Evidence map›Paper›PMID 16937189›Full record

ArticleMedical & biological engineering & computing2006

Inhibition of cardiomyocyte automaticity by electrotonic application of inward rectifier current from Kir2.1 expressing cells.

Teun P de Boer, Toon A B van Veen, Marien J C Houtman, John A Jansen, Shirley C M van Amersfoorth, Pieter A Doevendans, Marc A Vos, Marcel A G van der Heyden

Abstract read
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In one paragraph

Article in Medical & biological engineering & computing, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 26% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

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  7. Class III antiarrhythmic drugs amiodarone and dronedarone impair KJournal of cellular and molecular medicine · 2017
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  11. Genetic engineering of somatic cells to study and improve cardiac function.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 · 2012
    Article
  12. Human cardiomyocyte progenitor cells: a short history of nearly everything.Journal of cellular and molecular medicine · 2012
    Review
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  15. Regenerative therapies in electrophysiology and pacing: introducing the next steps.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2011
    Review
  16. Article
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  18. Article
  19. Article
  20. Computer modelling of the sinoatrial node.Medical & biological engineering & computing · 2007
    Review
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

8 authors at 3 institutions in 1 country.

Teun P de BoerDepartment of Medical Physiology, Heart Lung Center Utrecht, University Medical Center Utrecht, Yalelaan 50, 3584, Utrecht, The Netherlands.
Toon A B van Veen
Marien J C Houtman
John A Jansen
Shirley C M van Amersfoorth
Pieter A Doevendans
Marc A Vos
Marcel A G van der Heyden
University Medical Center Utrecht · NLNetherlands Heart Institute · NLUtrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A biological pacemaker might be created by generation of a cellular construct consisting of cardiac cells that display spontaneous membrane depolarization, and that are electrotonically coupled to surrounding myocardial cells by means of gap junctions. Depending on the frequency of the spontaneously beating cells, frequency regulation might be required. We hypothesized that application of Kir2.1 expressing non-cardiac cells, which provide I (K1) to spontaneously active neonatal cardiomyocytes (NCMs) by electrotonic coupling in such a cellular construct, would generate an opportunity for pacemaker frequency control. Non-cardiac Kir2.1 expressing cells were co-cultured with spontaneously active rat NCMs. Electrotonic coupling between the two cell types resulted in hyperpolarization of the cardiomyocyte membrane potential and silencing of spontaneous activity. Either blocking of gap-junctional communication by halothane or inhibition of I (K1) by BaCl(2) restored the original membrane potential and spontaneous activity of the NCMs. Our results demonstrate the power of electrotonic coupling for the application of specific ion currents into an engineered cellular construct such as a biological pacemaker.

Indexed as

Pacemaker, ArtificialAction PotentialsAnimalsCells, CulturedCoculture TechniquesMembrane PotentialsMiceMyocytes, CardiacPotassium Channels, Inwardly RectifyingRatsTissue EngineeringPotassium Channels, Inwardly Rectifying

Identifiers

PMID16937189
OpenAlexW2093362256

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.