Evidence map›Paper›PMID 36139853›Full record

ReviewAntioxidants (Basel, Switzerland)2022

Harnessing the Therapeutic Potential of the Nrf2/Bach1 Signaling Pathway in Parkinson's Disease.

Manuj Ahuja, Navneet Ammal Kaidery, Debashis Dutta, Otis C Attucks, Eliot H Kazakov, Irina Gazaryan, Mitsuyo Matsumoto, Kazuhiko Igarashi, Sudarshana M Sharma, Bobby Thomas

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Intersection of HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  3. Article
  4. Article
  5. Nrf2/Bach1 signaling axis: A promising multifaceted therapeutic strategy for Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  6. Review
  7. Review
  8. Reinforcing Nrf2 Signaling: Help in the Alzheimer's Disease Context.International journal of molecular sciences · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. The Nrf2-HO-1 system and inflammaging.Frontiers in immunology · 2024
    Review
  15. Emerging small molecule inhibitors of Bach1 as therapeutic agents: Rationale, recent advances, and future perspectives.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
    Article
  16. Review
  17. Article
  18. Implications of the Cultivation of Rosemary and Thyme (International journal of molecular sciences · 2023
    Article
  19. Review
  20. Review
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

10 authors at 5 institutions in 3 countries.

Manuj AhujaDarby Children's Research Institute, Medical University of South Carolina, Charleston, SC 29406, USA.
Navneet Ammal KaideryDarby Children's Research Institute, Medical University of South Carolina, Charleston, SC 29406, USA.
Debashis DuttaDarby Children's Research Institute, Medical University of South Carolina, Charleston, SC 29406, USA.
Otis C AttucksvTv Therapeutics LLC, High Point, NC 27263, USA.
Eliot H KazakovFordham University, Bronx, NY 10452, USA.
Irina GazaryanPace University, White Plains, NY 10601, USA.
Mitsuyo MatsumotoDepartment of Biochemistry, Graduate School of Medicine, Tohoku University, Sendai 980-8576, Japan.
Kazuhiko IgarashiDepartment of Biochemistry, Graduate School of Medicine, Tohoku University, Sendai 980-8576, Japan.
Sudarshana M SharmaDepartment of Biochemistry & Molecular Biology, Medical University of South Carolina, Charleston, SC 29406, USA.
Bobby ThomasDarby Children's Research Institute, Medical University of South Carolina, Charleston, SC 29406, USA.ORCID 0000-0001-9244-9726
Medical University of South Carolina · USTohoku University · JPFordham University · USNational Research University Higher School of Economics · RUvTv Therapeutics (United States) · US

Funding

Neuroprotective mechanisms of Bach1-Derepression in Alzheimer’s DiseaseRF1AG077396 · NIA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LEE, MICHAEL K, THOMAS, BOBBY · 2022 to 2022
$2.3M
Role of Bach-1-Mediated Transcriptional Regulation in NeuroprotectionR01NS101967 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI THOMAS, BOBBY · 2017 to 2021
$1.9M
Neuroprotective mechanisms of Bach1-Derepression in Alzheimer’s DiseaseR01AG077396 · NIA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MICHAEL K LEE, Bobby Thomas · 2025 to 2026
$1.5M
NIA NIH HHS R01 AG077396NIA NIH HHS RF1 AG077396NINDS NIH HHS R01 NS101967
6 · The paper itself

Abstract

Parkinson's disease (PD) is the second most common neurodegenerative movement disorder characterized by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Although a complex interplay of multiple environmental and genetic factors has been implicated, the etiology of neuronal death in PD remains unresolved. Various mechanisms of neuronal degeneration in PD have been proposed, including oxidative stress, mitochondrial dysfunction, neuroinflammation, α-synuclein proteostasis, disruption of calcium homeostasis, and other cell death pathways. While many drugs individually targeting these pathways have shown promise in preclinical PD models, this promise has not yet translated into neuroprotective therapies in human PD. This has consequently spurred efforts to identify alternative targets with multipronged therapeutic approaches. A promising therapeutic target that could modulate multiple etiological pathways involves drug-induced activation of a coordinated genetic program regulated by the transcription factor, nuclear factor E2-related factor 2 (Nrf2). Nrf2 regulates the transcription of over 250 genes, creating a multifaceted network that integrates cellular activities by expressing cytoprotective genes, promoting the resolution of inflammation, restoring redox and protein homeostasis, stimulating energy metabolism, and facilitating repair. However, FDA-approved electrophilic Nrf2 activators cause irreversible alkylation of cysteine residues in various cellular proteins resulting in side effects. We propose that the transcriptional repressor of BTB and CNC homology 1 (Bach1), which antagonizes Nrf2, could serve as a promising complementary target for the activation of both Nrf2-dependent and Nrf2-independent neuroprotective pathways. This review presents the current knowledge on the Nrf2/Bach1 signaling pathway, its role in various cellular processes, and the benefits of simultaneously inhibiting Bach1 and stabilizing Nrf2 using non-electrophilic small molecules as a novel therapeutic approach for PD.

Indexed as

antioxidantsBach1electrophileNrf2oxidative stressParkinson’s disease

Identifiers

PMID36139853
PMCPMC9495572
OpenAlexW4295548120

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.