Evidence map›Paper›PMID 39112467›Full record

ArticleNature communications2024

Skin hepcidin initiates psoriasiform skin inflammation via Fe-driven hyperproliferation and neutrophil recruitment.

Elise Abboud, Doha Chrayteh, Nadia Boussetta, Héloise Dalle, Mariangela Malerba, Ting-Di Wu, Morgane Le Gall, Olivier Reelfs, Charareh Pourzand, Mark Mellett and 9 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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Iron and the immune system.Nature reviews. Immunology · 2025
    Review
  12. Review
  13. How Cells Die in Psoriasis?International journal of molecular sciences · 2025
    Review
  14. Article
  15. Hepcidin and Tissue-Specific Iron Regulatory Networks.Advances in experimental medicine and biology · 2025
    Review
  16. Article
  17. Article
  18. Diagnostics: Markers of Body Iron Status.Advances in experimental medicine and biology · 2025
    Review
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

19 authors.

Elise Abboud *Université Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Doha Chrayteh *Université Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Nadia BoussettaUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Héloise DalleUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Mariangela MalerbaUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Ting-Di WuInstitut Curie, PSL University, Université Paris-Saclay, CNRS UAR2016, Inserm US43, Multimodal Imaging Center, Orsay, France.
Morgane Le GallProteom'IC facility, Université Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.ORCID 0000-0002-4935-7065
Olivier ReelfsDepartment of Life Sciences, University of Bath, Bath, United Kingdom.ORCID 0000-0002-7005-7411
Charareh PourzandDepartment of Life Sciences, University of Bath, Bath, United Kingdom.
Mark MellettDepartment of Dermatology, University Hospital Zürich (USZ), University of Zürich (UZH), Zürich, Switzerland.ORCID 0000-0002-6315-167X
Florence AssanLaboratory of Genetic Skin Diseases, INSERM U1163, Imagine Institute, Université Paris Cité, Paris, France.
Hervé BachelezLaboratory of Genetic Skin Diseases, INSERM U1163, Imagine Institute, Université Paris Cité, Paris, France.
Joël PouponLaboratoire de Toxicologie Biologique, Hôpital Lariboisière, Paris, France. Assistance Publique - Hôpitaux de Paris, AP-HP, Paris, France.
Selim AractingiUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Sophie VaulontUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Pierre SohierUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.ORCID 0000-0002-2341-6848
Bénédicte OulesUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Zoubida KarimUniversité de Toulouse, INSERM, CNRS, Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), Université Paul Sabatier (UPS), Toulouse, France.
Carole PeyssonnauxUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France. carole.peyssonnaux@inserm.fr.ORCID 0000-0002-1392-8225

Funding

Agence Nationale de la Recherche (French National Research Agency) ANR-11-IDEX-0005-02Agence Nationale de la Recherche (French National Research Agency) ANR-11-LABX-0051Fondation pour la Recherche Médicale (Foundation for Medical Research in France) DEQ20160334903Fondation pour la Recherche Médicale (Foundation for Medical Research in France) EQ202103012630Fondation pour la Recherche Médicale (Foundation for Medical Research in France) PMT202206015641Swiss National Science Foundation 341 310030_201242
6 · The paper itself

Abstract

Psoriasis is a multifactorial, chronic inflammatory skin disease with unresolved questions on its primary events. Iron overload has been described in the epidermis of psoriasis patients, but its relevance remains unknown. We found that the key iron regulatory hormone hepcidin was highly expressed in the epidermis of psoriasis patients, especially the pustular variants resistant to treatments. In a murine model of acute skin inflammation, keratinocyte-derived hepcidin was required for iron retention in keratinocytes, leading to hyperproliferation of the epidermal layer and neutrophil recruitment, two main features of psoriatic skin lesions. Keratinocytes overexpressing hepcidin were sufficient to elicit these psoriasiform features in a transgenic mouse model. Furthermore, transcriptome analysis of these keratinocytes revealed canonical pathways found in human psoriasis, pointing to a causal role for hepcidin in the pathogenesis of the disease. Altogether, our data suggest that hepcidin could be an actionable target for skin psoriasis treatment, in addition to current therapeutics, or targeted as maintenance therapy during remission to prevent recurrence.

Indexed as

Cell ProliferationHepcidinsIronKeratinocytesMice, TransgenicNeutrophil InfiltrationPsoriasisSkinAnimalsDisease Models, AnimalEpidermisFemaleHumansInflammationMaleMiceHepcidinsIron

Identifiers

PMID39112467
PMCPMC11306357

What OpenQuestion holds

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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.