferroptosis through phospholipid remodeling.Nature structural & molecular biology · 2026
    Article
  5. MiR-940 Suppresses Ferroptosis by Controlling Expression of Key Regulatory Genes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  17. Is Obesity a Modifiable Risk Factor in Multiple Sclerosis? Mechanistic Insights into Neuroinflammation and Oxidative Damage.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
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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

14 authors.

Juliane Tschuck *Research Unit Signaling and Translation, Helmholtz Zentrum München, Neuherberg, Germany.ORCID 0000-0002-3144-6027
Vidya Padmanabhan Nair *Endogenous Retrovirus Group, Institute of Virology, Helmholtz Zentrum München, Neuherberg, Germany.
Ana GalhozComputational Health Center, Helmholtz Zentrum München, Neuherberg, Germany.
Carole ZaratieguiInstitute of Functional Epigenetics, Helmholtz Zentrum München, Neuherberg, Germany.
Hin-Man TaiEndogenous Retrovirus Group, Institute of Virology, Helmholtz Zentrum München, Neuherberg, Germany.
Gabriele CiceriDevelopmental Biology and Center for Stem Cell Biology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID 0000-0002-8481-9771
Ina RothenaignerResearch Unit Signaling and Translation, Helmholtz Zentrum München, Neuherberg, Germany.
Jason TchieuDevelopmental Biology and Center for Stem Cell Biology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID 0000-0002-9793-9836
Brent R StockwellDepartment of Biological Sciences, Department of Chemistry, Herbert Irving Comprehensive Cancer Center, Irving Institute for Cancer Dynamics, Columbia University, New York, NY, USA.ORCID 0000-0002-3532-3868
Lorenz StuderDevelopmental Biology and Center for Stem Cell Biology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID 0000-0003-0741-7987
Daphne S CabiancaInstitute of Functional Epigenetics, Helmholtz Zentrum München, Neuherberg, Germany.
Michael P MendenComputational Health Center, Helmholtz Zentrum München, Neuherberg, Germany.ORCID 0000-0003-0267-5792
Michelle VincendeauEndogenous Retrovirus Group, Institute of Virology, Helmholtz Zentrum München, Neuherberg, Germany. michelle.vincendeau@helmholtz-munich.de.ORCID 0000-0002-8937-9277
Kamyar HadianResearch Unit Signaling and Translation, Helmholtz Zentrum München, Neuherberg, Germany. kamyar.hadian@helmholtz-munich.de.ORCID 0000-0001-8727-2575

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Deutsche Forschungsgemeinschaft (German Research Foundation) 435874434Deutsche Forschungsgemeinschaft (German Research Foundation) 496872373Deutsche Forschungsgemeinschaft (German Research Foundation) 497803923Deutsche Forschungsgemeinschaft (German Research Foundation) 498956525NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

The development of functional neurons is a complex orchestration of multiple signaling pathways controlling cell proliferation and differentiation. Because the balance of antioxidants is important for neuronal survival and development, we hypothesized that ferroptosis must be suppressed to gain neurons. We find that removal of antioxidants diminishes neuronal development and laminar organization of cortical organoids, which is fully restored when ferroptosis is inhibited by ferrostatin-1 or when neuronal differentiation occurs in the presence of vitamin A. Furthermore, iron-overload-induced developmental growth defects in C. elegans are ameliorated by vitamin E and A. We determine that all-trans retinoic acid activates the Retinoic Acid Receptor, which orchestrates the expression of anti-ferroptotic genes. In contrast, retinal and retinol show radical-trapping antioxidant activity. Together, our study reveals an unexpected function of vitamin A in coordinating the expression of essential cellular gatekeepers of ferroptosis, and demonstrates that suppression of ferroptosis by radical-trapping antioxidants or by vitamin A is required to obtain mature neurons and proper laminar organization in cortical organoids.

Indexed as

AntioxidantsCaenorhabditis elegansFerroptosisNeuronsVitamin AAnimalsCaenorhabditis elegans ProteinsCell DifferentiationCyclohexylaminesHumansMiceNeurogenesisOrganoidsPhenylenediaminesReceptors, Retinoic AcidSignal TransductionAntioxidantsCaenorhabditis elegans ProteinsCyclohexylaminesferrostatin-1PhenylenediaminesReceptors, Retinoic AcidTretinoinVitamin AVitamin E

Identifiers

PMID39218970
PMCPMC11366759

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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.