Evidence map›Paper›PMID 39443702›Full record

ReviewNature reviews. Cardiology2025

Translation of pathophysiological mechanisms of atrial fibrosis into new diagnostic and therapeutic approaches.

Ulrich Schotten, Andreas Goette, Sander Verheule

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
–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

31 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Prevalence and severity of atrial cardiomyopathy in patients with recently diagnosed atrial fibrillation and stroke risk factors and its association with early rhythm control: a secondary analysis of EAST-AFNET 4.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
    Trial
  3. Understanding the Diseased Atria.Physiology (Bethesda, Md.) · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Histological evaluation of clinically defined atrial cardiomyopathy stages and their association with atrial fibrillation burden under continuous monitoring for a 2.5-year follow-up.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 · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Differential effects of semaglutide and colchicine on atrial remodeling in rats with reduced ejection fraction after myocardial infarction.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 · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Clinical and prognostic impact of left atrial strain in non-ischemic cardiomyopathies.The international journal of cardiovascular imaging · 2026
    Review
  19. Review
  20. Article
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

3 authors.

Ulrich SchottenDepartment of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands. Schotten@maastrichtuniversity.nl.ORCID 0000-0003-1532-3315
Andreas GoetteDepartment of Cardiology and Intensive Care Medicine, St. Vincenz Hospital, Paderborn, Germany.
Sander VerheuleDepartment of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrosis is one of the main manifestations of atrial cardiomyopathy, an array of electrical, mechanical and structural alterations associated with atrial fibrillation (AF), stroke and heart failure. Atrial fibrosis can be both a cause and a consequence of AF and, once present, it accelerates the progression of AF. The pathophysiological mechanisms leading to atrial fibrosis are diverse and include stretch-induced activation of fibroblasts, systemic inflammatory processes, activation of coagulation factors and fibrofatty infiltrations. Importantly, atrial fibrosis can occur in different forms, such as reactive and replacement fibrosis. The diversity of atrial fibrosis mechanisms and patterns depends on sex, age and comorbidity profile, hampering the development of therapeutic strategies. In addition, the presence and severity of comorbidities often change over time, potentially causing temporal changes in the mechanisms underlying atrial fibrosis development. This Review summarizes the latest knowledge on the molecular and cellular mechanisms of atrial fibrosis, its association with comorbidities and the sex-related differences. We describe how the various patterns of atrial fibrosis translate into electrophysiological mechanisms that promote AF, and critically appraise the clinical applicability and limitations of diagnostic tools to quantify atrial fibrosis. Finally, we provide an overview of the newest therapeutic interventions under development and discuss relevant knowledge gaps related to the association between clinical manifestations and pathological mechanisms of atrial fibrosis and to the translation of this knowledge to a clinical setting.

Indexed as

Atrial FibrillationAtrial RemodelingHeart AtriaAnimalsFibrosisHumans

Identifiers

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.