Evidence map›Paper›PMID 29397400›Full record

ArticleArchives of toxicology2018

Cell death mechanisms of the anti-cancer drug etoposide on human cardiomyocytes isolated from pluripotent stem cells.

Harshal Nemade, Umesh Chaudhari, Aviseka Acharya, Jürgen Hescheler, Jan Georg Hengstler, Symeon Papadopoulos, Agapios Sachinidis

Open access · hybridAbstract read
In one paragraph

Article in Archives of toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Review
  5. Role of miR-182 in cardiovascular and cerebrovascular diseases.Frontiers in cell and developmental biology · 2023
    Review
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  7. Article
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  18. Article
  19. Review
  20. Veterinary world · 2021
    Article
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

7 authors at 2 institutions in 1 country.

Harshal NemadeInstitute of Neurophysiology and Center for Molecular Medicine Cologne (CMMC), University of Cologne (UKK), Robert-Koch-Str. 39, 50931, Cologne, Germany.
Umesh ChaudhariInstitute of Neurophysiology and Center for Molecular Medicine Cologne (CMMC), University of Cologne (UKK), Robert-Koch-Str. 39, 50931, Cologne, Germany.
Aviseka AcharyaInstitute of Neurophysiology and Center for Molecular Medicine Cologne (CMMC), University of Cologne (UKK), Robert-Koch-Str. 39, 50931, Cologne, Germany.
Jürgen HeschelerInstitute of Neurophysiology and Center for Molecular Medicine Cologne (CMMC), University of Cologne (UKK), Robert-Koch-Str. 39, 50931, Cologne, Germany.
Jan Georg HengstlerLeibniz Research Centre for Working Environment and Human Factors, Technical University of Dortmund (IfADo), 44139, Dortmund, Germany.
Symeon PapadopoulosCenter of Physiology and Pathophysiology, Institute of Vegetative Physiology, University of Cologne, Robert-Koch-Str. 39, 50931, Cologne, Germany.
Agapios SachinidisInstitute of Neurophysiology and Center for Molecular Medicine Cologne (CMMC), University of Cologne (UKK), Robert-Koch-Str. 39, 50931, Cologne, Germany. a.sachinidis@uni-koeln.de.
University of Cologne · DETU Dortmund University · DE

Funding

FP7 Health Programme, European Commission DETECTIVE
6 · The paper itself

Abstract

Etoposide (ETP) and anthracyclines are applied for wide anti-cancer treatments. However, the ETP-induced cardiotoxicity remains to be a major safety issue and the underlying cardiotoxic mechanisms are not well understood. This study is aiming to unravel the cardiotoxicity profile of ETP in comparison to anthracyclines using physiologically relevant human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs). Using xCELLigence real-time cell analyser (RTCA), we found that single high dose of ETP induces irreversible increase in hPSC-CMs beating rate and decrease in beating amplitude. We also identified 58 deregulated genes consisting of 33 upregulated and 25 downregulated genes in hPSC-CMs after ETP treatment. Gene ontology (GO) and pathway analysis showed that most upregulated genes are enriched in GO categories like positive regulation of apoptotic process, regulation of cell death, and mitochondria organization, whereas most downregulated genes were enriched in GO categories like cytoskeletal organization, muscle contraction, and Ca

Indexed as

AnthracyclinesAntineoplastic AgentsApoptosisBenzothiazolesCalcium-Binding ProteinsCalcium ChannelsCell DeathCells, CulturedCytoskeletal ProteinsDown-RegulationEtoposideGene ExpressionHumansMicroRNAsMitochondria, HeartMuscle ContractionAnthracyclinesAntineoplastic AgentsBenzothiazolesCalcium-Binding ProteinsCalcium ChannelsCytoskeletal ProteinsEtoposideliproxstatin-1MicroRNAspifithrinQuinoxalinesSpiro CompoundsTolueneApoptosisCalciumCardiomyocytesCardiotoxicityHuman pluripotent stem cellsNon-animal testingSafety assessment

Identifiers

PMID29397400
PMCPMC5882643
OpenAlexW2789179380

What OpenQuestion holds

Textmetadata
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.