Evidence map›Paper›PMID 40877415›Full record

ArticleScientific reports2025

Horse model of spontaneous atrial fibrillation share proteomic changes with humans.

Sarah Dalgas Nissen, Joakim Armstrong Bastrup, Simon Libak Haugaard, Rikke Marion-Knudsen, Mélodie Schneider, Sofie Troest Kjeldsen, Helena Carstensen, Charlotte Hopster-Iversen, Stanley Nattel, Thomas Andrew Jepps and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

11 authors.

Sarah Dalgas Nissen *Department of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Agrovej 8, Taastrup, 2630, Denmark. Sarahnissen@sund.ku.dk.ORCID http://orcid.org/0000-0001-8598-7147
Joakim Armstrong Bastrup *Physiology of Circulation, Kidney and Lung, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Simon Libak Haugaard *Department of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Agrovej 8, Taastrup, 2630, Denmark.
Rikke Marion-KnudsenCardiac Physiology Laboratory, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Mélodie SchneiderDepartment of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Agrovej 8, Taastrup, 2630, Denmark.
Sofie Troest KjeldsenDepartment of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Agrovej 8, Taastrup, 2630, Denmark.
Helena CarstensenDepartment of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Agrovej 8, Taastrup, 2630, Denmark.
Charlotte Hopster-IversenDepartment of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Agrovej 8, Taastrup, 2630, Denmark.
Stanley NattelDepartment of Medicine, Institut de Cardiologie de Montréal and Université de Montréal, Montreal, Canada.
Thomas Andrew JeppsPhysiology of Circulation, Kidney and Lung, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Rikke BuhlDepartment of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Agrovej 8, Taastrup, 2630, Denmark.

Funding

Danish Independent Research Foundation 1032-00053BLundbeck Foundation R400-2022-1213Novo Nordisk Fonden NNF20SA0067242Novo Nordisk Fonden PhD 2022002-HF
6 · The paper itself

Abstract

Horses and humans are among the few mammals susceptible to spontaneous atrial fibrillation (AF), both suffering from high recurrence rates after treatment. Treatment resistance is often attributed to progressive atrial remodeling, but current treatment options fail to effectively address this aspect. Here, we introduce a novel horse model of spontaneous AF to investigate the biological pathway changes in early stages of the disease. Through data-independent acquisition mass spectrometry on biopsies from the right and left atrium and left ventricular chamber of horses with early-stage persistent AF (n = 8) and controls (n = 8), we identify several differentially regulated proteins across all three chambers. Pathway enrichment analyses and histological stainings highlight a significant role of atrial extracellular matrix (ECM) remodeling in early AF. Other key proteomic changes relate to metabolism, contractility, and protein-folding, and overlap with findings from publicly available human datasets. Our results demonstrate that horses and humans share several AF-related proteomic changes, providing translational insights into the early atrial remodeling processes that are likely to contribute to treatment resistance. These protein-level changes could serve as biomarkers or pharmacological targets for preventing AF-associated atrial remodeling and improve treatment outcomes across species.

Indexed as

Atrial FibrillationProteomeProteomicsAnimalsAtrial RemodelingBiomarkersDisease Models, AnimalExtracellular MatrixFemaleHeart AtriaHorsesHumansMaleBiomarkersProteomeAtrial fibrillationAtrial remodelingExtracellular matrixGlycoproteinsHorsesProteomics

Identifiers

PMID40877415
PMCPMC12394609

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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.