Evidence map›Paper›PMID 34471171›Full record

ArticleScientific reports2021

Comparison of the antiremodeling effects of losartan and mirabegron in a rat model of uremic cardiomyopathy.

Zsuzsanna Z A Kovács, Gergő Szűcs, Marah Freiwan, Mónika G Kovács, Fanni M Márványkövi, Hoa Dinh, Andrea Siska, Katalin Farkas, Ferenc Kovács, András Kriston and 7 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Scientific reports, 2021. 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
2.7field-weighted citation impact, top 9% 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, 26 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

17 authors at 3 institutions in 2 countries.

Zsuzsanna Z A KovácsMEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, Albert Szent-Györgyi Medical School, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary.
Gergő SzűcsMEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, Albert Szent-Györgyi Medical School, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary.
Marah FreiwanMEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, Albert Szent-Györgyi Medical School, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary.
Mónika G KovácsMEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, Albert Szent-Györgyi Medical School, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary.
Fanni M MárványköviMEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, Albert Szent-Györgyi Medical School, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary.
Hoa DinhMEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, Albert Szent-Györgyi Medical School, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary.
Andrea SiskaDepartment of Laboratory Medicine, Albert Szent-Györgyi Medical School, University of Szeged, Semmelweis utca 6, Szeged, 6720, Hungary.
Katalin FarkasDepartment of Laboratory Medicine, Albert Szent-Györgyi Medical School, University of Szeged, Semmelweis utca 6, Szeged, 6720, Hungary.
Ferenc KovácsSynthetic and Systems Biology Unit, Biological Research Centre, Eötvös Loránd Research Network, Temesvári krt. 62, Szeged, 6726, Hungary.
András KristonSynthetic and Systems Biology Unit, Biological Research Centre, Eötvös Loránd Research Network, Temesvári krt. 62, Szeged, 6726, Hungary.
Péter HorváthSynthetic and Systems Biology Unit, Biological Research Centre, Eötvös Loránd Research Network, Temesvári krt. 62, Szeged, 6726, Hungary.
Bence KőváriDepartment of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Állomás utca 1, Szeged, 6720, Hungary.
Bálint Gábor CserniDepartment of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Állomás utca 1, Szeged, 6720, Hungary.
Gábor CserniDepartment of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Állomás utca 1, Szeged, 6720, Hungary.
Imre FöldesiDepartment of Laboratory Medicine, Albert Szent-Györgyi Medical School, University of Szeged, Semmelweis utca 6, Szeged, 6720, Hungary.
Tamás CsontMEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, Albert Szent-Györgyi Medical School, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary. csont.tamas@med.u-szeged.hu.ORCID http://orcid.org/0000-0001-5792-2768
Márta SárközyMEDICS Research Group, Department of Biochemistry, Interdisciplinary Center of Excellence, Albert Szent-Györgyi Medical School, University of Szeged, Dóm tér 9, Szeged, 6720, Hungary. sarkozy.marta@med.u-szeged.hu.ORCID http://orcid.org/0000-0002-5929-2146
University of Szeged · HUHUN-REN Szegedi Biológiai Kutatóközpont · HUUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uremic cardiomyopathy is characterized by diastolic dysfunction (DD), left ventricular hypertrophy (LVH), and fibrosis. Angiotensin-II plays a major role in the development of uremic cardiomyopathy via nitro-oxidative and inflammatory mechanisms. In heart failure, the beta-3 adrenergic receptor (β3-AR) is up-regulated and coupled to endothelial nitric oxide synthase (eNOS)-mediated pathways, exerting antiremodeling effects. We aimed to compare the antiremodeling effects of the angiotensin-II receptor blocker losartan and the β3-AR agonist mirabegron in uremic cardiomyopathy. Chronic kidney disease (CKD) was induced by 5/6th nephrectomy in male Wistar rats. Five weeks later, rats were randomized into four groups: (1) sham-operated, (2) CKD, (3) losartan-treated (10 mg/kg/day) CKD, and (4) mirabegron-treated (10 mg/kg/day) CKD groups. At week 13, echocardiographic, histologic, laboratory, qRT-PCR, and Western blot measurements proved the development of uremic cardiomyopathy with DD, LVH, fibrosis, inflammation, and reduced eNOS levels, which were significantly ameliorated by losartan. However, mirabegron showed a tendency to decrease DD and fibrosis; but eNOS expression remained reduced. In uremic cardiomyopathy, β3-AR, sarcoplasmic reticulum ATPase (SERCA), and phospholamban levels did not change irrespective of treatments. Mirabegron reduced the angiotensin-II receptor 1 expression in uremic cardiomyopathy that might explain its mild antiremodeling effects despite the unchanged expression of the β3-AR.

Indexed as

AcetanilidesAdrenergic beta-3 Receptor AgonistsAnimalsAntihypertensive AgentsCardiomyopathiesLosartanMaleNephrectomyNitric Oxide Synthase Type IIIRatsRats, WistarRenal Insufficiency, ChronicThiazolesUremiaAcetanilidesAdrenergic beta-3 Receptor AgonistsAntihypertensive AgentsLosartanmirabegronNitric Oxide Synthase Type IIINos3 protein, ratThiazoles

Identifiers

PMID34471171
PMCPMC8410807
OpenAlexW3197000865

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.