Evidence map›Paper›PMID 22447020›Full record

ArticleCirculation journal : official journal of the Japanese Circulation Society2012

Triggered firing and atrial fibrillation in transgenic mice with selective atrial fibrosis induced by overexpression of TGF-β1.

Eue-Keun Choi, Po-Cheng Chang, Young-Soo Lee, Shien-Fong Lin, Wuqiang Zhu, Mitsunori Maruyama, Michael C Fishbein, Zhenhui Chen, Michael Rubart-von der Lohe, Loren J Field and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Circulation journal : official journal of the Japanese Circulation Society, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Transcriptional factors in calcium mishandling and atrial fibrillation development.Pflugers Archiv : European journal of physiology · 2021
    Review
  16. LncRNA TUG1 Regulates Proliferation of Cardiac FibroblastFrontiers in cardiovascular medicine · 2021
    Article
  17. hsa-miR-4443 inhibits myocardial fibroblast proliferation by targeting THBS1 to regulate TGF-β1/α-SMA/collagen signaling in atrial fibrillation.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
    Article
  18. AGE-RAGE Stress in the Pathophysiology of Atrial Fibrillation and Its Treatment.The International journal of angiology : official publication of the International College of Angiology, Inc · 2020
    Article
  19. Doxycycline Improves Fibrosis-Induced Abnormalities in Atrial Conduction and Vulnerability to Atrial Fibrillation in Chronic Intermittent Hypoxia Rats.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  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

11 authors at 3 institutions in 1 country.

Eue-Keun ChoiKrannert Institute of Cardiology and the Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.
Po-Cheng Chang
Young-Soo Lee
Shien-Fong Lin
Wuqiang Zhu
Mitsunori Maruyama
Michael C Fishbein
Zhenhui Chen
Michael Rubart-von der Lohe
Loren J Field
Peng-Sheng Chen
Indiana University · USIndiana University School of MedicineUniversity of California, Los Angeles · US

Funding

WAVE DYNAMICS IN NORMAL AND DISEASED RABBIT HEARTSP01HL078931 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WEISS, JAMES · 2005 to 2015
$20.7M
REGULATION OF CARDIOMYOCYTE SURVIVALP01HL085098 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FIELD, LOREN J · 2007 to 2011
$10.9M
Thoracic Veins and Sustained Atrial FibrillationR01HL071140 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI CHEN, PENG-SHENG · 2002 to 2014
$4.7M
Genetic Enhancement of Cardiac Repair with Adult Stem CellsR01HL083126 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FIELD, LOREN J · 2006 to 2015
$2.9M
Fibrillation and DefibrillationR01HL078932 · NHLBI · TRUSTEES OF INDIANA UNIVERSITY · PI CHEN, PENG-SHENG · 2005 to 2010
$2.3M
Functional assessment of donor-host cell couplingR01HL075165 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI RUBART-VAN DER LOHE, MICHAEL · 2005 to 2009
$2.1M
Cell cycle activation for cardiac repairR01HL109205 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI FIELD, LOREN J · 2011 to 2015
$1.9M
Transgenic Reporters for Cardiac Growth and RegenerationR21HL091189 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI FIELD, LOREN J · 2009 to 2010
$424k
NHLBI NIH HHS P01 HL078931NHLBI NIH HHS P01 HL085098NHLBI NIH HHS P01 HL78931NHLBI NIH HHS P01 HL85098NHLBI NIH HHS R01 HL071140NHLBI NIH HHS R01 HL075165NHLBI NIH HHS R01 HL078932NHLBI NIH HHS R01 HL083126NHLBI NIH HHS R01 HL109205NHLBI NIH HHS R01 HL71140NHLBI NIH HHS R01 HL75165NHLBI NIH HHS R01 HL78932NHLBI NIH HHS R01 HL83126NHLBI NIH HHS R21 HL091189
6 · The paper itself

Abstract

backgroundCalcium transient triggered firing (CTTF) is induced by large intracellular calcium (Ca(i)) transient and short action potential duration (APD). We hypothesized that CTTF underlies the mechanisms of early afterdepolarization (EAD) and spontaneous recurrent atrial fibrillation (AF) in transgenic (Tx) mice with overexpression of transforming growth factor β1 (TGF-β1). METHODS AND

resultsMHC-TGFcys(33)ser Tx mice develop atrial fibrosis because of elevated levels of TGF-β1. We studied membrane potential and Ca(i)transients of isolated superfused atria from Tx and wild-type (Wt) littermates. Short APD and persistently elevated Ca(i) transients promoted spontaneous repetitive EADs, triggered activity and spontaneous AF after cessation of burst pacing in Tx but not Wt atria (39% vs. 0%, P=0.008). We were able to map optically 4 episodes of spontaneous AF re-initiation. All first and second beats of spontaneous AF originated from the right atrium (4/4, 100%), which is more severely fibrotic than the left atrium. Ryanodine and thapsigargin inhibited spontaneous re-initiation of AF in all 7 Tx atria tested. Western blotting showed no significant changes of calsequestrin or sarco/endoplasmic reticulum Ca(2+)-ATPase 2a.

conclusionsSpontaneous AF may occur in the Tx atrium because of CTTF, characterized by APD shortening, prolonged Ca(i) transient, EAD and triggered activity. Inhibition of Ca(2+) release from the sarcoplasmic reticulum suppressed spontaneous AF. Our results indicate that CTTF is an important arrhythmogenic mechanism in TGF-β1 Tx atria.

Indexed as

Atrial FunctionCalcium SignalingAction PotentialsAnimalsAtrial FibrillationBlotting, WesternCardiac Pacing, ArtificialDisease Models, AnimalElectrophysiologic Techniques, CardiacEnzyme InhibitorsFibrosisHeart AtriaHeart Conduction SystemMiceMice, TransgenicRyanodineAtp2a2 protein, mouseEnzyme InhibitorsRyanodineSarcoplasmic Reticulum Calcium-Transporting ATPasesThapsigarginTransforming Growth Factor beta1

Identifiers

PMID22447020
PMCPMC3593311
OpenAlexW2016274258

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.