ReviewBiological psychiatry2020
Potential Roles of Redox Dysregulation in the Development of Schizophrenia.
Review in Biological psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 2 of them syntheses that pooled 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.
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
61 citing papers in PubMed, 2 syntheses or guidelines pooled it, 100 citations in OpenAlex.
- The role of anti-inflammatory diets and supplementation in metabolic syndrome and symptom remission in adults with schizophrenia: a systematic review.Frontiers in psychiatry · 2024Pooled it
- Matrix Metalloproteinase 9 Blood Alterations in Patients With Schizophrenia Spectrum Disorders: A Systematic Review and Meta-Analysis.Schizophrenia bulletin · 2021Pooled it
- Pilot study indicates that a gluten-free diet lowers oxidative stress for gluten-sensitive persons with schizophrenia.Schizophrenia research · 2024Trial
- Accelerated aging in schizophrenia: integrating epigenetic clocks, telomere dynamics, senescence-associated secretory phenotype, and oxidative stress.European archives of psychiatry and clinical neuroscience · 2026Review
- Redox Homeostasis and Oxidative Stress in Schizophrenia: Glutathione-NMDA-Neuroimmune Convergence and a Hypothesis-Generating Iron-Lipid Redox Extension.International journal of molecular sciences · 2026Review
- Glutathione deficiency in the early postnatal developmental period as a neurodevelopmental animal model of schizophrenia.Pharmacological reports : PR · 2026Review
- Transcription Factors in the Pathogenesis of Schizophrenia.Life (Basel, Switzerland) · 2026Review
- Novel drug treatments for schizophrenia.Nature reviews. Drug discovery · 2026Review
- Effects of Liposome-Encapsulated α-Pinene on In Vitro Oocyte Maturation and Embryo Development in Bovine Species.Molecular reproduction and development · 2026Article
- Altered lipid peroxidation, perineuronal net and oligodendrocyte markers in the frontal cortex of a dual-hit neurodevelopmental model support its relevance to schizophrenia.Frontiers in cellular neuroscience · 2026Article
- Curcumin as an Antioxidant Against Ziprasidone Induced Lipid Peroxidation in Human Plasma: Potential Relevance to Cortico Subcortical Circuit Function.International journal of molecular sciences · 2025Article
- The antioxidant N-acetylcysteine prevents cortical neuropathological phenotypes caused by adolescent Δ-9-tetrahydrocannabinol exposure in male rats.Translational psychiatry · 2025Article
- Electrochemistry as a Tool for Redox-Based Bio-Information Processing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Association of GRM7 Polymorphisms with Bilateral Auditory Regions Glutamate and Coupling with Glutathione in ARHL Patients.Molecular neurobiology · 2025Article
- Novel chlorine-containing curcumin analogue CAK06 promotes neuroprotection and rapid antidepressant through Nrf2-induced anti-inflammatory and antioxidant effects.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Measuring oxidative stress by the iridium reducing capacity assay (Ir-RCA).Advances in redox research · 2025Article
- Body fluid biomarkers and psychosis risk in The Accelerating Medicines Partnership® Schizophrenia Program: design considerations.Schizophrenia (Heidelberg, Germany) · 2025Article
- Adolescent Stress-Induced Ventral Hippocampus Redox Dysregulation Underlies Behavioral Deficits and Excitatory/Inhibitory Imbalance Related to Schizophrenia.Schizophrenia bulletin · 2025Article
- Can artificial intelligence be the future solution to the enormous challenges and suffering caused by Schizophrenia?Schizophrenia (Heidelberg, Germany) · 2025Review
- Corticolimbic circuitry as a druggable target in schizophrenia spectrum disorders: a narrative review.Translational psychiatry · 2025Review
1 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
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Converging evidence implicates redox dysregulation as a pathological mechanism driving the emergence of psychosis. Increased oxidative damage and decreased capacity of intracellular redox modulatory systems are consistent findings in persons with schizophrenia as well as in persons at clinical high risk who subsequently developed frank psychosis. Levels of glutathione, a key regulator of cellular redox status, are reduced in the medial prefrontal cortex, striatum, and thalamus in schizophrenia. In humans with schizophrenia and in rodent models recapitulating various features of schizophrenia, redox dysregulation is linked to reductions of parvalbumin containing gamma-aminobutyric acid (GABA) interneurons and volumes of their perineuronal nets, white matter abnormalities, and microglia activation. Importantly, the activity of transcription factors, kinases, and phosphatases regulating diverse aspects of neurodevelopment and synaptic plasticity varies according to cellular redox state. Molecules regulating interneuron function under redox control include NMDA receptor subunits GluN1 and GluN2A as well as KEAP1 (regulator of transcription factor NRF2). In a rodent schizophrenia model characterized by impaired glutathione synthesis, the Gclm knockout mouse, oxidative stress activated MMP9 (matrix metalloprotease 9) via its redox-responsive regulatory sites, causing a cascade of molecular events leading to microglia activation, perineural net degradation, and impaired NMDA receptor function. Molecular pathways under redox control are implicated in the etiopathology of schizophrenia and are attractive drug targets for individualized drug therapy trials in the contexts of prevention and treatment of psychosis.
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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.