Evidence map›Paper›PMID 34761510›Full record

ArticleJournal of cellular and molecular medicine2021

Calcium dysregulation increases right ventricular outflow tract arrhythmogenesis in rabbit model of chronic kidney disease.

Shih-Yu Huang, Yao-Chang Chen, Yu-Hsun Kao, Yen-Yu Lu, Yung-Kuo Lin, Satoshi Higa, Shih-Ann Chen, Yi-Jen Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  7. Atrial cardiomyocytes contribute to the inflammatory status associated with atrial fibrillation in right heart disease.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
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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

8 authors at 4 institutions in 2 countries.

Shih-Yu HuangDivision of Cardiac Electrophysiology, Cardiovascular Center, Cathay General Hospital, Taipei City, Taiwan.
Yao-Chang ChenDepartment of Biomedical Engineering, National Defense Medical Center, Taipei City, Taiwan.
Yu-Hsun KaoGraduate Institute of Clinical Medicine, Taipei Medical University, Taipei City, Taiwan.
Yen-Yu LuSchool of Medicine, Fu Jen Catholic University, New Taipei City, Taiwan.
Yung-Kuo LinDivision of Cardiovascular Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei City, Taiwan.
Satoshi HigaCardiac Electrophysiology and Pacing Laboratory, Division of Cardiovascular Medicine, Makiminato Central Hospital, Urasoe, Japan.
Shih-Ann ChenDivision of Cardiology, Department of Medicine, Heart Rhythm Center, Taipei Veterans General Hospital, Taipei City, Taiwan.
Yi-Jen ChenGraduate Institute of Clinical Medicine, Taipei Medical University, Taipei City, Taiwan.ORCID 0000-0001-7224-4491
Wan Fang Hospital · TWFu Jen Catholic University · TWTaipei Veterans General Hospital · TWTomishiro Central Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) increases the risk of arrhythmia. The right ventricular outflow tract (RVOT) is a crucial site of ventricular tachycardia (VT) origination. We hypothesize that CKD increases RVOT arrhythmogenesis through its effects on calcium dysregulation. We analysed measurements obtained using conventional microelectrodes, patch clamp, confocal microscopy, western blotting, immunohistochemical examination and lipid peroxidation for both control and CKD (induced by 150 mg/kg neomycin and 500 mg/kg cefazolin daily) rabbit RVOT tissues or cardiomyocytes. The RVOT of CKD rabbits exhibited a short action potential duration, high incidence of tachypacing (20 Hz)-induced sustained VT, and long duration of isoproterenol and tachypacing-induced sustained and non-sustained VT. Tachypacing-induced sustained and non-sustained VT in isoproterenol-treated CKD RVOT tissues were attenuated by KB-R7943 and partially inhibited by KN93 and H89. The CKD RVOT myocytes had high levels of phosphorylated CaMKII and PKA, and an increased expression of tyrosine hydroxylase-positive neural density. The CKD RVOT myocytes exhibited large levels of I

Indexed as

Disease SusceptibilityAction PotentialsAnimalsArrhythmias, CardiacBiomarkersCalciumDisease Models, AnimalElectrocardiographyHeart Function TestsHeart VentriclesHumansImmunohistochemistryMyocytes, CardiacOxidative StressPatch-Clamp TechniquesRabbitsBiomarkersCalciumcalcium homeostasischronic kidney diseaseright ventricular outflow tractventricular tachycardia

Identifiers

PMID34761510
PMCPMC8650029
OpenAlexW3213366360

What OpenQuestion holds

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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.