Evidence map›Paper›PMID 38769293›Full record

ArticleNature communications2024

Fatal COVID-19 pulmonary disease involves ferroptosis.

Baiyu Qiu, Fereshteh Zandkarimi, Anjali Saqi, Candace Castagna, Hui Tan, Miroslav Sekulic, Lisa Miorin, Hanina Hibshoosh, Shinya Toyokuni, Koji Uchida and 1 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 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing 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

44 citing papers in PubMed.

  1. Review
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  5. Iron and the lung: emerging roles of iron metabolism in pulmonary disease pathogenesis and therapy.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Trophoblast ferroptosis restricts SARS-CoV-2 spread in the placenta.bioRxiv : the preprint server for biology · 2026
    Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
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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

11 authors.

Baiyu Qiu *Department of Chemistry, Columbia University, New York, NY, 10027, USA.
Fereshteh Zandkarimi *Department of Chemistry, Columbia University, New York, NY, 10027, USA.ORCID http://orcid.org/0000-0001-8618-3669
Anjali Saqi *Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY, 10032, USA.
Candace CastagnaInstitute of Comparative Medicine, Columbia University Irving Medical Center, New York, NY, 10032, USA.ORCID http://orcid.org/0000-0003-2410-9361
Hui TanDepartment of Chemistry, Columbia University, New York, NY, 10027, USA.
Miroslav SekulicDepartment of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY, 10032, USA.
Lisa MiorinDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Hanina HibshooshDepartment of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY, 10032, USA.
Shinya ToyokuniDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.ORCID http://orcid.org/0000-0002-5757-1109
Koji UchidaGraduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, 113-8657, Japan.
Brent R StockwellDepartment of Chemistry, Columbia University, New York, NY, 10027, USA. bstockwell@columbia.edu.ORCID http://orcid.org/0000-0002-3532-3868

Funding

Tumor Biology and Microenvironment ProgramP30CA013696 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Anil K Rustgi · 1985 to 2026
$115.3M
Defining the functions and translational potential of ferroptosisR35CA209896 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI STOCKWELL, BRENT R. · 2016 to 2022
$6.5M
NCI NIH HHS P30 CA013696NCI NIH HHS R35 CA209896U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R35CA209896
6 · The paper itself

Abstract

SARS-CoV-2 infection causes severe pulmonary manifestations, with poorly understood mechanisms and limited treatment options. Hyperferritinemia and disrupted lung iron homeostasis in COVID-19 patients imply that ferroptosis, an iron-dependent cell death, may occur. Immunostaining and lipidomic analysis in COVID-19 lung autopsies reveal increases in ferroptosis markers, including transferrin receptor 1 and malondialdehyde accumulation in fatal cases. COVID-19 lungs display dysregulation of lipids involved in metabolism and ferroptosis. We find increased ferritin light chain associated with severe COVID-19 lung pathology. Iron overload promotes ferroptosis in both primary cells and cancerous lung epithelial cells. In addition, ferroptosis markers strongly correlate with lung injury severity in a COVID-19 lung disease model using male Syrian hamsters. These results reveal a role for ferroptosis in COVID-19 pulmonary disease; pharmacological ferroptosis inhibition may serve as an adjuvant therapy to prevent lung damage during SARS-CoV-2 infection.

Indexed as

COVID-19FerroptosisLungMesocricetusSARS-CoV-2AdultAgedAnimalsCricetinaeDisease Models, AnimalFemaleHumansIronIron OverloadLung InjuryMaleIron

Identifiers

PMID38769293
PMCPMC11106344

What OpenQuestion holds

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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.