Evidence map›Paper›PMID 30140996›Full record

ArticleJournal of molecular neuroscience : MN2018

Nrf2 Signaling in Sodium Azide-Treated Oligodendrocytes Restores Mitochondrial Functions.

Annette Liessem-Schmitz, Nico Teske, Miriam Scheld, Stella Nyamoya, Adib Zendedel, Cordian Beyer, Tim Clarner, Athanassios Fragoulis

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2018. 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
0.6field-weighted citation impact, top 34% 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, 17 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 2 institutions in 1 country.

Annette Liessem-SchmitzInstitute of Neuroanatomy, Uniklinik RWTH Aachen University, Wendlingweg 2, 52074, Aachen, Germany.
Nico TeskeDepartment of Anatomy II, Ludwig-Maximilians-University of Munich, 80336, Munich, Germany.
Miriam ScheldInstitute of Neuroanatomy, Uniklinik RWTH Aachen University, Wendlingweg 2, 52074, Aachen, Germany.
Stella NyamoyaInstitute of Neuroanatomy, Uniklinik RWTH Aachen University, Wendlingweg 2, 52074, Aachen, Germany.
Adib ZendedelInstitute of Neuroanatomy, Uniklinik RWTH Aachen University, Wendlingweg 2, 52074, Aachen, Germany.
Cordian BeyerInstitute of Neuroanatomy, Uniklinik RWTH Aachen University, Wendlingweg 2, 52074, Aachen, Germany.
Tim ClarnerInstitute of Neuroanatomy, Uniklinik RWTH Aachen University, Wendlingweg 2, 52074, Aachen, Germany.
Athanassios FragoulisDepartment of Anatomy and Cell Biology, Medical Faculty, Uniklinik RWTH Aachen University, Wendlingweg 2, 52074, Aachen, Germany. afragoulis@ukaachen.de.ORCID http://orcid.org/0000-0002-6973-3080
Universitätsklinikum Aachen · DELudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunctions mark a critical step in many central nervous system (CNS) pathologies, including multiple sclerosis (MS). Such dysfunctions lead to depolarization of mitochondrial membranes and imbalanced redox homeostasis. In this context, reactive oxygen species (ROS) are potentially deleterious but can also act as an important signaling step for cellular maintenance. The transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2), the key regulator in the cellular oxidative stress-response, induces a battery of genes involved in repair and regeneration. Here, we investigated the relevance of Nrf2 signaling for the prevention of cellular damage caused by dysfunctional mitochondria. We employed sodium azide (SA) as mitochondrial inhibitor on oligodendroglial OliNeu cells in vitro, and the cuprizone model with wild type and GFAP-Cre

Indexed as

Signal TransductionAnimalsCell LineCells, CulturedEnzyme InhibitorsGlial Fibrillary Acidic ProteinKelch-Like ECH-Associated Protein 1Membrane Potential, MitochondrialMiceMitochondriaNF-E2-Related Factor 2OligodendrogliaSodium AzideEnzyme InhibitorsGlial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseKeap1 protein, mouseKelch-Like ECH-Associated Protein 1Nfe2l2 protein, mouseNF-E2-Related Factor 2Sodium AzideComplex IVDepolarizationMitochondrial dysfunctionNrf2OligodendrocytesSodium azide

Identifiers

PMID30140996
OpenAlexW2888486643

What OpenQuestion holds

Textmetadata
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.