ReviewAntioxidants & redox signaling2012
Glutathione efflux and cell death.
Review in Antioxidants & redox signaling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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
107 citing papers in PubMed, 240 citations in OpenAlex.
- The mechanism of 45S5 bioactive glass-mediated, cell-type-specific death of bone tumor cells.Cell death discovery · 2026Article
- Cytotoxic and Antimelanoma Activity of Selected 3-Methyl-1,6-diazaphenothiazines in Human Melanoma Cells-In Vitro Studies.Current issues in molecular biology · 2026Article
- Tissue-resident macrophage survival depends on mitochondrial function regulated by SerpinB2 in chronic inflammation.Nature communications · 2026Article
- Current Insights into Glutathione Depletion in Adult Septic Patients.Antioxidants (Basel, Switzerland) · 2025Review
- Plumage polymorphism in the black sparrowhawk (Accipiter melanoleucus) is strongly associated with the expression level of agouti signaling protein.The Journal of heredity · 2025Article
- Vitamin C: From Self-Sufficiency to Dietary Dependence in the Framework of Its Biological Functions and Medical Implications.Life (Basel, Switzerland) · 2025Review
- Effect of soluble dietary fiber extracted fromFrontiers in nutrition · 2025Article
- NFE2L2 and SLC25A39 drive cuproptosis resistance through GSH metabolism.Scientific reports · 2024Article
- Mitigating hemoglobin-induced nephropathy: ApoHb-hp protection of podocytes.Physiological reports · 2024Article
- Modeling the oxygen effect in DNA strand break induced by gamma-rays with TOPAS-nBio.Physics in medicine and biology · 2024Article
- Article
- GSH and Ferroptosis: Side-by-Side Partners in the Fight against Tumors.Antioxidants (Basel, Switzerland) · 2024Review
- Ferroptosis: a critical mechanism of NScience China. Life sciences · 2024Review
- Review
- Article
- A Computational Model of Endogenous Hydrogen Peroxide Metabolism in Hepatocytes, Featuring a Critical Role for GSH.Computational toxicology (Amsterdam, Netherlands) · 2024Article
- Glutathione supplementation improves fat graft survival by inhibiting ferroptosis via the SLC7A11/GPX4 axis.Stem cell research & therapy · 2024Article
- Iron toxicity, ferroptosis and microbiota in Parkinson's disease: Implications for novel targets.Advances in neurotoxicology · 2024Article
- Pharmacological profile of dicaffeoylquinic acids and their role in the treatment of respiratory diseases.Frontiers in pharmacology · 2024Review
- EGR1 Promotes Erastin-induced Ferroptosis Through Activating Nrf2-HMOX1 Signaling Pathway in Breast Cancer Cells.Journal of Cancer · 2024Article
47 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
significanceGlutathione (GSH) depletion is a central signaling event that regulates the activation of cell death pathways. GSH depletion is often taken as a marker of oxidative stress and thus, as a consequence of its antioxidant properties scavenging reactive species of both oxygen and nitrogen (ROS/RNS). RECENT ADVANCES: There is increasing evidence demonstrating that GSH loss is an active phenomenon regulating the redox signaling events modulating cell death activation and progression. CRITICAL ISSUES: In this work, we review the role of GSH depletion by its efflux, as an important event regulating alterations in the cellular redox balance during cell death independent from oxidative stress and ROS/RNS formation. We discuss the mechanisms involved in GSH efflux during cell death progression and the redox signaling events by which GSH depletion regulates the activation of the cell death machinery. FUTURE DIRECTIONS: The evidence summarized here clearly places GSH transport as a central mechanism mediating redox signaling during cell death progression. Future studies should be directed toward identifying the molecular identity of GSH transporters mediating GSH extrusion during cell death, and addressing the lack of sensitive approaches to quantify GSH efflux.
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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.