Evidence map›Paper›PMID 41085167›Full record

ArticleMolecular omics2025

Cytokine-induced memory-like responses in endothelial cells link chronic inflammation to vascular disease risk.

Kieu T T Le, Nick Keur, Heleen Middelkamp, Thuy Linh Do, Albert van den Berg, Valeria Orlova, Leo A B Joosten, Mihai G Netea, Cisca Wijmenga, Iris Jonkers and 3 more

Abstract read
In one paragraph

Article in Molecular omics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Innate Immune Memory Responses in Organ Transplantation.Arteriosclerosis, thrombosis, and vascular biology · 2026
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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

13 authors.

Kieu T T LeDepartment of Genetics, University Medical Center Groningen, University of Groningen, The Netherlands.
Nick KeurDepartment of Internal Medicine and Radboud Institute of Molecular Life Sciences (RIMLS), Radboud University Medical Center, Nijmegen, The Netherlands. v.kumar@radboudumc.nl.ORCID http://orcid.org/0000-0002-0142-0811
Heleen MiddelkampBIOS lab-on-a-chip group, University of Twente, Enschede, The Netherlands.ORCID http://orcid.org/0000-0003-0267-8811
Thuy Linh DoDepartment of Genetics, University Medical Center Groningen, University of Groningen, The Netherlands.
Albert van den BergBIOS lab-on-a-chip group, University of Twente, Enschede, The Netherlands.ORCID http://orcid.org/0000-0001-9019-933X
Valeria OrlovaDepartment of Developmental Biology, Leiden UMC, The Netherlands.
Leo A B JoostenDepartment of Internal Medicine and Radboud Institute of Molecular Life Sciences (RIMLS), Radboud University Medical Center, Nijmegen, The Netherlands. v.kumar@radboudumc.nl.
Mihai G NeteaDepartment of Internal Medicine and Radboud Institute of Molecular Life Sciences (RIMLS), Radboud University Medical Center, Nijmegen, The Netherlands. v.kumar@radboudumc.nl.
Cisca WijmengaDepartment of Genetics, University Medical Center Groningen, University of Groningen, The Netherlands.
Iris JonkersDepartment of Genetics, University Medical Center Groningen, University of Groningen, The Netherlands.ORCID http://orcid.org/0000-0003-2304-7939
Sebo WithoffDepartment of Genetics, University Medical Center Groningen, University of Groningen, The Netherlands.
Andries D Van der MeerDepartment of Applied Stem Cell Technologies, University of Twente, The Netherlands.ORCID http://orcid.org/0000-0002-8761-4077
Vinod KumarDepartment of Genetics, University Medical Center Groningen, University of Groningen, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation plays a central role in the progression of both infectious and vascular diseases, yet its impact on endothelial cells (ECs), which form the interface between blood and tissue, remains poorly understood. Given their constant exposure to inflammatory cytokines such as TNF-α and IFN-γ, we set out to investigate how cytokine induced inflammation shapes EC function at the molecular level. Using primary human umbilical vein endothelial cells (HUVECs), we modeled repeated cytokine exposure to simulate a chronically inflamed microenvironment. Transcriptomic and epigenetic profiling revealed that ECs respond to this chronic stimulation with durable transcriptional and chromatin changes. These responses included phenotypes resembling immune cell priming, training, and tolerance, which are commonly associated with innate immune memory, a phenomenon whereby innate immune cells mount altered responses following previous stimulation. Although we did not observe classical trained immunity pathways, several genes known to mediate immune training, including

Indexed as

CytokinesEndothelial CellsImmunologic MemoryInflammationVascular DiseasesChronic DiseaseCOVID-19Epigenesis, GeneticHumansHuman Umbilical Vein Endothelial CellsImmunity, InnateInterferon-gammaTumor Necrosis Factor-alphaCytokinesInterferon-gammaTumor Necrosis Factor-alpha

Identifiers

PMID41085167
PMCPMC12519785

What OpenQuestion holds

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LicenceCC BY
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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.