ArticleScientific reports2016
Pharmacological targeting of glucose-6-phosphate dehydrogenase in human erythrocytes by Bay 11-7082, parthenolide and dimethyl fumarate.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- Molecular mechanisms and targeted therapeutic strategies for glycolytic reprogramming in osteosarcoma.Genes & diseases · 2027Review
- Tasisulam-induced suicidal death of human erythrocytes.Biochemistry and biophysics reports · 2026Article
- Redefining the concept of erythrocyte senescence: is eryptosis fundamentally different from erythrocyte senescence.GeroScience · 2025Review
- Current understanding of eryptosis: mechanisms, physiological functions, role in disease, pharmacological applications, and nomenclature recommendations.Cell death & disease · 2025Review
- Glucose-6-phosphate dehydrogenase regulates mitophagy by maintaining PINK1 stability.Life metabolism · 2025Article
- Inheritance of Hb S and G6PD deficiency in a familiar group.Archives of medical science : AMS · 2024Article
- Relationships between blood bone metabolic biomarkers and anemia in patients with chronic kidney disease.Renal failure · 2023Article
- Desipramine induces eryptosis in human erythrocytes, an effect blunted by nitric oxide donor sodium nitroprusside and N-acetyl-L-cysteine but enhanced by Calcium depletion.Cell cycle (Georgetown, Tex.) · 2023Article
- Casein kinase 1α mediates eryptosis: a review.Apoptosis : an international journal on programmed cell death · 2023Review
- Article
- Myostatin Knockout Limits Exercise-Induced Reduction in Bovine Erythrocyte Oxidative Stress by Enhancing the Efficiency of the Pentose Phosphate Pathway.Animals : an open access journal from MDPI · 2022Article
- Review
- Preliminary Study of Structural Changes of Glucose-6-Phosphate Dehydrogenase Deficiency Variants.BioMedicine · 2022Article
- Human erythrocytes, nuclear factor kappaB (NFκB) and hydrogen sulfide (HCell cycle (Georgetown, Tex.) · 2021Article
- The specific PKC-α inhibitor chelerythrine blunts costunolide-induced eryptosis.Apoptosis : an international journal on programmed cell death · 2020Article
- Targeting immunometabolism as an anti-inflammatory strategy.Cell research · 2020Review
- Proliferating tumor cells mimick glucose metabolism of mature human erythrocytes.Cell cycle (Georgetown, Tex.) · 2019Review
- Target identification reveals protein arginine methyltransferase 1 is a potential target of phenyl vinyl sulfone and its derivatives.Bioscience reports · 2018Article
- Signaling Pathways Regulating Redox Balance in Cancer Metabolism.Frontiers in oncology · 2018Review
- Manipulating Eryptosis of Human Red Blood Cells: A Novel Antimalarial Strategy?Frontiers in cellular and infection microbiology · 2018Review
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Authors and funding
15 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mature erythrocytes, glucose-6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate dehydrogenase (6PGDH) yield NADPH, a crucial cofactor of the enzyme glutathione reductase (GR) converting glutathione disulfide (GSSG) into its reduced state (GSH). GSH is essential for detoxification processes in and survival of erythrocytes. We explored whether the anti-inflammatory compounds Bay 11-7082, parthenolide and dimethyl fumarate (DMF) were able to completely deplete a common target (GSH), and to impair the function of upstream enzymes of GSH recycling and replenishment. Treatment of erythrocytes with Bay 11-7082, parthenolide or DMF led to concentration-dependent eryptosis resulting from complete depletion of GSH. GSH depletion was due to strong inhibition of G6PDH activity. Bay 11-7082 and DMF, but not parthenolide, were able to inhibit the GR activity. This approach "Inhibitors, Detection of their common target that is completely depleted or inactivated when pharmacologically relevant concentrations of each single inhibitor are applied, Subsequent functional analysis of upstream enzymes for this target" (IDS), can be applied to a broad range of inhibitors and cell types according to the selected target. The specific G6PDH inhibitory effect of these compounds may be exploited for the treatment of human diseases with high NADPH and GSH consumption rates, including malaria, trypanosomiasis, cancer or obesity.
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