Evidence map›Paper›PMID 38097808›Full record

ArticleNature metabolism2023

Iron accumulation drives fibrosis, senescence and the senescence-associated secretory phenotype.

Mate Maus, Vanessa López-Polo, Lidia Mateo, Miguel Lafarga, Mònica Aguilera, Eugenia De Lama, Kathleen Meyer, Anna Sola, Cecilia Lopez-Martinez, Ines López-Alonso and 17 more

Open access · hybridAbstract read
In one paragraph

Article in Nature metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed
27.4field-weighted citation impact, top 1% of its field
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

144 citing papers in PubMed, 164 citations in OpenAlex.

  1. Article
  2. Impact of renal iron overload on sickle cell nephropathy in a humanized mouse model.American journal of physiology. Renal physiology · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Dysregulated iron metabolism in remodeling of aging asthmatic human airways.American journal of physiology. Cell physiology · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. A practical toolbox for modelling fibrosis in vitro.Nature biomedical engineering · 2026
    Review
  11. Article
  12. Article
  13. Article
  14. 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
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

84 more citing papers are in PubMed but not listed here.

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

27 authors at 14 institutions in 3 countries.

Mate Maus *Institute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain. matemaus@vhio.net.ORCID 0000-0002-2128-2479
Vanessa López-Polo *Institute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.ORCID 0000-0001-6165-2510
Lidia MateoInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.ORCID 0000-0002-9076-4025
Miguel LafargaDepartamento de Anatomía y Biología Celular, Universidad de Cantabria-IDIVAL, Santander, Spain.
Mònica AguileraInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.ORCID 0000-0003-0763-7947
Eugenia De LamaRadiology Department, Hospital Universitari de Bellvitge, IDIBELL, L'Hospitalet de Llobregat, Barcelona, Spain.
Kathleen MeyerInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Anna SolaNephrology and Renal Transplantation Research Group. Bellvitge Biomedical Research Institute (IDIBELL), Hospitalet de Llobregat, Barcelona, Spain.ORCID 0000-0003-2379-9313
Cecilia Lopez-MartinezDepartamento de Biología Funcional, Instituto Universitario de Oncología del principado de Asturias, Universidad de Oviedo, Oviedo, Spain.ORCID 0000-0001-7269-4126
Ines López-AlonsoDepartamento de Morfología y Biología Celular, Universidad de Oviedo, Instituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain.
Marc Guasch-PiquerasVall d'Hebron Institute of Oncology, Barcelona, Spain.ORCID 0000-0003-2392-2860
Fernanda Hernandez-GonzalezInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.ORCID 0000-0001-5113-4285
Selim ChaibInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.ORCID 0000-0003-0497-2002
Miguel RoviraInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.ORCID 0000-0002-1391-8465
Mayka SanchezIron Metabolism: Regulation and Diseases Group, Department of Basic Sciences, Universitat Internacional de Catalunya (UIC), Sant Cugat del Vallès, Spain.ORCID 0000-0002-6499-5989
Rosa FanerBiomedicine Department, University of Barcelona, IDIBAPS, CIBERES, Barcelona, Spain.
Alvar AgustiUniversitat de Barcelona, Institut Respiratori, Hospital Clinic, IDIBAPS, CIBERES, Barcelona, Spain.ORCID 0000-0003-3271-3788
Rodrigo Diéguez-HurtadoDeparment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Sagrario OrtegaTransgenics Unit, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Anna ManonellesNephrology and Renal Transplantation Research Group. Bellvitge Biomedical Research Institute (IDIBELL), Hospitalet de Llobregat, Barcelona, Spain.ORCID 0000-0003-2456-388X
Stefan EngelhardtInstitute of Pharmacology and Toxicology, Technical University of Munich (TUM), Munich, Germany.ORCID 0000-0001-5378-8661
Freddy MonteiroInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.ORCID 0000-0002-9080-6715
Camille Stephan-Otto AttoliniInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.ORCID 0000-0001-8045-320X
Neus PratsInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Guillermo AlbaicetaDepartamento de Biología Funcional, Instituto Universitario de Oncología del principado de Asturias, Universidad de Oviedo, Oviedo, Spain.ORCID 0000-0002-9276-3253
Josep M CruzadoNephrology and Renal Transplantation Research Group. Bellvitge Biomedical Research Institute (IDIBELL), Hospitalet de Llobregat, Barcelona, Spain.ORCID 0000-0003-1388-8558
Manuel SerranoInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), Barcelona, Spain. mserrano@altoslabs.com.ORCID 0000-0001-7177-9312
Institute for Research in Biomedicine · ESBellvitge University Hospital · ESUniversidad de Oviedo · ESCentro de Investigación Biomédica en Red de Enfermedades Respiratorias · ESGerman Centre for Cardiovascular Research · DEHospital Clínic de Barcelona · ESInstitució Catalana de Recerca i Estudis Avançats · ESInstitut d'Investigació Biomédica de Bellvitge · ESMax Planck Institute for Molecular Biomedicine · DESpanish National Cancer Research Centre · ESUniversidad de Cantabria · ESUniversitat Internacional de Catalunya · ESVall d'Hebron Institut de Recerca · ESVall d'Hebron Institute of Oncology · ES

Funding

European Research Council"la Caixa" Foundation (Caixa Foundation) SAF2017-82613-R
6 · The paper itself

Abstract

Fibrogenesis is part of a normal protective response to tissue injury that can become irreversible and progressive, leading to fatal diseases. Senescent cells are a main driver of fibrotic diseases through their secretome, known as senescence-associated secretory phenotype (SASP). Here, we report that cellular senescence, and multiple types of fibrotic diseases in mice and humans are characterized by the accumulation of iron. We show that vascular and hemolytic injuries are efficient in triggering iron accumulation, which in turn can cause senescence and promote fibrosis. Notably, we find that senescent cells persistently accumulate iron, even when the surge of extracellular iron has subdued. Indeed, under normal conditions of extracellular iron, cells exposed to different types of senescence-inducing insults accumulate abundant ferritin-bound iron, mostly within lysosomes, and present high levels of labile iron, which fuels the generation of reactive oxygen species and the SASP. Finally, we demonstrate that detection of iron by magnetic resonance imaging might allow non-invasive assessment of fibrotic burden in the kidneys of mice and in patients with renal fibrosis. Our findings suggest that iron accumulation plays a central role in senescence and fibrosis, even when the initiating events may be independent of iron, and identify iron metabolism as a potential therapeutic target for senescence-associated diseases.

Indexed as

Cellular SenescenceSenescence-Associated Secretory PhenotypeFibrosisHumansIronKidneyIron

Identifiers

PMID38097808
PMCPMC10730403
OpenAlexW4389736224

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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.