Evidence map›Paper›PMID 29997171›Full record

ArticleEMBO molecular medicine2018

Aberrant regulation of the GSK-3β/NRF2 axis unveils a novel therapy for adrenoleukodystrophy.

Pablo Ranea-Robles, Nathalie Launay, Montserrat Ruiz, Noel Ylagan Calingasan, Magali Dumont, Alba Naudí, Manuel Portero-Otín, Reinald Pamplona, Isidre Ferrer, M Flint Beal and 2 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 61 citations in OpenAlex.

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  20. Evolution of adrenoleukodystrophy model systems.Journal of inherited metabolic disease · 2021
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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

12 authors at 5 institutions in 3 countries.

Pablo Ranea-RoblesNeurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat Barcelona, Spain.ORCID 0000-0001-6478-3815
Nathalie LaunayNeurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat Barcelona, Spain.
Montserrat RuizNeurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat Barcelona, Spain.
Noel Ylagan CalingasanFeil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY, USA.
Magali DumontUMR S 1127, Inserm, U1127, CNRS, UMR 7225, Institut du Cerveau et de la Moelle épinière, Sorbonne Universités, UPMC Université Paris 06, Paris, France.
Alba NaudíExperimental Medicine Department, University of Lleida-IRB Lleida, Lleida, Spain.
Manuel Portero-OtínExperimental Medicine Department, University of Lleida-IRB Lleida, Lleida, Spain.
Reinald PamplonaExperimental Medicine Department, University of Lleida-IRB Lleida, Lleida, Spain.
Isidre FerrerDepartment of Pathology and Experimental Therapeutics, Faculty of Medicine, University of Barcelona, L'Hospitalet de Llobregat Barcelona, Spain.
M Flint BealFeil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY, USA.
Stéphane FourcadeNeurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat Barcelona, Spain sfourcade@idibell.cat apujol@idibell.cat.ORCID 0000-0002-8031-5007
Aurora PujolNeurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat Barcelona, Spain sfourcade@idibell.cat apujol@idibell.cat.ORCID 0000-0002-9606-0600
Instituto de Salud Carlos III · ESUniversitat de Lleida · ESCornell University · USCentre National de la Recherche Scientifique · FRInstitució Catalana de Recerca i Estudis Avançats · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nuclear factor erythroid 2-like 2 (NRF2) is the master regulator of endogenous antioxidant responses. Oxidative damage is a shared and early-appearing feature in X-linked adrenoleukodystrophy (X-ALD) patients and the mouse model (

Indexed as

AdrenoleukodystrophyAnimalsAnti-Inflammatory AgentsAntioxidantsATP Binding Cassette Transporter, Subfamily D, Member 1Dimethyl FumarateDisease Models, AnimalGliosisGlycogen Synthase Kinase 3 betaHumansMaleMiceMice, KnockoutNF-E2-Related Factor 2Organelle BiogenesisOxidative StressAbcd1 protein, mouseAnti-Inflammatory AgentsAntioxidantsATP Binding Cassette Transporter, Subfamily D, Member 1Dimethyl FumarateGlycogen Synthase Kinase 3 betaNFE2L2 protein, humanNfe2l2 protein, mouseNF-E2-Related Factor 2Proto-Oncogene Proteins c-aktReactive Oxygen Speciesadrenoleukodystrophydimethyl fumarateGSK‐3NRF2oxidative stress

Identifiers

PMID29997171
PMCPMC6079538
OpenAlexW2861844602

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.