Evidence map›Paper›PMID 34572150›Full record

ReviewCells2021

Are Interactions between Epicardial Adipose Tissue, Cardiac Fibroblasts and Cardiac Myocytes Instrumental in Atrial Fibrosis and Atrial Fibrillation?

Anirudh Krishnan, Emily Chilton, Jaishankar Raman, Pankaj Saxena, Craig McFarlane, Alexandra F Trollope, Robert Kinobe, Lisa Chilton

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.0field-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

41 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  3. Interstitial cells and arrhythmia.American journal of physiology. Cell physiology · 2026
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  16. Immune Regulation in Atrial Cardiomyopathy.Reviews in cardiovascular medicine · 2025
    Review
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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

8 authors at 5 institutions in 3 countries.

Anirudh KrishnanCollege of Medicine and Dentistry, James Cook University, Townsville, QLD 4811, Australia.
Emily ChiltonDepartment of Biomedical Physiology and Kinesiology, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
Jaishankar RamanAustin & St Vincent's Hospitals, Melbourne University, Melbourne, VIC 3010, Australia.
Pankaj SaxenaDepartment of Cardiothoracic Surgery, Townsville University Hospital, Townsville, QLD 4814, Australia.
Craig McFarlaneCentre for Tropical Bioinformatics and Molecular Biology, Australian Institute of Tropical Health and Medicine, College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, QLD 4811, Australia.ORCID 0000-0002-7056-8887
Alexandra F TrollopeCentre for Molecular Therapeutics, Australian Institute of Tropical Health and Medicine, College of Medicine and Dentistry, James Cook University, Townsville, QLD 4811, Australia.
Robert KinobeCentre for Molecular Therapeutics, Australian Institute of Tropical Health and Medicine, College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, QLD 4811, Australia.ORCID 0000-0003-1166-0947
Lisa ChiltonCentre for Molecular Therapeutics, Australian Institute of Tropical Health and Medicine, College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, QLD 4811, Australia.
Australian Institute of Tropical Health and Medicine · AUDeakin University · AUJames Cook University · AUSimon Fraser University · CATownsville Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrillation is very common among the elderly and/or obese. While myocardial fibrosis is associated with atrial fibrillation, the exact mechanisms within atrial myocytes and surrounding non-myocytes are not fully understood. This review considers the potential roles of myocardial fibroblasts and myofibroblasts in fibrosis and modulating myocyte electrophysiology through electrotonic interactions. Coupling with (myo)fibroblasts in vitro and in silico prolonged myocyte action potential duration and caused resting depolarization; an optogenetic study has verified in vivo that fibroblasts depolarized when coupled myocytes produced action potentials. This review also introduces another non-myocyte which may modulate both myocardial (myo)fibroblasts and myocytes: epicardial adipose tissue. Epicardial adipocytes are in intimate contact with myocytes and (myo)fibroblasts and may infiltrate the myocardium. Adipocytes secrete numerous adipokines which modulate (myo)fibroblast and myocyte physiology. These adipokines are protective in healthy hearts, preventing inflammation and fibrosis. However, adipokines secreted from adipocytes may switch to pro-inflammatory and pro-fibrotic, associated with reactive oxygen species generation. Pro-fibrotic adipokines stimulate myofibroblast differentiation, causing pronounced fibrosis in the epicardial adipose tissue and the myocardium. Adipose tissue also influences myocyte electrophysiology, via the adipokines and/or through electrotonic interactions. Deeper understanding of the interactions between myocytes and non-myocytes is important to understand and manage atrial fibrillation.

Indexed as

Action PotentialsAdipocytesAdipokinesAdipose TissueAtrial FibrillationCardiomyopathiesElectrophysiological PhenomenaEndomyocardial FibrosisEpicardial MappingFibroblastsFibrosisHeartHeart AtriaHumansMyocardiumMyocytes, CardiacAdipokinesadipokinecurrent sinkelectrotonic couplingmyofibroblast

Identifiers

PMID34572150
PMCPMC8467050
OpenAlexW3200958559

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.