Evidence map›Paper›PMID 41868610›Full record

ArticleFrontiers in immunology2025

GJA5 and ATP1A1 perturbations recapitulate inflammation-related beat irregularities in iPSC-based atrial myocardium tissue model.

Thomas Hutschalik, Albert Dasí, Leto L Riebel, Maury Wiendels, Frederikus Bakker, Lucas J A M Beckers, Koen C Kriege, Susanne M Valster, Roland C M Vulders, Ozan Özgül and 5 more

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In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Thomas HutschalikNcardia Services B.V., Leiden, Netherlands.
Albert DasíDepartment of Computer Science, University of Oxford, Oxford, United Kingdom.
Leto L RiebelDepartment of Computer Science, University of Oxford, Oxford, United Kingdom.
Maury WiendelsAnatomy and Embryology, Leiden University Medical Center (LUMC), Leiden, Netherlands.
Frederikus BakkerDepartment of Digital Standardization and Licensing Research, Intellectual Property and Standards, Royal Philips, Eindhoven, Netherlands.
Lucas J A M BeckersDepartment of Digital Standardization and Licensing Research, Intellectual Property and Standards, Royal Philips, Eindhoven, Netherlands.
Koen C KriegeDepartment of Digital Standardization and Licensing Research, Intellectual Property and Standards, Royal Philips, Eindhoven, Netherlands.
Susanne M ValsterDepartment of Digital Standardization and Licensing Research, Intellectual Property and Standards, Royal Philips, Eindhoven, Netherlands.
Roland C M VuldersDepartment of Digital Standardization and Licensing Research, Intellectual Property and Standards, Royal Philips, Eindhoven, Netherlands.
Ozan ÖzgülDepartment of Physiology, Cardiovascular Research Institute Maastricht, Maastricht, Netherlands.
Rémi PeyronnetInstitute for Experimental Cardiovascular Medicine, University Heart Center Freiburg Bad Krozingen, and Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Blanca RodriguezDepartment of Computer Science, University of Oxford, Oxford, United Kingdom.
Mariana ArgenzianoNcardia Services B.V., Leiden, Netherlands.
Ulrich SchottenDepartment of Physiology, Cardiovascular Research Institute Maastricht, Maastricht, Netherlands.
Elena MatsaNcardia Services B.V., Leiden, Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrillation (AF) is the most common cardiac arrhythmia, linked to greater risk of heart failure, stroke and death. Inflammation has been connected to AF emergence, however mechanisms of inflammation-caused AF remain thus far elusive, leading to a lack of mechanism-based treatments. An isogenic, 3D tissue model containing hiPSC-derived atrial-like cardiomyocytes (aCM), cardiac fibroblasts (cfb), and cardiac macrophages was engineered using custom injection-molded pillar devices. Electrophysiological changes were examined via sharp electrode recordings, calcium imaging, and multi-electrode assays. Gene function was interrogated using siRNA knock-down, lentiviral overexpression, and pharmacological modulation. In silico tissue and whole-heart models validated findings under simulated stress and heterogeneous conditions. Activation of M1 macrophages led to a 50% reduction in contraction amplitude, action potential spike amplitude (aCM+cfb+M1: 61.3 mV ±13.9

Indexed as

Atrial FibrillationConnexinsHeart AtriaInduced Pluripotent Stem CellsInflammationMyocardiumAction PotentialsAnimalsGap Junction alpha-5 ProteinHumansMacrophagesMyocytes, CardiacConnexinsGap Junction alpha-5 Proteinatrial fibrillationengineered 3D tissueinflammationIPSCmacrophage

Identifiers

PMID41868610
PMCPMC13002374

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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.