Evidence map›Paper›PMID 37713664›Full record

ArticleCardiovascular research2023

Cardiomyocyte and endothelial cells play distinct roles in the tumour necrosis factor (TNF)-dependent atrial responses and increased atrial fibrillation vulnerability induced by endurance exercise training in mice.

Robert Lakin, Nazari Polidovitch, Sibao Yang, Mihir Parikh, Xueyan Liu, Ryan Debi, Xiaodong Gao, Wenliang Chen, Camilo Guzman, Simona Yakobov and 7 more

Open access · greenAbstract read
In one paragraph

Article in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. [Integrating Bioinformatics and Machine Learning Algorithms to Screen Inflammatory Biomarkers for Atrial Fibrillation and Experimental Validation].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
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  7. From moderate to strenuous training: unravelling mechanistic contributors and biomarkers for atrial fibrillation in exercise.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025
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  9. Targeted intervention in obesity-associated atrial fibrosis using nanoparticle-loaded fusion protein.Apoptosis : an international journal on programmed cell death · 2025
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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

17 authors at 6 institutions in 4 countries.

Robert LakinDepartment of Biology, York University, 354 & 357 Farquharson Building, 4700 Keele Street, Toronto, ON M3J 1P3, Canada.ORCID 0000-0003-2169-0488
Nazari PolidovitchDepartment of Biology, York University, 354 & 357 Farquharson Building, 4700 Keele Street, Toronto, ON M3J 1P3, Canada.
Sibao YangDepartment of Biology, York University, 354 & 357 Farquharson Building, 4700 Keele Street, Toronto, ON M3J 1P3, Canada.
Mihir ParikhDepartment of Biology, York University, 354 & 357 Farquharson Building, 4700 Keele Street, Toronto, ON M3J 1P3, Canada.
Xueyan LiuDepartment of Biology, York University, 354 & 357 Farquharson Building, 4700 Keele Street, Toronto, ON M3J 1P3, Canada.
Ryan DebiDepartment of Biology, York University, 354 & 357 Farquharson Building, 4700 Keele Street, Toronto, ON M3J 1P3, Canada.
Xiaodong GaoDepartment of Biology, York University, 354 & 357 Farquharson Building, 4700 Keele Street, Toronto, ON M3J 1P3, Canada.
Wenliang ChenDepartment of Biology, York University, 354 & 357 Farquharson Building, 4700 Keele Street, Toronto, ON M3J 1P3, Canada.
Camilo GuzmanDepartment of Biology, York University, 354 & 357 Farquharson Building, 4700 Keele Street, Toronto, ON M3J 1P3, Canada.
Simona YakobovDepartment of Biology, York University, 354 & 357 Farquharson Building, 4700 Keele Street, Toronto, ON M3J 1P3, Canada.
Farzad IzaddoustdarDepartment of Physiology, University of Toronto, Toronto, ON M5S 3E2, Canada.
Marianne WauchopDepartment of Physiology, University of Toronto, Toronto, ON M5S 3E2, Canada.
Qian LeiDepartment of Anesthesiology, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, China.
Weimin XuDepartment of Cardiology, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130022, China.
Sergei A NedospasovLaboratory of Molecular Mechanisms of Immunity, Engelhardt Institute of Molecular Biology, Moscow 119991, Russia.
Vincent M ChristoffelsDepartment of Medical Biology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Amsterdam, The Netherlands.
Peter H BackxDepartment of Biology, York University, 354 & 357 Farquharson Building, 4700 Keele Street, Toronto, ON M3J 1P3, Canada.ORCID 0000-0003-0497-776X
York University · CAUniversity of Toronto · CAAmsterdam University Medical Centers · NLEngelhardt Institute of Molecular Biology · RUJilin University · CNUniversity of Electronic Science and Technology of China · CN

Funding

CIHR MOP-83453
6 · The paper itself

Abstract

aimsEndurance exercise is associated with an increased risk of atrial fibrillation (AF). We previously established that adverse atrial remodelling and AF susceptibility induced by intense exercise in mice require the mechanosensitive and pro-inflammatory cytokine tumour necrosis factor (TNF). The cellular and mechanistic basis for these TNF-mediated effects is unknown. METHODS AND

resultsWe studied the impact of Tnf excision, in either atrial cardiomyocytes or endothelial cells (using Cre-recombinase expression controlled by Nppa or Tie2 promoters, respectively), on the cardiac responses to six weeks of intense swim exercise training. TNF ablation, in either cell type, had no impact on the changes in heart rate, autonomic tone, or left ventricular structure and function induced by exercise training. Tnf excision in atrial cardiomyocytes did, however, prevent atrial hypertrophy, fibrosis, and macrophage infiltration as well as conduction slowing and increased AF susceptibility arising from exercise training. In contrast, endothelial-specific excision only reduced the training-induced atrial hypertrophy. Consistent with these cell-specific effects of Tnf excision, inducing TNF loss from atrial cardiomyocytes prevented activation of p38MAPKinase, a strain-dependent downstream mediator of TNF signalling, without affecting the atrial stretch as assessed by atrial pressures induced by exercise. Despite TNF's established role in innate immune responses and inflammation, neither acute nor chronic exercise training caused measurable NLRP3 inflammasome activation.

conclusionsOur findings demonstrate that adverse atrial remodelling and AF vulnerability induced by intense exercise require TNF in atrial cardiomyocytes whereas the impact of endothelial-derived TNF is limited to hypertrophy modulation. The implications of the cell autonomous effects of TNF and crosstalk between cells in the atria are discussed.

Indexed as

Atrial FibrillationAtrial RemodelingCardiomyopathiesAnimalsEndothelial CellsHeart AtriaHypertrophyMiceMyocytes, CardiacTumor Necrosis Factor-alphaTumor Necrosis Factor-alphaAtrial fibrillationExerciseHeartInflammationTumour necrosis factor

Identifiers

PMID37713664
PMCPMC10730243
OpenAlexW4386793927

What Socratic holds

Textmetadata
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 Socratic graph.