ReviewAntioxidants (Basel, Switzerland)2022
Protein Glutathionylation and Glutaredoxin: Role in Neurodegenerative Diseases.
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 23 papers.
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
23 citing papers in PubMed, 34 citations in OpenAlex.
- Glutathione Biology in Neurodegenerative and Metabolic Diseases: Molecular Mechanisms, Pathophysiological Roles, and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Redox Molecules in Aging and Neurodegenerative Disorders.International journal of molecular sciences · 2026Review
- Metabolic drivers of genome instability in cancer: mechanisms and therapeutic opportunities.Experimental hematology & oncology · 2026Review
- Salivary Oxidative Stress and Antioxidant Markers in Oral Leukoplakia: A Systematic Review and Meta-Analysis.Antioxidants (Basel, Switzerland) · 2026Review
- Genome-wide identification and expression analysis under selenium stress of glutaredoxin system genes in Cardamine hupingshanensis.BMC plant biology · 2026Article
- Serum Aberrant Expression of miR-431-5p and Their Diagnostic Value in Parkinson's Disease.Neurochemical research · 2026Article
- Post-translational modifications in ferroptosis: mechanisms and therapeutic potential.International journal of biological sciences · 2026Review
- Changes in the brain [NADFrontiers in aging neuroscience · 2026Review
- Glutaredoxin 2 Protects Lens Epithelial Cells From Ferroptosis by Preventing HNRNPA2B1 S-Glutathionylation in Diabetes-Mediated Cataractogenesis.Investigative ophthalmology & visual science · 2025Article
- PSMD4 Alleviates Aβ₁₋₄₂-Induced Mitochondrial Dysfunction and Oxidative Stress via the PGC-1α/Nrf Axis in Alzheimer's Disease Models.Molecular neurobiology · 2025Article
- Molecular signatures of disulfidptosis: interplay with programmed cell death pathways and therapeutic implications in oncology.Cellular & molecular biology letters · 2025Review
- Protein S-glutathionylation confers cellular resistance to ferroptosis induced by glutathione depletion.Redox biology · 2025Article
- HSPBiomedicines · 2025Article
- Redox Regulation of cAMP-Dependent Protein Kinase and Its Role in Health and Disease.Life (Basel, Switzerland) · 2025Review
- Influence of the Degree of Unsaturation in Fish Oil Supplements on Oxidative Stress and Protein Carbonylation in the Cerebral Cortex and Cerebellum of Healthy Rats.Antioxidants (Basel, Switzerland) · 2024Article
- Disulfide stress and its role in cardiovascular diseases.Redox biology · 2024Review
- Role of the telomeric factor TRF2 in post-hypoxic brain damages.Redox biology · 2024Article
- The Interplay of Protein Aggregation, Genetics, and Oxidative Stress in Alzheimer's Disease: Role for Natural Antioxidants and Immunotherapeutics.Antioxidants (Basel, Switzerland) · 2024Review
- Protein Oxidative Modifications in Neurodegenerative Diseases: From Advances in Detection and Modelling to Their Use as Disease Biomarkers.Antioxidants (Basel, Switzerland) · 2024Review
- Glutaredoxin 2 Protein (Grx2) as an Independent Prognostic Factor Associated with the Survival of Colon Adenocarcinoma Patients.International journal of molecular sciences · 2024Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress has been implicated in the pathogenesis and progression of many neurodegenerative disorders including Parkinson's disease and Alzheimer's disease. One of the major enzyme systems involved in the defense against reactive oxygen species are the tripeptide glutathione and oxidoreductase glutaredoxin. Glutathione and glutaredoxin system are very important in the brain because of the oxidative modification of protein thiols to protein glutathione mixed disulfides with the concomitant formation of oxidized glutathione during oxidative stress. Formation of Pr-SSG acts as a sink in the brain and is reduced back to protein thiols during recovery, thus restoring protein functions. This is unlike in the liver, which has a high turnover of glutathione, and formation of Pr-SSG is very minimal as liver is able to quickly quench the prooxidant species. Given the important role glutathione and glutaredoxin play in the brain, both in normal and pathologic states, it is necessary to study ways to augment the system to help maintain the protein thiol status. This review details the importance of glutathione and glutaredoxin systems in several neurodegenerative disorders and emphasizes the potential augmentation of this system as a target to effectively protect the brain during aging.
Indexed as
Identifiers
What OpenQuestion holds
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.