Evidence map›Paper›PMID 37280612›Full record

ArticleJournal of translational medicine2023

Atrial epicardial adipose tissue abundantly secretes myeloperoxidase and activates atrial fibroblasts in patients with atrial fibrillation.

Eva R Meulendijks, Rushd F M Al-Shama, Makiri Kawasaki, Benedetta Fabrizi, Jolien Neefs, Robin Wesselink, Auriane C Ernault, Sander Piersma, Thang V Pham, Connie R Jimenez and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

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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

19 authors at 5 institutions in 2 countries.

Eva R Meulendijks *Amsterdam UMC, Heart Center, Department of Clinical and Experimental Cardiology and Cardiothoracic Surgery, University of Amsterdam, Amsterdam, The Netherlands. e.r.meulendijks@amsterdamumc.nl.
Rushd F M Al-Shama *Amsterdam UMC, Heart Center, Department of Clinical and Experimental Cardiology and Cardiothoracic Surgery, University of Amsterdam, Amsterdam, The Netherlands.
Makiri KawasakiAmsterdam UMC, Heart Center, Department of Clinical and Experimental Cardiology and Cardiothoracic Surgery, University of Amsterdam, Amsterdam, The Netherlands.
Benedetta FabriziAmsterdam UMC, Heart Center, Department of Clinical and Experimental Cardiology and Cardiothoracic Surgery, University of Amsterdam, Amsterdam, The Netherlands.
Jolien NeefsAmsterdam UMC, Heart Center, Department of Clinical and Experimental Cardiology and Cardiothoracic Surgery, University of Amsterdam, Amsterdam, The Netherlands.
Robin WesselinkAmsterdam UMC, Heart Center, Department of Clinical and Experimental Cardiology and Cardiothoracic Surgery, University of Amsterdam, Amsterdam, The Netherlands.
Auriane C ErnaultAmsterdam UMC, Heart Center, Department of Clinical and Experimental Cardiology and Cardiothoracic Surgery, University of Amsterdam, Amsterdam, The Netherlands.
Sander PiersmaAmsterdam UMC, VU Medical Center, Department of Medical Oncology, VU university, Amsterdam, The Netherlands.
Thang V PhamAmsterdam UMC, VU Medical Center, Department of Medical Oncology, VU university, Amsterdam, The Netherlands.
Connie R JimenezAmsterdam UMC, VU Medical Center, Department of Medical Oncology, VU university, Amsterdam, The Netherlands.
Jaco C KnolAmsterdam UMC, VU Medical Center, Department of Medical Oncology, VU university, Amsterdam, The Netherlands.
Wim J P van BovenAmsterdam UMC, Heart Center, Department of Clinical and Experimental Cardiology and Cardiothoracic Surgery, University of Amsterdam, Amsterdam, The Netherlands.
Antoine H G DriessenAmsterdam UMC, Heart Center, Department of Clinical and Experimental Cardiology and Cardiothoracic Surgery, University of Amsterdam, Amsterdam, The Netherlands.
Tim A C de VriesAmsterdam UMC, Heart Center, Department of Clinical and Experimental Cardiology and Cardiothoracic Surgery, University of Amsterdam, Amsterdam, The Netherlands.
Britt van der LeedenAmsterdam Cardiovascular Sciences, Heart Failure and Arrhythmias, Amsterdam, The Netherlands.
Hans W M NiessenAmsterdam Cardiovascular Sciences, Heart Failure and Arrhythmias, Amsterdam, The Netherlands.
Onno J de BoerAmsterdam UMC, Department of Pathology, University of Amsterdam, Amsterdam, The Netherlands.
Sébastien P J KrulAmsterdam UMC, Heart Center, Department of Clinical and Experimental Cardiology and Cardiothoracic Surgery, University of Amsterdam, Amsterdam, The Netherlands.
Joris R de GrootAmsterdam UMC, Heart Center, Department of Clinical and Experimental Cardiology and Cardiothoracic Surgery, University of Amsterdam, Amsterdam, The Netherlands.
Amsterdam University Medical Centers · NLAmsterdam UMC Location VUmc · NLUniversity of Amsterdam · NLIsala · NLRijnstate Hospital · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpicardial adipose tissue (EAT) secretome induces fibrosis. Fibrosis, primarily extracellular matrix (ECM) produced by fibroblasts, creates a substrate for atrial fibrillation (AF). Whether the EAT secretome from patients with AF activates human atrial fibroblasts and through which components, remains unexplored. RESEARCH

aims(a) To investigate if the EAT secretome from patients with versus without AF increases ECM production in atrial fibroblasts. (b) To identify profibrotic proteins and processes in the EAT secretome and EAT from patients with, who will develop (future onset), and without AF.

methodsAtrial EAT was obtainded during thoracoscopic ablation (AF, n = 20), or open-heart surgery (future onset and non-AF, n = 35). ECM gene expression of human atrial fibroblasts exposed to the EAT secretome and the proteomes of EAT secretome and EAT were assessed in patients with and without AF. Myeloperoxidase and neutrophil extracellular traps (NETs) were assessed immunohistochemically in patients with paroxysmal, persistent, future onset, and those who remain free of AF (non-AF).

resultsThe expression of COL1A1 and FN1 in fibroblasts exposed to secretome from patients with AF was 3.7 and 4.7 times higher than in patients without AF (p < 0.05). Myeloperoxidase was the most increased protein in the EAT secretome and EAT from patients with versus without AF (FC 18.07 and 21.57, p < 0.005), as was the gene-set neutrophil degranulation. Immunohistochemically, myeloperoxidase was highest in persistent (FC 13.3, p < 0.0001) and increased in future onset AF (FC 2.4, p = 0.02) versus non-AF. Myeloperoxidase aggregated subepicardially and around fibrofatty infiltrates. NETs were increased in patients with persistent versus non-AF (p = 0.03).

conclusionIn AF, the EAT secretome induces ECM gene expression in atrial fibroblasts and contains abundant myeloperoxidase. EAT myeloperoxidase was increased prior to AF onset, and both myeloperoxidase and NETs were highest in persistent AF, highlighting the role of EAT neutrophils in the pathophysiology of AF.

Indexed as

Atrial FibrillationAdipose TissueFibrosisHeart AtriaHumansPericardiumPeroxidaseMPO protein, humanPeroxidase

Identifiers

PMID37280612
PMCPMC10245533
OpenAlexW4379538102

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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.