Evidence map›Paper›PMID 35492601›Full record

ReviewFrontiers in physiology2022

Role of Inflammation in the Pathogenesis of Atrial Fibrillation.

Kensuke Ihara, Tetsuo Sasano

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 6 pooled it
16.3field-weighted citation impact, top 1% 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

82 citing papers in PubMed, 6 syntheses or guidelines pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Beyond the beats: a systematic review of the underlying inflammatory pathways between atrial fibrillation and cognitive decline.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Trial
  8. Article
  9. Prediabetes and the risk of atrial fibrillation and heart failure: a propensity-matched analysis in a real-world cohort.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Review
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  16. Osteopontin in Atrial Fibrillation and Atrial Remodeling.Journal of the American Heart Association · 2026
    Review
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  18. Article
  19. Impact of anemia prior to catheter ablation for atrial fibrillation on clinical outcomes: a U.S. retrospective cohort analysis.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2026
    Article
  20. Article

22 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Kensuke IharaDepartment of Bio-informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Tetsuo SasanoDepartment of Cardiovascular Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
The University of Tokyo · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrillation (AF) is one of the most common arrhythmias encountered in clinical practice. AF is a major risk factor for stroke, which is associated with high mortality and great disability and causes a significant burden on society. With the development of catheter ablation, AF has become a treatable disease, but its therapeutic outcome has been limited so far. In persistent and long-standing AF, the expanded AF substrate is difficult to treat only by ablation, and a better understanding of the mechanism of AF substrate formation will lead to the development of a new therapeutic strategy for AF. Inflammation is known to play an important role in the substrate formation of AF. Inflammation causes and accelerates the electrical and structural remodeling of the atria via pro-inflammatory cytokines and other inflammatory molecules, and enhances the AF substrate, leading to the maintenance of AF and further inflammation, which forms a vicious spiral, so-called "AF begets AF". Breaking this vicious cycle is expected to be a key therapeutic intervention in AF. In this review, we will discuss the relationship between AF and inflammation, the inflammatory molecules included in the AF-related inflammatory process, and finally the potential of those molecules as a therapeutic target.

Indexed as

arrhythmogenic substrateatrial fibrillationcytokinefibrosisinflammation

Identifiers

PMID35492601
PMCPMC9047861
OpenAlexW4224058616

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.