Evidence map›Paper›PMID 33440248›Full record

ReviewHeart rhythm2021

Epigenetics in atrial fibrillation: A reappraisal.

Rosa Doñate Puertas, Rishi Arora, Sophie Rome, Babken Asatryan, H Llewelyn Roderick, Philippe Chevalier

Open access · greenAbstract readReview
In one paragraph

Review in Heart rhythm, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

12 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Targeted intervention in obesity-associated atrial fibrosis using nanoparticle-loaded fusion protein.Apoptosis : an international journal on programmed cell death · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Nucleoplasmic CaCirculation research · 2021
    Article
  12. 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

6 authors at 5 institutions in 5 countries.

Rosa Doñate PuertasLaboratory of Experimental Cardiology, Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium. Electronic address: rosa.donatepuertas@kuleuven.be.
Rishi AroraFeinberg Cardiovascular and Renal Research Institute, Northwestern University-Feinberg School of Medicine, Chicago, Illinois.
Sophie RomeCarMeN Laboratory (UMR INSERM 1060-INRA 1397, INSA), Lyon-Sud Faculty of Medicine, University of Lyon, Pierre-Bénite, France.
Babken AsatryanDepartment of Cardiology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
H Llewelyn RoderickLaboratory of Experimental Cardiology, Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium; K.G. Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.
Philippe ChevalierRhythmology Unit, Hospices Civils de Lyon, University of Lyon, Lyon, France. Electronic address: philippe.chevalier@chu-lyon.fr.
Université Claude Bernard Lyon 1 · FRKU Leuven · BENorthwestern University · USUniversity of Bern · CHUniversity of Oslo · NO

Funding

The identification and pathophysiology of non-infarcted but injured myocardium in the post-ischemic heartR01HL152712 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ARORA, RISHI, ZHAO, MING · 2021 to 2024
$3.0M
Pathophysiological Significance of Atrial Fibrillation Electrogram PatternsR01HL125881 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ARORA, RISHI · 2015 to 2019
$2.4M
Oxidative stress contributes to atrial fibrillation by causing remodeling of the autonomic nervous systemR01HL140061 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ARORA, RISHI · 2018 to 2021
$2.3M
NHLBI NIH HHS R01 HL125881NHLBI NIH HHS R01 HL140061NHLBI NIH HHS R01 HL152712
6 · The paper itself

Abstract

Atrial fibrillation (AF) is the most common cardiac arrhythmia and an important cause of morbidity and mortality globally. Atrial remodeling includes changes in ion channel expression and function, structural alterations, and neural remodeling, which create an arrhythmogenic milieu resulting in AF initiation and maintenance. Current therapeutic strategies for AF involving ablation and antiarrhythmic drugs are associated with relatively high recurrence and proarrhythmic side effects, respectively. Over the last 2 decades, in an effort to overcome these issues, research has sought to identify the genetic basis for AF thereby gaining insight into the regulatory mechanisms governing its pathophysiology. Despite identification of multiple gene loci associated with AF, thus far none has led to a therapy, indicating additional contributors to pathology. Recently, in the context of expanding knowledge of the epigenome (DNA methylation, histone modifications, and noncoding RNAs), its potential involvement in the onset and progression of AF pathophysiology has started to emerge. Probing the role of various epigenetic mechanisms that contribute to AF may improve our knowledge of this complex disease, identify potential therapeutic targets, and facilitate targeted therapies. Here, we provide a comprehensive review of growing epigenetic features involved in AF pathogenesis and summarize the emerging epigenomic targets for therapy that have been explored in preclinical models of AF.

Indexed as

Atrial FibrillationAtrial RemodelingEpigenomicsHeart AtriaHumansAtrial fibrillationEpidrugEpigeneticPersonalized therapySystems biology

Identifiers

PMID33440248
PMCPMC9414202
OpenAlexW3120755824

What OpenQuestion holds

Textmetadata
LicenceTDM
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.