Evidence map›Paper›PMID 33728024›Full record

ArticleOxidative medicine and cellular longevity2021

Modulation of Mitochondrial Quality Control Processes by BGP-15 in Oxidative Stress Scenarios: From Cell Culture to Heart Failure.

Orsolya Horvath, Katalin Ordog, Kitti Bruszt, Nikoletta Kalman, Dominika Kovacs, Balazs Radnai, Ferenc Gallyas, Kalman Toth, Robert Halmosi, Laszlo Deres

RetractedOpen access · hybridAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Orsolya Horvath1st Department of Medicine, University of Pecs, Medical School, Pecs, Hungary.ORCID https://orcid.org/0000-0002-5456-7200
Katalin Ordog1st Department of Medicine, University of Pecs, Medical School, Pecs, Hungary.ORCID https://orcid.org/0000-0002-8269-7256
Kitti Bruszt1st Department of Medicine, University of Pecs, Medical School, Pecs, Hungary.ORCID https://orcid.org/0000-0002-7544-009X
Nikoletta KalmanDepartment of Biochemistry and Medical Chemistry, University of Pecs, Medical School, Pecs, Hungary.ORCID https://orcid.org/0000-0001-6827-9894
Dominika KovacsDepartment of Biochemistry and Medical Chemistry, University of Pecs, Medical School, Pecs, Hungary.ORCID https://orcid.org/0000-0002-8904-3976
Balazs RadnaiDepartment of Biochemistry and Medical Chemistry, University of Pecs, Medical School, Pecs, Hungary.ORCID https://orcid.org/0000-0002-7147-0080
Ferenc GallyasSzentágothai Research Centre, University of Pecs, Pecs, Hungary.ORCID https://orcid.org/0000-0002-1906-4333
Kalman Toth1st Department of Medicine, University of Pecs, Medical School, Pecs, Hungary.ORCID https://orcid.org/0000-0002-0114-5231
Robert Halmosi1st Department of Medicine, University of Pecs, Medical School, Pecs, Hungary.ORCID https://orcid.org/0000-0002-6965-7743
Laszlo Deres1st Department of Medicine, University of Pecs, Medical School, Pecs, Hungary.ORCID https://orcid.org/0000-0003-1808-3724
University of Pecs · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure (HF) is a complex chronic clinical disease characterized by among others the damage of the mitochondrial network. The disruption of the mitochondrial quality control and the imbalance in fusion-fission processes lead to a lack of energy supply and, finally, to cell death. BGP-15 (O-[3-piperidino-2-hydroxy-1-propyl]-nicotinic acid amidoxime dihydrochloride) is an insulin sensitizer molecule and has a cytoprotective effect in a wide variety of experimental models. In our recent work, we aimed to clarify the mitochondrial protective effects of BGP-15 in a hypertension-induced heart failure model and "in vitro." Spontaneously hypertensive rats (SHRs) received BGP-15 or placebo for 18 weeks. BGP-15 treatment preserved the normal mitochondrial ultrastructure and enhanced the mitochondrial fusion. Neonatal rat cardiomyocytes (NRCMs) were stressed by hydrogen-peroxide. BGP-15 treatment inhibited the mitochondrial fission processes, promoted mitochondrial fusion, maintained the integrity of the mitochondrial genome, and moreover enhanced the de novo biogenesis of the mitochondria. As a result of these effects, BGP-15 treatment also supports the maintenance of mitochondrial function through the preservation of the mitochondrial structure during hydrogen peroxide-induced oxidative stress as well as in an "in vivo" heart failure model. It offers the possibility, which pharmacological modulation of mitochondrial quality control under oxidative stress could be a novel therapeutic approach in heart failure.

Indexed as

Oxidative StressAnimalsAnimals, NewbornCell Culture TechniquesCitrate (si)-SynthaseDNADNA DamageDNA, MitochondrialDynaminsElectron TransportEnergy MetabolismGenome, MitochondrialHeart FailureHypertensionMaleMembrane Potential, MitochondrialBGP 15Citrate (si)-SynthaseDNADNA, MitochondrialDnm1l protein, ratDynaminsMitochondrial ProteinsNatriuretic Peptide, BrainOximesPiperidines

Identifiers

PMID33728024
PMCPMC7937466
OpenAlexW3134499334

What Socratic holds

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LicenceCC BY
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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 Socratic graph.