Evidence map›Paper›PMID 39910039›Full record

ArticleNature communications2025

Testosterone exacerbates neutrophilia and cardiac injury in myocardial infarction via actions in bone marrow.

Elin Svedlund Eriksson, Marta Lantero Rodriguez, Bente Halvorsen, Inger Johansson, Anna K F Mårtensson, Anna S Wilhelmson, Camilla Huse, Thor Ueland, Pål Aukrust, Kaspar Broch and 15 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Metabolic Messengers: testosterone.Nature metabolism · 2026
    Review
  10. Review
  11. Review
  12. 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

25 authors.

Elin Svedlund ErikssonWallenberg Laboratory for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0009-0006-0169-6929
Marta Lantero Rodriguez *Wallenberg Laboratory for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0002-9912-6716
Bente Halvorsen *Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.ORCID http://orcid.org/0000-0002-6529-6485
Inger JohanssonWallenberg Laboratory for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0009-0008-3579-9031
Anna K F MårtenssonWallenberg Laboratory for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0002-8786-4965
Anna S WilhelmsonWallenberg Laboratory for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0003-0640-0251
Camilla HuseResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.ORCID http://orcid.org/0000-0002-7694-5196
Thor UelandResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Pål AukrustResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.ORCID http://orcid.org/0000-0003-0919-836X
Kaspar BrochDepartment of Cardiology, Oslo University Hospital Rikshospitalet, Oslo, Norway.ORCID http://orcid.org/0000-0003-4316-805X
Lars GullestadFaculty of Medicine, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Brage Høyem AmundsenClinic of Cardiology, St. Olav's Hospital, Trondheim University Hospital, Trondheim, Norway.ORCID http://orcid.org/0000-0001-7914-7395
Geir Øystein AndersenDepartment of Cardiology, Oslo University Hospital Ullevål, Oslo, Norway.ORCID http://orcid.org/0000-0003-1578-6440
Mikael C I KarlssonDepartment of Microbiology, Tumor, and Cell Biology, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-5582-614X
Malin Hagberg ThulinDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0002-8673-1247
Alessandro CamponeschiDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0002-6472-2438
Dana TrompetDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0001-9472-6184
Ola HammarstenDepartment of Laboratory Medicine, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
Björn RedforsWallenberg Laboratory for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Jan BorénWallenberg Laboratory for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Elmir OmerovicWallenberg Laboratory for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Malin C LevinWallenberg Laboratory for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Andrei S ChaginDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0002-2696-5850
Tuva B DahlResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.ORCID http://orcid.org/0000-0001-7818-9411
Åsa TivestenWallenberg Laboratory for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden. asa.tivesten@medic.gu.se.ORCID http://orcid.org/0000-0002-8318-0486

Funding

Hjärt-Lungfonden (Swedish Heart-Lung Foundation) 20210492Novo Nordisk Fonden (Novo Nordisk Foundation) NNF18OC0034464Vetenskapsrådet (Swedish Research Council) 2021-01856
6 · The paper itself

Abstract

Men develop larger infarct sizes than women after a myocardial infarction (MI), but the mechanism underlying this sex difference is unknown. Here, we demonstrated that blood neutrophil counts post-MI were higher in male than female mice. Castration-induced testosterone deficiency reduced blood neutrophil counts to the level in females and increased survival post-MI. These effects were mimicked by Osterix-directed ablation of the androgen receptor in bone marrow (BM). Mechanistically, androgens downregulated the leukocyte retention factor CXCL12 in BM stromal cells. Post-hoc analysis of clinical trial data showed that neutrophilia was greater in men than women after reperfusion of first-time ST-elevation MI, and tocilizumab, an interleukin-6 receptor inhibitor, reduced blood neutrophil counts and infarct size to a greater extent in men than women. Our work reveals a previously unknown mechanism connecting testosterone with neutrophilia and MI injury via BM and identifies the importance of considering sex when developing anti-inflammatory strategies to treat MI.

Indexed as

Bone MarrowMyocardial InfarctionNeutrophilsTestosteroneAnimalsChemokine CXCL12Disease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLReceptors, AndrogenChemokine CXCL12Receptors, AndrogenTestosterone

Identifiers

PMID39910039
PMCPMC11799197

What Socratic holds

Textmetadata
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 Socratic graph.