ReviewAntioxidants & redox signaling2017
Redox Signaling Mediated by Thioredoxin and Glutathione Systems in the Central Nervous System.
Review in Antioxidants & redox signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers, 2 of them syntheses that pooled it.
What it found
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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.
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.
Who cites it
167 citing papers in PubMed, 2 syntheses or guidelines pooled it, 333 citations in OpenAlex.
- Glutathione in Skin Aging and Tissue Regeneration: A Systematic Review of Molecular Mechanisms, Redox Modulation, and Biomedical Implications.Molecules (Basel, Switzerland) · 2026Pooled it
- Involvement of heat shock proteins HSP70 in the mechanisms of endogenous neuroprotection: the prospect of using HSP70 modulators.Frontiers in cellular neuroscience · 2023Pooled it
- The central role of mitochondrial dysfunction in neurodegeneration: implications for therapy.Molecular and cellular biochemistry · 2026Review
- Crosstalk of thioredoxin system and programmed cell death: from pathophysiology to novel therapy.Redox biology · 2026Review
- How Polyphenol Metabolites Spatiotemporally Reprogram Transcription Factors and Human Proteostasis: A Metabolite-Centric Framework.Current issues in molecular biology · 2026Review
- Redox rewiring in glioblastoma: the thioredoxin system as a precision therapeutic target.Pharmacological reports : PR · 2026Review
- EndMT in vascular cognitive impairment and dementia: mechanisms, evidence gaps, and therapeutic opportunities.Molecular medicine (Cambridge, Mass.) · 2026Review
- Sensing and Filtering Environmental Fluctuations: The Case of Biomolecular Condensates in Plants.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Monitoring in real time and far-red imaging of HNature chemical biology · 2026Article
- Combined Expression of hRdCVF and hRdCVFL Through AAV-Mediated Delivery for the Treatment of Retinitis Pigmentosa.Investigative ophthalmology & visual science · 2026Article
- Active Components ofAntioxidants (Basel, Switzerland) · 2026Article
- Pathophysiology of reactive oxygen species (ROS).Archives of toxicology · 2026Review
- Reactive oxygen species promotion drives auranofin's antiviral activity against hepatitis E virus.Journal of virology · 2026Article
- Review
- Therapeutic potential of pycnogenol: antioxidant, anti-inflammatory, immunomodulatory, antiviral, and anticancer effects.Frontiers in pharmacology · 2026Review
- Evaluation of Oxidative Stress and Antioxidant Effects of Methylxanthines in Adult Zebrafish Exposed to Zinc Oxide Nanoparticles (ZnO-NPs).Medicina (Kaunas, Lithuania) · 2025Article
- Mercury-induced neurotoxicity in rat: in vivo and in silico studies of thymoquinone modulatory effect via oxidative stress and inflammation, HO-1/NRF/Trx/Trx-R trajectories.BMC veterinary research · 2025Article
- Review
- Investigation of the effects of monosodium glutamate and tannic acid on the glutathione and thioredoxin systems in the liver of rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- SOD1, A Crucial Protein for Neural Biochemistry: Dysfunction and Risk of Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2025Review
107 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
significanceThe thioredoxin (Trx) and glutathione (GSH) systems play important roles in maintaining the redox balance in the brain, a tissue that is prone to oxidative stress due to its high-energy demand. These two disulfide reductase systems are active in various areas of the brain and are considered to be critical antioxidant systems in the central nervous system (CNS). Various neuronal disorders have been characterized to have imbalanced redox homeostasis. Recent Advances: In addition to their detrimental effects, recent studies have highlighted that reactive oxygen species/reactive nitrogen species (ROS/RNS) act as critical signaling molecules by modifying thiols in proteins. The Trx and GSH systems, which reversibly regulate thiol modifications, regulate redox signaling involved in various biological events in the CNS. CRITICAL ISSUES: In this review, we focus on the following: (i) how ROS/RNS are produced and mediate signaling in CNS; (ii) how Trx and GSH systems regulate redox signaling by catalyzing reversible thiol modifications; (iii) how dysfunction of the Trx and GSH systems causes alterations of cellular redox signaling in human neuronal diseases; and (iv) the effects of certain small molecules that target thiol-based signaling pathways in the CNS. FUTURE DIRECTIONS: Further study on the roles of thiol-dependent redox systems in the CNS will improve our understanding of the pathogenesis of many human neuronal disorders and also help to develop novel protective and therapeutic strategies against neuronal diseases. Antioxid. Redox Signal. 27, 989-1010.
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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.