Evidence map›Paper›PMID 34663413›Full record

ReviewMolecular neurodegeneration2021

Impaired antioxidant KEAP1-NRF2 system in amyotrophic lateral sclerosis: NRF2 activation as a potential therapeutic strategy.

Silvia Bono, Marco Feligioni, Massimo Corbo

Open access · goldAbstract readReview
In one paragraph

Review in Molecular neurodegeneration, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 73 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

3 authors at 3 institutions in 1 country.

Silvia BonoNeed Institute, Laboratory of Neurobiology for Translational Medicine, c/o Casa di Cura del Policlinico (CCP), Via Dezza 48, 20144, Milan, Italy. silvia.bono@needinstitute.org.ORCID 0000-0002-5958-4499
Marco FeligioniNeed Institute, Laboratory of Neurobiology for Translational Medicine, c/o Casa di Cura del Policlinico (CCP), Via Dezza 48, 20144, Milan, Italy.
Massimo CorboDepartment of Neurorehabilitation Sciences, Casa di Cura del Policlinico (CCP), Via Dezza 48, 20144, Milan, Italy. m.corbo@ccppdezza.it.ORCID 0000-0003-0793-9830
Casa di Cura Columbus · ITCentro Clinico Nemo · ITEuropean Brain Research Institute · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOxidative stress (OS) is an imbalance between oxidant and antioxidant species and, together with other numerous pathological mechanisms, leads to the degeneration and death of motor neurons (MNs) in amyotrophic lateral sclerosis (ALS). MAIN BODY: Two of the main players in the molecular and cellular response to OS are NRF2, the transcription nuclear factor erythroid 2-related factor 2, and its principal negative regulator, KEAP1, Kelch-like ECH (erythroid cell-derived protein with CNC homology)-associated protein 1. Here we first provide an overview of the structural organization, regulation, and critical role of the KEAP1-NRF2 system in counteracting OS, with a focus on its alteration in ALS. We then examine several compounds capable of promoting NRF2 activity thereby inducing cytoprotective effects, and which are currently in different stages of clinical development for many pathologies, including neurodegenerative diseases.

conclusionsAlthough challenges associated with some of these compounds remain, important advances have been made in the development of safer and more effective drugs that could actually represent a breakthrough for fatal degenerative diseases such as ALS.

Indexed as

Amyotrophic Lateral SclerosisNF-E2-Related Factor 2Oxidative StressAntioxidantsHumansKelch-Like ECH-Associated Protein 1Signal TransductionAntioxidantsKEAP1 protein, humanKelch-Like ECH-Associated Protein 1NFE2L2 protein, humanNF-E2-Related Factor 2Amyotrophic lateral sclerosisAntioxidantKEAP1-NRF2NeuroprotectionOxidative stressTherapeutic target

Identifiers

PMID34663413
PMCPMC8521937
OpenAlexW3207478950

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.