ArticleJournal of neurochemistry2008
Induction of sulfiredoxin expression and reduction of peroxiredoxin hyperoxidation by the neuroprotective Nrf2 activator 3H-1,2-dithiole-3-thione.
Article in Journal of neurochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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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.
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Who cites it
74 citing papers in PubMed, 137 citations in OpenAlex.
- Crosstalk Between Nrf2 and Metabolic Pathways: Redox Regulation, Glutaminolysis, and Cellular Proliferation.Cell biochemistry and biophysics · 2026Review
- An antioxidant therapy elicits distinct transcriptome responses in 22q11-deleted upper layer cortical projection neurons.Disease models & mechanisms · 2026Article
- The role of histone demethylase PHF2 as a tumour suppressor in hepatocellular carcinoma by regulating SRXN1.Oncogenesis · 2026Article
- Distinct cellular and transcriptional mechanisms mediate an antioxidant therapeutic response in 22q11-deleted upper layer cortical projection neurons.bioRxiv : the preprint server for biology · 2025Article
- SRXN1 is a novel protective factor against methylmercury-induced apoptosis in C17.2 mouse neural stem cells.Toxicological research · 2025Article
- Role of NRF2 in Pathogenesis of Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Altered responsiveness of the antioxidant system in chronically stressed animals: modulation by chronic lurasidone treatment.Psychopharmacology · 2022Article
- Review
- The Potential Role of Curcumin in Modulating the Master Antioxidant Pathway in Diabetic Hypoxia-Induced Complications.Molecules (Basel, Switzerland) · 2021Review
- Genetic mutations and molecular mechanisms of Fuchs endothelial corneal dystrophy.Eye and vision (London, England) · 2021Review
- Article
- Hyperoxidation of Peroxiredoxins and Effects on Physiology ofAntioxidants (Basel, Switzerland) · 2021Article
- Targeted de-repression of neuronal Nrf2 inhibits α-synuclein accumulation.Cell death & disease · 2021Article
- Apigenin-7-Aging · 2020Article
- The Transcriptomic Response of the Murine Thyroid Gland to Iodide Overload and the Role of the Nrf2 Antioxidant System.Antioxidants (Basel, Switzerland) · 2020Article
- Article
- Nrf2 Suppresses Oxidative Stress and Inflammation inMolecular and cellular biology · 2020Article
- Sulfiredoxin as a Potential Therapeutic Target for Advanced and Metastatic Prostate Cancer.Oxidative medicine and cellular longevity · 2020Article
- Loss of Oxidation Resistance 1, OXR1, Is Associated with an Autosomal-Recessive Neurological Disease with Cerebellar Atrophy and Lysosomal Dysfunction.American journal of human genetics · 2019Article
- The redox regulator sulfiredoxin forms a complex with thioredoxin domain-containing 5 protein in response to ER stress in lung cancer cells.The Journal of biological chemistry · 2019Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Peroxiredoxins are an important family of cysteine-based antioxidant enzymes that exert a neuroprotective effect in several models of neurodegeneration. However, under oxidative stress they are vulnerable to inactivation through hyperoxidation of their active site cysteine residues. We show that in cortical neurons, the chemopreventive inducer 3H-1,2-dithiole-3-thione (D3T), that activates the transcription factor Nuclear factor erythroid 2-related factor (Nrf2), inhibits the formation of inactivated, hyperoxidized peroxiredoxins following oxidative trauma, and protects neurons against oxidative stress. In both neurons and glia, Nrf2 expression and treatment with chemopreventive Nrf2 activators, including D3T and sulforaphane, up-regulates sulfiredoxin, an enzyme responsible for reducing hyperoxidized peroxiredoxins. Induction of sulfiredoxin expression is mediated by Nrf2, acting via a cis-acting antioxidant response element (ARE) in its promoter. The ARE element in Srxn1 contains an embedded activator protein-1 (AP-1) site which directs induction of Srxn1 by synaptic activity. Thus, raising Nrf2 activity in neurons prevents peroxiredoxin hyperoxidation and induces a new member of the ARE-gene family, whose enzymatic function of reducing hyperoxidized peroxiredoxins may contribute to the neuroprotective effects of Nrf2 activators.
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Registered trials
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.