Evidence map›Paper›PMID 30639418›Full record

ArticleEBioMedicine2019

Primary cardiac manifestation of autosomal dominant polycystic kidney disease revealed by patient induced pluripotent stem cell-derived cardiomyocytes.

Jia-Jung Lee, Sin-Jhong Cheng, Ching-Ying Huang, Chen-Yun Chen, Li Feng, Daw-Yang Hwang, Timothy J Kamp, Hung-Chun Chen, Patrick C H Hsieh

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 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
2.5field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

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  7. Human iPSC banking: barriers and opportunities.Journal of biomedical science · 2019
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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

9 authors at 4 institutions in 3 countries.

Jia-Jung LeePh.D. Program in Translational Medicine, Kaohsiung Medical University and Academia Sinica, Taiwan; Division of Nephrology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan; Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Faculty of Renal Care, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Sin-Jhong ChengInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; Neuroscience Program of Academia Sinica, Academia Sinica, Taipei, Taiwan.
Ching-Ying HuangInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Chen-Yun ChenInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Li FengCellular and Molecular Arrhythmia Research Program, University of Wisconsin-Madison, Madison, WI, United States; Department of Cardiology, Beijing AnZhen Hospital, Capital Medical University, Beijing, China.
Daw-Yang HwangDivision of Nephrology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan; Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Timothy J KampCellular and Molecular Arrhythmia Research Program, University of Wisconsin-Madison, Madison, WI, United States; Department of Cell and Regenerative Biology, University of Wisconsin-Madison, Madison, WI, United States; Department of Medicine, University of Wisconsin-Madison, Madison, WI, United States.
Hung-Chun ChenDivision of Nephrology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan; Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Faculty of Renal Care, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan. Electronic address: chenhc@kmu.edu.tw.
Patrick C H HsiehInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; Cellular and Molecular Arrhythmia Research Program, University of Wisconsin-Madison, Madison, WI, United States; Department of Medicine, University of Wisconsin-Madison, Madison, WI, United States. Electronic address: phsieh@ibms.sinica.edu.tw.
Institute of Biomedical Sciences, Academia Sinica · TWUniversity of Wisconsin–Madison · USKaohsiung Medical University Chung-Ho Memorial Hospital · TWAcademia Sinica · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMutations in PKD1 or PKD2 gene lead to autosomal dominant polycystic kidney disease (ADPKD). The mechanism of ADPKD progression and its link to increased cardiovascular mortality is still elusive.

methodsWe differentiated ADPKD patient induced pluripotent stem cells (iPSCs) to cardiomyocytes (CMs). The electrophysiological properties at the cellular level were analyzed by calcium imaging and whole cell patch clamping.

findingsThe ADPKD patient iPSC-CMs had decreased sarcoplasmic reticulum calcium content compared with Control-CMs. Spontaneous action potential of the PKD2 mutation line-derived CMs demonstrated slower beating rate and longer action potential duration. The PKD1 mutation line-derived CMs showed a comparable dose-dependent shortening of phase II repolarization with the Control-CMs, but a significant increase in beating frequency in response to L-type calcium channel blocker. The PKD1-mutant iPSC-CMs also showed a relatively unstable baseline as a greater percentage of cells exhibited delayed afterdepolarizations (DADs). Both the ADPKD patient iPSC-CMs showed more β-adrenergic agonist-elicited DADs compared with Control-CMs.

interpretationCharacterization of ADPKD patient iPSC-CMs provides new insights into the increased clinical risk of arrhythmias, and the results enable disease modeling and drug screening for cardiac manifestations of ADPKD. FUND: Ministry of Science and Technology, National Health Research Institutes, Academia Sinica Program for Technology Supporting Platform Axis Scheme, Thematic Research Program and Summit Research Program, and Kaohsiung Medical University Hospital, Taiwan.

Indexed as

Adrenergic beta-AgonistsBiomarkersCalciumCalcium Channel BlockersCalcium Channels, L-TypeCell DifferentiationCell LineElectrophysiological PhenomenaGene ExpressionHeart DiseasesHumansInduced Pluripotent Stem CellsMolecular ImagingMutationMyocytes, CardiacPhenotypeAdrenergic beta-AgonistsBiomarkersCalciumCalcium Channel BlockersCalcium Channels, L-TypeTRPP Cation ChannelsArrhythmiaAutosomal dominant polycystic kidney diseaseCardiomyocyteHuman iPS cell

Identifiers

PMID30639418
PMCPMC6413318
OpenAlexW2909427345

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.