Evidence map›Paper›PMID 30794687›Full record

ArticlePloS one2019

Omentin protects H9c2 cells against docetaxel cardiotoxicity.

Ricardo Lage, María Cebro-Márquez, Moisés Rodríguez-Mañero, José Ramón González-Juanatey, Isabel Moscoso

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

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  10. Inhibition of TNF-Applied bionics and biomechanics · 2022
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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

5 authors at 1 institution in 1 country.

Ricardo LageCardiology Group, Center for Research in Molecular Medicine and Chronic Diseases (CIMUS), Universidade de Santiago de Compostela and Health Research Institute, University Clinical Hospital of Santiago de Compostela-Santiago de Compostela, Spain.
María Cebro-MárquezCardiology Group, Center for Research in Molecular Medicine and Chronic Diseases (CIMUS), Universidade de Santiago de Compostela and Health Research Institute, University Clinical Hospital of Santiago de Compostela-Santiago de Compostela, Spain.ORCID 0000-0001-6427-7955
Moisés Rodríguez-MañeroCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
José Ramón González-JuanateyCardiology Group, Center for Research in Molecular Medicine and Chronic Diseases (CIMUS), Universidade de Santiago de Compostela and Health Research Institute, University Clinical Hospital of Santiago de Compostela-Santiago de Compostela, Spain.
Isabel MoscosoCardiology Group, Center for Research in Molecular Medicine and Chronic Diseases (CIMUS), Universidade de Santiago de Compostela and Health Research Institute, University Clinical Hospital of Santiago de Compostela-Santiago de Compostela, Spain.ORCID 0000-0002-6078-4666
Universidade de Santiago de Compostela · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAssociation between obesity and cardiovascular diseases is well known, however increased susceptibility of obese patients to develop several cancer types is not so commonly known. Current data suggest that poorer overall survival in cancer patients might be associated to non-cancer-related causes such as higher risk of cardiotoxicity in obese patients treated with chemotherapeutic agents. Omentin, a novel adipokine decreased in obesity, is actually in the spotlight due to its favourable effects on inflammation, glucose homeostasis and cardiovascular diseases. Also, recent data showed that in vitro anthracycline-induced cardiomyocyte apoptosis is counteracted by omentin suggesting its cardioprotective role.

objectiveOur aim was to evaluate omentin effects against docetaxel toxicity.

resultsOur data indicate that omentin inhibits docetaxel-induced viability loss and that increased viability is associated to decreased caspase-3 expression and cell death. Although omentin reduces NOX4 expression, it failed to reduce docetaxel-induced reactive oxygen species production. Our results indicate that omentin decreases docetaxel-induced endoplasmic reticulum stress, suggesting that cardioprotective role might be associated to ERS inhibition.

conclusionThese data suggest that omentin treatment may contribute to decrease susceptibility to DTX-induced cardiotoxicity.

Indexed as

CardiotoxicityMyocytes, CardiacAnimalsCaspase 3Cell LineCytokinesDocetaxelGene Expression Regulation, EnzymologicLectinsNADPH Oxidase 4RatsReactive Oxygen SpeciesCasp3 protein, ratCaspase 3CytokinesDocetaxelLectinsNADPH Oxidase 4Nox4 protein, ratomentin protein, ratReactive Oxygen Species

Identifiers

PMID30794687
PMCPMC6386316
OpenAlexW2916906313

What OpenQuestion holds

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LicenceCC BY
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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.