Evidence map›Paper›PMID 30766898›Full record

ArticleRegenerative therapy2019

Inhibitory effects of class I antiarrhythmic agents on Na

Sayaka Yonemizu, Keiichiro Masuda, Yasutaka Kurata, Tomomi Notsu, Yuhei Higashi, Kenta Fukumura, Peili Li, Haruaki Ninomiya, Junichiro Miake, Motokazu Tsuneto and 2 more

Abstract read
In one paragraph

Article in Regenerative therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Beneficial effects of chronic mexiletine treatment in a human model of SCN5A overlap syndrome.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
    Article
  2. Article
  3. Regenerative therapy · 2022
    Article
  4. Article
  5. Review
  6. Article
  7. Article
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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

12 authors.

Sayaka YonemizuDivision of Regenerative Medicine and Therapeutics, Department of Genetic Medicine and Regenerative Therapeutics, Tottori University Graduate School of Medical Science, 86 Nishi-cho, Yonago 683-8503, Japan.
Keiichiro MasudaDivision of Regenerative Medicine and Therapeutics, Department of Genetic Medicine and Regenerative Therapeutics, Tottori University Graduate School of Medical Science, 86 Nishi-cho, Yonago 683-8503, Japan.
Yasutaka KurataDepartment of Physiology II, Kanazawa Medical University, 1-1 Daigaku, Uchinada-machi, Kahoku-gun, Ishikawa 920-0293, Japan.
Tomomi NotsuDivision of Regenerative Medicine and Therapeutics, Department of Genetic Medicine and Regenerative Therapeutics, Tottori University Graduate School of Medical Science, 86 Nishi-cho, Yonago 683-8503, Japan.
Yuhei HigashiDivision of Regenerative Medicine and Therapeutics, Department of Genetic Medicine and Regenerative Therapeutics, Tottori University Graduate School of Medical Science, 86 Nishi-cho, Yonago 683-8503, Japan.
Kenta FukumuraDivision of Regenerative Medicine and Therapeutics, Department of Genetic Medicine and Regenerative Therapeutics, Tottori University Graduate School of Medical Science, 86 Nishi-cho, Yonago 683-8503, Japan.
Peili LiDivision of Regenerative Medicine and Therapeutics, Department of Genetic Medicine and Regenerative Therapeutics, Tottori University Graduate School of Medical Science, 86 Nishi-cho, Yonago 683-8503, Japan.
Haruaki NinomiyaDepartment of Biological Regulation, Tottori University Faculty of Medicine, Yonago 683-8503, Japan.
Junichiro MiakeDepartment of Pharmacology, Tottori University Faculty of Medicine, Yonago 683-8503, Japan.
Motokazu TsunetoDivision of Regenerative Medicine and Therapeutics, Department of Genetic Medicine and Regenerative Therapeutics, Tottori University Graduate School of Medical Science, 86 Nishi-cho, Yonago 683-8503, Japan.
Yasuaki ShirayoshiDivision of Regenerative Medicine and Therapeutics, Department of Genetic Medicine and Regenerative Therapeutics, Tottori University Graduate School of Medical Science, 86 Nishi-cho, Yonago 683-8503, Japan.
Ichiro HisatomeDivision of Regenerative Medicine and Therapeutics, Department of Genetic Medicine and Regenerative Therapeutics, Tottori University Graduate School of Medical Science, 86 Nishi-cho, Yonago 683-8503, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionHuman induced pluripotent stem cells (hiPSCs) harboring cardiac myosin heavy chain 6 promoter can differentiate into functional cardiomyocytes called "iCell cardiomyocytes" under blasticidin treatment condition. While iCell cardiomyocytes are expected to be used for predicting cardiotoxicity of drugs, their responses to antiarrhythmic agents remain to be elucidated. We first examined electrophysiological properties of iCell cardiomyocytes and mRNA levels of ion channels and Ca handling proteins, and then evaluated effects of class I antiarrhythmic agents on their Na

methodsiCell cardiomyocytes were cultured for 8-14 days (38-44 days after inducing their differentiation), according to the manufacturer's protocol. We determined their action potentials (APs) and sarcolemmal ionic currents using whole-cell patch clamp techniques, and also mRNA levels of ion channels and Ca handling proteins by RT-PCR. Effects of three class I antiarrhythmic agents, pirmenol, pilsicainide and mexiletine, on Na

resultsiCell cardiomyocytes revealed sinoatrial node-type (18%), atrial-type (18%) and ventricular-type (64%) spontaneous APs. The maximum peak amplitudes of I

conclusionsIn iCell cardiomyocytes, I

Indexed as

APA, AP amplitudeAP, action potentialAPD, AP durationclass I antiarrhythmic agentsET-1, Endothelin 1hiPSC, human induced pluripotent stem cellHP, holding potentialiCell cardiomyocytesIGF-1, insulin-like growth factor-1L-type Ca2+ channel currentMDP, maximum diastolic potentialminK, minimal potassium channel subunitMiRP, minK related proteinMYH, myosin heavy chainNa+ channel currentOS, overshoot potentialSAN, sinoatrial node

Identifiers

PMID30766898
PMCPMC6360514

What OpenQuestion holds

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Registered trials

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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.