Evidence map›Paper›PMID 41236081›Full record

ArticleEquine veterinary journal2026

The horse cardiac transcriptome: Moving towards a molecular understanding of atrial fibrillation.

Simon Libak Haugaard, Sarah Dalgas Nissen, Mélodie Jil Schneider, Jesper Bratz Birk, Helena Carstensen, Charlotte Hopster-Iversen, Ali Altıntaş, Romain Barrès, Rasmus Kjøbsted, Jørgen F P Wojtaszewski and 3 more

Abstract read
In one paragraph

Article in Equine veterinary journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

13 authors.

Simon Libak HaugaardDepartment of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Taastrup, Denmark.ORCID https://orcid.org/0000-0003-1787-134X
Sarah Dalgas NissenDepartment of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Taastrup, Denmark.ORCID https://orcid.org/0000-0001-8598-7147
Mélodie Jil SchneiderDepartment of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Taastrup, Denmark.ORCID https://orcid.org/0000-0001-8739-8223
Jesper Bratz BirkAugust Krogh Section for Human and Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.ORCID https://orcid.org/0000-0001-9775-4789
Helena CarstensenDepartment of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Taastrup, Denmark.ORCID https://orcid.org/0000-0001-8952-9637
Charlotte Hopster-IversenDepartment of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Taastrup, Denmark.ORCID https://orcid.org/0000-0003-3606-2484
Ali AltıntaşNovo Nordisk Foundation Centre for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.ORCID https://orcid.org/0000-0002-8932-0160
Romain BarrèsNovo Nordisk Foundation Centre for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.ORCID https://orcid.org/0000-0002-0158-519X
Rasmus KjøbstedAugust Krogh Section for Human and Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.ORCID https://orcid.org/0000-0002-0628-4994
Jørgen F P WojtaszewskiAugust Krogh Section for Human and Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.ORCID https://orcid.org/0000-0001-8185-3408
Kate M HerumResearch and Early Development, Novo Nordisk A/S, Måløv, Denmark.
Thomas JespersenCardiac Physiology Laboratory, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.ORCID https://orcid.org/0000-0001-6575-360X
Rikke BuhlDepartment of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Taastrup, Denmark.ORCID https://orcid.org/0000-0002-8201-0186

Funding

Danish Cardiovascular Academy NNF20SA0067242Danish Cardiovascular Academy PhD 2022002-HFIndependent Research Fund Denmark 1032-00053B
6 · The paper itself

Abstract

backgroundHigh recurrence rates after atrial fibrillation (AF) treatment may be driven by myocardial changes induced by the arrhythmia itself. Understanding the molecular mechanisms behind these changes is crucial for developing targeted therapies and improving outcomes.

objectivesTo characterise the cardiac transcriptome of healthy horses and explore transcriptional changes associated with persistent AF (naturally occurring and tachypacing-induced). STUDY

designCase-control study.

methodsRNA-sequencing was performed on atrial and ventricular tissue samples collected from six horses with naturally occurring persistent AF (lasting 2-12 weeks) and six healthy controls. Differential gene expression and pathway enrichment analyses were conducted to identify chamber-specific differences and molecular pathways associated with AF. Findings were integrated with proteomic data and compared with transcriptional changes in a separate cohort of 10 horses with tachypacing-induced AF. Atrial metabolic remodelling was further investigated by evaluating the activity of AMP-activated protein kinase (AMPK), a central metabolic regulator and measuring local glycogen content.

resultsThe transcriptomes of the four heart chambers had distinct molecular identities. Expression of ion channels and genes encoding calcium handling proteins was largely similar to humans, despite important differences in the ventricular expression of repolarising potassium channels. Persistent AF was associated with minimal ion channel changes but significant upregulation of metabolic, fibrotic and myofibrillar pathways. Metabolic remodeling included upregulation of fatty acid and glycolytic pathways, increased glycogen content in the left atrium and preserved AMPK activity in the right atrium. Transcriptomic profiles of naturally occurring persistent AF correlated well with those of tachypacing-induced AF. MAIN LIMITATIONS: The study cannot distinguish changes predisposing to AF from those caused by it.

conclusionPersistent AF was associated with changes in metabolic and fibrotic pathways in the atria, with minimal ion channel remodeling. Targeting these pathways, rather than focusing solely on the electrical disturbance, may improve treatment outcomes in equine AF.

Indexed as

Atrial FibrillationHorse DiseasesMyocardiumTranscriptomeAnimalsCase-Control StudiesFemaleGene Expression RegulationHorsesMaleAMP‐activated protein kinaseatrial remodellingequine cardiologyfibrosishorseion channelsRNA‐sequencing

Identifiers

PMID41236081
PMCPMC13447889

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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.