Evidence map›Paper›PMID 30353147›Full record

ArticleScientific reports2018

Ionic and cellular mechanisms underlying TBX5/PITX2 insufficiency-induced atrial fibrillation: Insights from mathematical models of human atrial cells.

Jieyun Bai, Patrick A Gladding, Martin K Stiles, Vadim V Fedorov, Jichao Zhao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Modulation of NOX2 causes obesity-mediated atrial fibrillation.The Journal of clinical investigation · 2024
    Article
  4. Review
  5. Review
  6. Identification of atrial-enriched lncRNA Walras linked to cardiomyocyte cytoarchitecture and atrial fibrillation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  7. Review
  8. Transcriptional factors in calcium mishandling and atrial fibrillation development.Pflugers Archiv : European journal of physiology · 2021
    Review
  9. Review
  10. In Silico Assessment of Class I Antiarrhythmic Drug Effects onInternational journal of molecular sciences · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Differential Modulation ofFrontiers in physiology · 2019
    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

5 authors at 4 institutions in 3 countries.

Jieyun BaiAuckland Bioengineering Institute, The University of Auckland, Auckland, New Zealand. jieyun.bai@auckland.ac.nz.ORCID http://orcid.org/0000-0002-2847-350X
Patrick A GladdingDepartment of Cardiology, Waitemata District Health Board, Auckland, New Zealand.
Martin K StilesWaikato Hospital, Hamilton, New Zealand.
Vadim V FedorovDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, United States of America.
Jichao ZhaoAuckland Bioengineering Institute, The University of Auckland, Auckland, New Zealand. j.zhao@auckland.ac.nz.
Auckland Institute of Studies · NZThe Ohio State University Wexner Medical Center · USWaikato Hospital · NZWaitemata District Health Board · NZ

Funding

Targeting the Arrhythmogenic Sources of Human Atrial FibrillationR01HL135109 · NHLBI · OHIO STATE UNIVERSITY · PI Vadim V Fedorov · 2017 to 2026
$6.0M
Integration of structure and signaling in cardiac pacemaker functionR01HL115580 · NHLBI · OHIO STATE UNIVERSITY · PI FEDOROV, VADIM V · 2013 to 2021
$4.2M
NHLBI NIH HHS R01 HL115580NHLBI NIH HHS R01 HL135109
6 · The paper itself

Abstract

Transcription factors TBX5 and PITX2 involve in the regulation of gene expression of ion channels and are closely associated with atrial fibrillation (AF), the most common cardiac arrhythmia in developed countries. The exact cellular and molecular mechanisms underlying the increased susceptibility to AF in patients with TBX5/PITX2 insufficiency remain unclear. In this study, we have developed and validated a novel human left atrial cellular model (TPA) based on the ten Tusscher-Panfilov ventricular cell model to systematically investigate how electrical remodeling induced by TBX5/PITX2 insufficiency leads to AF. Using our TPA model, we have demonstrated that spontaneous diastolic depolarization observed in atrial myocytes with TBX5-deletion can be explained by altered intracellular calcium handling and suppression of inward-rectifier potassium current (I

Indexed as

Models, CardiovascularAction PotentialsAnimalsAtrial FibrillationCalciumHeart AtriaHomeobox Protein PITX2Homeodomain ProteinsHumansIon ChannelsIonsMiceMyocytes, CardiacPhenotypeT-Box Domain ProteinsTranscription FactorsCalciumHomeobox Protein PITX2Homeodomain ProteinsIon ChannelsIonsT-Box Domain ProteinsT-box transcription factor 5Transcription Factors

Identifiers

PMID30353147
PMCPMC6199257
OpenAlexW2895885670

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.