Evidence map›Paper›PMID 30390173›Full record

ArticleMolecular and cellular biochemistry2019

The increased expression of the inducible Hsp70 (HSP70A1A) in serum of patients with heart failure and its protective effect against the cardiotoxic agent doxorubicin.

Stelios Zerikiotis, Charalampos Angelidis, Irida Dhima, Katerina K Naka, Panagiota Kasioumi, Vasiliki Kalfakakou, Dimitrios Peschos, Patra Vezyraki

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Article in Molecular and cellular biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

16 citing papers in PubMed, 24 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

8 authors at 1 institution in 1 country.

Stelios ZerikiotisLaboratory of Experimental Physiology, Molecular and Cellular Physiology Unit, Medical School, University of Ioannina, 45110, Ioannina, Greece. szerik@cc.uoi.gr.ORCID http://orcid.org/0000-0003-0745-3224
Charalampos AngelidisLaboratory of General Biology, Medical School, University of Ioannina, 45110, Ioannina, Greece.
Irida DhimaLaboratory of Experimental Physiology, Molecular and Cellular Physiology Unit, Medical School, University of Ioannina, 45110, Ioannina, Greece.
Katerina K NakaDepartment of Cardiology and Michaelidion Cardiac Center, Medical School, University of Ioannina, 45110, Ioannina, Greece.
Panagiota KasioumiLaboratory of General Biology, Medical School, University of Ioannina, 45110, Ioannina, Greece.
Vasiliki KalfakakouLaboratory of Experimental Physiology, Molecular and Cellular Physiology Unit, Medical School, University of Ioannina, 45110, Ioannina, Greece.
Dimitrios PeschosLaboratory of Experimental Physiology, Molecular and Cellular Physiology Unit, Medical School, University of Ioannina, 45110, Ioannina, Greece.
Patra VezyrakiLaboratory of Experimental Physiology, Molecular and Cellular Physiology Unit, Medical School, University of Ioannina, 45110, Ioannina, Greece.
University of Ioannina · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to examine the potential association between the expression of Hsp70 protein and heart failure and to investigate the possible protective effect of Hsp70 against the doxorubicin-induced toxicity. Initially, at clinical level, the expression levels of the inducible Hsp70 were quantified in serum from patients with heart failure. Our results showed that in heart failure, Hsp70 concentration appeared to be increased in blood sera of patients compared to that of healthy individuals. The enhanced expression of Hsp70 in serum of patients with heart failure seemed to be associated with various features, such as gender, age and the type of heart failure, but not with its etiology. Next, in our study at cellular level, we used primary cell cultures isolated from embryos of Hsp70-transgenic mice (Tg/Tg) overexpressing human HSP70 and wild-type mice (F1/F1). After exposure to a wide range of doxorubicin concentrations and incubation times, the dose- and time-dependent toxicity of the drug, which appeared to be reduced in Tg/Tg cells, was demonstrated. In addition, doxorubicin administration appeared to result in a dose- and time-dependent decrease in the activity of two of the major endogenous antioxidant enzymes (SOD and GPx). The increased activity of these enzymes in Tg/Tg cells compared to the control F1/F1 cells was obvious, suggesting that the presence of Hsp70 confers enhanced tolerance against DOX-induced oxidative stress. Overall, it has been indicated that Hsp70 protein exerts a very important protective action and renders cells more resistant to the harmful effects of doxorubicin.

Indexed as

AnimalsCardiotoxinsDoxorubicinFemaleGene Expression RegulationHeart FailureHSP70 Heat-Shock ProteinsHumansMaleMiceMice, TransgenicOxidative StressCardiotoxinsDoxorubicinHSP70 Heat-Shock ProteinsDoxorubicinGPxHeart failureHsp70SerumSOD

Identifiers

PMID30390173
OpenAlexW2898766707

What OpenQuestion holds

Textmetadata
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Registered trials

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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.