Evidence map›Paper›PMID 30965670›Full record

ArticleMolecules (Basel, Switzerland)2019

Regulation of the Nrf2 Pathway by Glycogen Synthase Kinase-3β in MPP⁺-Induced Cell Damage.

Güliz Armagan, Elvin Sevgili, Fulya Tuzcu Gürkan, Fadime Aydın Köse, Tuğçe Bilgiç, Taner Dagcı, Luciano Saso

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  7. HarnessingInternational journal of molecular sciences · 2025
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  10. Article
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  14. Heteronemin promotes iron-dependent cell death in pancreatic cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Article
  15. Review
  16. Review
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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 2 institutions in 2 countries.

Güliz ArmaganDepartment of Biochemistry, Faculty of Pharmacy, Ege University, 35100 Bornova, Izmir, Turkey. guliz.armagan@ege.edu.tr.
Elvin SevgiliDepartment of Biochemistry, Faculty of Pharmacy, Ege University, 35100 Bornova, Izmir, Turkey. elvinsevgili@windowslive.com.
Fulya Tuzcu GürkanDepartment of Physiology, School of Medicine, Ege University, 35100 Bornova, Izmir, Turkey. fulya_tuzcu@yahoo.com.
Fadime Aydın KöseDepartment of Biochemistry, Faculty of Pharmacy, Ege University, 35100 Bornova, Izmir, Turkey. fadime.aydin@ege.edu.tr.
Tuğçe BilgiçDepartment of Physiology, School of Medicine, Ege University, 35100 Bornova, Izmir, Turkey. tugce_bilgic@icloud.com.
Taner DagcıDepartment of Physiology, School of Medicine, Ege University, 35100 Bornova, Izmir, Turkey. tanerdagci@gmail.com.
Luciano SasoDepartment of Physiology and Pharmacology "Vittorio Erspamer", Sapienza University of Rome, 00185 Rome, Italy. luciano.saso@uniroma1.it.
Ege University · TRSapienza University of Rome · IT

Funding

Ege Üniversitesi 15/ECZ/012, 2016/BIL/004Türkiye Bilimsel ve Teknolojik Araştirma Kurumu 215S528
6 · The paper itself

Abstract

Recently, nuclear translocation and stability of nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) have gained increasing attention in the prevention of oxidative stress. The present study was aimed to evaluate the regulatory role of glycogen synthase kinase-3β (GSK-3β) inhibition by tideglusib through the Nrf2 pathway in a cellular damage model. Gene silencing (siRNA-mediated) was performed to examine the responses of Nrf2-target genes (i.e., heme oxygenase-1, NAD(P)H:quinone oxidoreductase1) to siRNA depletion of Nrf2 in MPP⁺-induced dopaminergic cell death. Nrf2 and its downstream regulated genes/proteins were analyzed using Real-time PCR and Western Blotting techniques, respectively. Moreover, free radical production, the changes in mitochondrial membrane potential, total glutathione, and glutathione-S-transferase were examined. The possible contribution of peroxisome proliferator-activated receptor gamma (PPARγ) to tideglusib-mediated neuroprotection was evaluated. The number of viable cells and mitochondrial membrane potential were increased following GSK-3β enzyme inhibition against MPP⁺. HO-1, NQO1 mRNA/protein expressions and Nrf2 nuclear translocation significantly triggered by tideglusib. Moreover, the neuroprotection by tideglusib was not observed in the presence of siRNA Nrf2. Our study supports the idea that GSK-3β enzyme inhibition may modulate the Nrf2/ARE pathway in cellular damage and the inhibitory role of tideglusib on GSK-3β along with PPARγ activation may be responsible for neuroprotection.

Indexed as

1-Methyl-4-phenylpyridiniumCell DeathCell LineGlycogen Synthase Kinase 3 betaHeme Oxygenase-1HumansMembrane Potential, MitochondrialNAD(P)H Dehydrogenase (Quinone)NeuronsNF-E2-Related Factor 2PioglitazoneSignal TransductionThiadiazoles1-Methyl-4-phenylpyridiniumGlycogen Synthase Kinase 3 betaGSK3B protein, humanHeme Oxygenase-1HMOX1 protein, humanNAD(P)H Dehydrogenase (Quinone)NFE2L2 protein, humanNF-E2-Related Factor 2NQO1 protein, humanPioglitazoneThiadiazolestideglusibglycogen synthase kinase-3βMPP+-induced cellular damageNrf2 pathway

Identifiers

PMID30965670
PMCPMC6480928
OpenAlexW2931131301

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.