Evidence map›Paper›PMID 34502501›Full record

ReviewInternational journal of molecular sciences2021

An Overview of the Nrf2/ARE Pathway and Its Role in Neurodegenerative Diseases.

Emilia Zgorzynska, Barbara Dziedzic, Anna Walczewska

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed
8.6field-weighted citation impact, top 1% 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

109 citing papers in PubMed, 171 citations in OpenAlex.

  1. Review
  2. International journal of molecular sciences · 2026
    Review
  3. Obstacles and Trials in Treating Primary Brain Tumors.International journal of molecular sciences · 2026
    Review
  4. Nrf2 signaling pathway and its molecular regulatory mechanism.Journal of Zhejiang University. Science. B · 2026
    Review
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49 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Emilia ZgorzynskaDepartment of Cell-to-Cell Communication, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland.ORCID 0000-0002-5411-3778
Barbara DziedzicDepartment of Cell-to-Cell Communication, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland.ORCID 0000-0002-4122-4882
Anna WalczewskaDepartment of Cell-to-Cell Communication, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland.
Medical University of Lodz · PL

Funding

Uniwersytet Medyczny w Lodzi 502-03/0-079-04/502-04-035Uniwersytet Medyczny w Lodzi 503/0-079-04/503-01-001
6 · The paper itself

Abstract

Nrf2 is a basic region leucine-zipper transcription factor that plays a pivotal role in the coordinated gene expression of antioxidant and detoxifying enzymes, promoting cell survival in adverse environmental or defective metabolic conditions. After synthesis, Nrf2 is arrested in the cytoplasm by the Kelch-like ECH-associated protein 1 suppressor (Keap1) leading Nrf2 to ubiquitin-dependent degradation. One Nrf2 activation mechanism relies on disconnection from the Keap1 homodimer through the oxidation of cysteine at specific sites of Keap1. Free Nrf2 enters the nucleus, dimerizes with small musculoaponeurotic fibrosarcoma proteins (sMafs), and binds to the antioxidant response element (ARE) sequence of the target genes. Since oxidative stress, next to neuroinflammation and mitochondrial dysfunction, is one of the hallmarks of neurodegenerative pathologies, a molecular intervention into Nrf2/ARE signaling and the enhancement of the transcriptional activity of particular genes are targets for prevention or delaying the onset of age-related and inherited neurogenerative diseases. In this study, we review evidence for the Nrf2/ARE-driven pathway dysfunctions leading to various neurological pathologies, such as Alzheimer's, Parkinson's, and Huntington's diseases, as well as amyotrophic lateral sclerosis, and the beneficial role of natural and synthetic molecules that are able to interact with Nrf2 to enhance its protective efficacy.

Indexed as

Alzheimer DiseaseAntioxidant Response ElementsAntioxidantsHumansHuntington DiseaseKelch-Like ECH-Associated Protein 1Neurodegenerative DiseasesNF-E2-Related Factor 2Oxidative StressSignal TransductionAntioxidantsKEAP1 protein, humanKelch-Like ECH-Associated Protein 1NFE2L2 protein, humanNF-E2-Related Factor 2Alzheimer’s diseaseamyotrophic lateral sclerosisHuntington’s diseaseKeap1neurodegenerative diseasesneuroprotectionNrf2oxidative stressParkinson’s disease

Identifiers

PMID34502501
PMCPMC8431732
OpenAlexW3198533851

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.