Evidence map›Paper›PMID 23612580›Full record

ArticleCardiovascular research2013

Molecular basis of selective atrial fibrosis due to overexpression of transforming growth factor-β1.

Dolkun Rahmutula, Gregory M Marcus, Emily E Wilson, Chun-Hua Ding, Yuanyuan Xiao, Agnes C Paquet, Rebecca Barbeau, Andrea J Barczak, David J Erle, Jeffrey E Olgin

2 registry-linked trialsOpen access · hybridAbstract read
In one paragraph

Article in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 61 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 2 pooled it
6.7field-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.

NCT04404465 enrolling by invitationnot on this mapstarted 2020, after this paper: background citation

Health eHeart BEAT-AFib - Health eHeart Biomarkers of Early Atrial Transformation in Atrial Fibrillation

TypeobservationalSponsorUniversity of California, San FranciscoRan2020 to 2040Enrolled3,000ConditionsAtrial Fibrillation
NCT06976502 enrolling by invitationnot on this mapstarted 2025, after this paper: background citation

Health eHeart BioBank

Typeobservational_patient_registrySponsorUniversity of California, San FranciscoRan2025 to 2035Enrolled500,000ConditionsHeart Diseases, Cardiac Diseases, Vascular Diseases, Cardiovascular DiseasesArmsBlood Draw, Tissue Collection, DNA Collection, Medical Chart Review
3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 2 syntheses or guidelines pooled it, 96 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Sphingomyelin as a key negative mediator in atrial fibrillation via lipid profiling analysis and functional identification.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
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  11. Gene therapy for atrial fibrillation.Journal of molecular and cellular cardiology · 2024
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Sphingolipids: drivers of cardiac fibrosis and atrial fibrillation.Journal of molecular medicine (Berlin, Germany) · 2024
    Review
  17. Atrial fibrillation in human patients is associated with increased collagen type V and TGFbeta1.International journal of cardiology. Heart & vasculature · 2024
    Article
  18. Review
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Dolkun RahmutulaDivision of Cardiology, University of California, San Francisco, CA 94143, USA.
Gregory M Marcus
Emily E Wilson
Chun-Hua Ding
Yuanyuan Xiao
Agnes C Paquet
Rebecca Barbeau
Andrea J Barczak
David J Erle
Jeffrey E Olgin
University of California, San Francisco · USUniversity of California System · USGuangdong Provincial Hospital of Traditional Chinese Medicine · CN

Funding

UCSF CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTEUL1RR024131 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JOHNSTON, S. CLAIBORNE · 2006 to 2011
$111.2M
CTSA: K12 COMPONENTKL2RR024130 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JOHNSTON, S. CLAIBORNE · 2006 to 2011
$19.3M
Electrophysiology of the pulmonary vein myocardium in AFR01HL072854 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI OLGIN, JEFFREY E · 2003 to 2006
$1.5M
UCSF Living Heart ResourceRC1HL099789 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BAKER, ANTHONY J., EVERETT, THOMAS H · 2009 to 2010
$1000k
NCRR NIH HHS KL2 RR024130NCRR NIH HHS UL1 RR024131NHLBI NIH HHS R01-HL072854NHLBI NIH HHS RC1-HL099789
6 · The paper itself

Abstract

aimsAnimal studies show that transforming growth factor-β1 (TGF-β1) is an important mediator of atrial fibrosis and atrial fibrillation (AF). This study investigated the role of TGF-β1 in human AF and the mechanism of atrial-selective fibrosis. METHODS AND

resultsAtrial specimens from 17 open heart surgery patients and left atrial and ventricular specimens from 17 explanted hearts were collected to assess the relationship between TGF-β1, AF, and differential atrial vs. ventricular TGF-β1 levels. A transgenic mouse model overexpressing active TGF-β1 was used to study the mechanisms underlying the resultant atrial-selective fibrosis. Higher right atrial total TGF-β1 levels (2.58 ± 0.16-fold, P < 0.0001) and active TGF-β1 (3.7 ± 0.7-fold, P = 0.013) were observed in those that developed post-operative AF. Although no ventricular differences were observed, 11 explanted heart failure hearts exhibited higher atrial TGF-β1 levels than 6 non-failing hearts (2.30 ± 0.87 fold higher, P < 0.001). In the transgenic mouse, TGF-β1 receptor-1 kinase blockade resulted in decreased atrial expression of fibrosis-related genes. By RNA microarray analyses in that model, 80 genes in the atria and only 2 genes in the ventricle were differentially expressed. Although these mice atria, but not the ventricles, exhibited increased expression of fibrosis-related genes and phosphorylation of Smad2, there were no differences in TGF-β1 receptor levels or Smads in the atria compared with the ventricles.

conclusionsTGF-β1 mediates selective atrial fibrosis in AF that occurs via TGF-β Receptor 1/2 and the classical Smad pathway. The differential atrial vs. ventricular fibrotic response occurs at the level of TGF-β1 receptor binding or phosphorylation.

Indexed as

AnimalsAtrial FibrillationFibrosisHeart AtriaHumansMiceMice, TransgenicMinkReceptors, Transforming Growth Factor betaTransforming Growth Factor beta1Receptors, Transforming Growth Factor betaTransforming Growth Factor beta1Atrial fibrillationCardiac fibrosisGene expressionHeart failureTransforming growth factor-beta1

Identifiers

PMID23612580
PMCPMC3746950
OpenAlexW1983904548

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.