Evidence map›Paper›PMID 26714926›Full record

ArticleCardiovascular research2016

Pitx2c increases in atrial myocytes from chronic atrial fibrillation patients enhancing IKs and decreasing ICa,L.

Marta Pérez-Hernández, Marcos Matamoros, Adriana Barana, Irene Amorós, Ricardo Gómez, Mercedes Núñez, Sandra Sacristán, Ángel Pinto, Francisco Fernández-Avilés, Juan Tamargo and 2 more

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Cardiovascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.2field-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

44 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Single-Nucleotide Polymorphisms,International journal of molecular sciences · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Modulation of NOX2 causes obesity-mediated atrial fibrillation.The Journal of clinical investigation · 2024
    Article
  11. Human induced pluripotent stem cell-derived atrial cardiomyocytes recapitulate contribution of the slowly activating delayed rectifier currents IKs to repolarization in the human atrium.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 · 2024
    Article
  12. Review
  13. Non-coding RNA and arrhythmias: expression, function, and molecular mechanism.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 · 2023
    Review
  14. New Insights into Cardiac Ion Channel Regulation 2.0.International journal of molecular sciences · 2023
    Article
  15. Article
  16. Article
  17. Review
  18. 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
  19. Article
  20. Zfhx3 Transcription Factor Represses the Expression ofInternational journal of molecular sciences · 2021
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Marta Pérez-HernándezDepartment of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
Marcos MatamorosDepartment of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
Adriana BaranaDepartment of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
Irene AmorósDepartment of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
Ricardo GómezDepartment of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
Mercedes NúñezDepartment of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
Sandra SacristánDepartment of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
Ángel PintoInstituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain Cardiology and Cardiovascular Surgery Services, Hospital General Universitario Gregorio Marañón, Madrid 28007, Spain.
Francisco Fernández-AvilésInstituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain Cardiology and Cardiovascular Surgery Services, Hospital General Universitario Gregorio Marañón, Madrid 28007, Spain.
Juan TamargoDepartment of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
Eva DelpónDepartment of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain edelpon@med.ucm.es.
Ricardo CaballeroDepartment of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid 28040, Spain Instituto de Investigación Sanitaria Gregorio Marañón, School of Medicine, Universidad Complutense, Madrid 28040, Spain.
Hospital General Universitario Gregorio Marañón · ESUniversidad Complutense de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsAtrial fibrillation (AF) produces rapid changes in the electrical properties of the atria (electrical remodelling) that promote its own recurrence. In chronic AF (CAF) patients, up-regulation of the slow delayed rectifier K(+) current (IKs) and down-regulation of the voltage-gated Ca(2+) current (ICa,L) are hallmarks of electrical remodelling and critically contribute to the abbreviation of action potential duration and atrial refractory period. Recent evidences suggested that Pitx2c, a bicoid-related homeodomain transcription factor involved in directing cardiac asymmetric morphogenesis, could play a role in atrial remodelling. However, its effects on IKs and ICa,L are unknown. METHODS AND

resultsReal-time quantitative polymerase chain reaction analysis showed that Pitx2c mRNA expression was significantly higher in human atrial myocytes from CAF patients than those from sinus rhythm patients. The expression of Pitx2c was positively and negatively correlated with IKs and ICa,L densities, respectively. Expression of Pitx2c in HL-1 cells increased IKs density and reduced ICa,L density. Luciferase assays demonstrated that Pitx2c increased transcriptional activity of KCNQ1 and KCNE1 genes. Conversely, its effects on ICa,L could be mediated by the atrial natriuretic peptide.

conclusionOur results demonstrated for the first time that CAF increases Pitx2c expression in isolated human atrial myocytes and suggested that this transcription factor could contribute to the CAF-induced IKs increase and ICa,L reduction observed in humans.

Indexed as

Action PotentialsAnimalsAtrial FibrillationCalciumDown-RegulationHeart AtriaHomeobox Protein PITX2Homeodomain ProteinsHumansMiceMyocytes, CardiacPatch-Clamp TechniquesPotassiumTranscription FactorsUp-RegulationCalciumHomeobox Protein PITX2Homeodomain ProteinsPotassiumTranscription FactorsChronic atrial fibrillationHuman atrial myocytesICa,LIKsPitx2c

Identifiers

PMID26714926
OpenAlexW2199847870

What OpenQuestion 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 OpenQuestion graph.