Evidence map›Paper›PMID 37456854›Full record

ArticleiScience2023

Peripheral blood mononuclear cell hyperresponsiveness in patients with premature myocardial infarction without traditional risk factors.

Jan-Quinten Mol, Julia van Tuijl, Siroon Bekkering, Charlotte D C C van der Heijden, Sander A J Damen, Benjamin C Cossins, Liesbeth van Emst, Tim M Nielen, Laura Rodwell, Yang Li and 5 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. 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

15 authors at 3 institutions in 3 countries.

Jan-Quinten MolDepartment of Cardiology, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Julia van TuijlDepartment of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Siroon BekkeringDepartment of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Charlotte D C C van der HeijdenDepartment of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Sander A J DamenDepartment of Cardiology, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Benjamin C CossinsDepartment of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Liesbeth van EmstDepartment of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Tim M NielenDepartment of Cardiology, Canisius Wilhelmina Hospital, 6532 SZ Nijmegen, the Netherlands.
Laura RodwellSection Biostatistics, Department for Health Evidence, Radboud Institute for Health Sciences, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Yang LiDepartment of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Gheorghe A M PopDepartment of Cardiology, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Mihai G NeteaDepartment of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Niels van RoyenDepartment of Cardiology, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Niels P RiksenDepartment of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Saloua El MessaoudiDepartment of Cardiology, Radboud University Medical Center, 6525 GA Nijmegen, the Netherlands.
Radboud University Nijmegen · NLCanisius-Wilhelmina Ziekenhuis · NLUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An increasing number of patients develop an atherothrombotic myocardial infarction (MI) in the absence of standard modifiable risk factors (SMuRFs). Monocytes and macrophages regulate the development of atherosclerosis, and monocytes can adopt a long-term hyperinflammatory phenotype by epigenetic reprogramming, which can contribute to atherogenesis (called "trained immunity"). We assessed circulating monocyte phenotype and function and specific histone marks associated with trained immunity in SMuRFless patients with MI and matched healthy controls. Even in the absence of systemic inflammation, monocytes from SMuRFless patients with MI had an increased overall cytokine production capacity, with the strongest difference for LPS-induced interleukin-10 production, which was associated with an enrichment of the permissive histone marker H3K4me3 at the promoter region. Considering the lack of intervenable risk factors in these patients, trained immunity could be a promising target for future therapy.

Indexed as

Cardiovascular medicineComponents of the immune systemMolecular mechanism of gene regulationTranscriptomics

Identifiers

PMID37456854
PMCPMC10338301
OpenAlexW4381251349

What OpenQuestion 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 OpenQuestion graph.