Evidence map›Paper›PMID 26137186›Full record

ArticleOxidative medicine and cellular longevity2015

High Throughput Screening Identifies a Novel Compound Protecting Cardiomyocytes from Doxorubicin-Induced Damage.

Szabolcs Gergely, Csaba Hegedűs, Petra Lakatos, Katalin Kovács, Renáta Gáspár, Tamás Csont, László Virág

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Szabolcs GergelyDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen 4032, Hungary ; Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen 4032, Hungary.
Csaba HegedűsDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen 4032, Hungary.
Petra LakatosDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen 4032, Hungary.
Katalin KovácsDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen 4032, Hungary ; MTA-DE Cell Biology and Signaling Research Group of the Hungarian Academy of Sciences, Debrecen 4032, Hungary.
Renáta GáspárDepartment of Biochemistry, Faculty of Medicine, University of Szeged, Szeged 6720, Hungary.
Tamás CsontDepartment of Biochemistry, Faculty of Medicine, University of Szeged, Szeged 6720, Hungary.
László VirágDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen 4032, Hungary ; MTA-DE Cell Biology and Signaling Research Group of the Hungarian Academy of Sciences, Debrecen 4032, Hungary.
University of Debrecen · HUUniversity of Szeged · HUHungarian Academy of Sciences · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antracyclines are effective antitumor agents. One of the most commonly used antracyclines is doxorubicin, which can be successfully used to treat a diverse spectrum of tumors. Application of these drugs is limited by their cardiotoxic effect, which is determined by a lifetime cumulative dose. We set out to identify by high throughput screening cardioprotective compounds protecting cardiomyocytes from doxorubicin-induced injury. Ten thousand compounds of ChemBridge's DIVERSet compound library were screened to identify compounds that can protect H9C2 rat cardiomyocytes against doxorubicin-induced cell death. The most effective compound proved protective in doxorubicin-treated primary rat cardiomyocytes and was further characterized to demonstrate that it significantly decreased doxorubicin-induced apoptotic and necrotic cell death and inhibited doxorubicin-induced activation of JNK MAP kinase without having considerable radical scavenging effect or interfering with the antitumor effect of doxorubicin. In fact the compound identified as 3-[2-(4-ethylphenyl)-2-oxoethyl]-1,2-dimethyl-1H-3,1-benzimidazol-3-ium bromide was toxic to all tumor cell lines tested even without doxorubicine treatment. This benzimidazole compound may lead, through further optimalization, to the development of a drug candidate protecting the heart from doxorubicin-induced injury.

Indexed as

AnimalsAntibiotics, AntineoplasticApoptosisBenzimidazolesCell ProliferationCells, CulturedDoxorubicinHigh-Throughput Screening AssaysJNK Mitogen-Activated Protein KinasesMyocytes, CardiacProtective AgentsRatsRats, WistarReactive Nitrogen SpeciesReactive Oxygen Species3-(2-(4-ethylphenyl)-2-oxoethyl)-1,2-dimethyl-1H-3,1-benzimidazol-3-iumAntibiotics, AntineoplasticBenzimidazolesDoxorubicinJNK Mitogen-Activated Protein KinasesProtective AgentsReactive Nitrogen SpeciesReactive Oxygen Species

Identifiers

PMID26137186
PMCPMC4475553
OpenAlexW1527034886

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.