ArticleNature communications2018
Correcting glucose-6-phosphate dehydrogenase deficiency with a small-molecule activator.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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.
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Who cites it
66 citing papers in PubMed, 119 citations in OpenAlex.
- Activation of Glucose-6-Phosphate Dehydrogenase Promotes Cardiomyocyte Cell Cycle.Circulation · 2026Article
- PANX2 Suppresses Lung Adenocarcinoma Progression by Inducing Disulfidptosis and Enhancing Antitumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Evidence for G6PD variant classification from multiplexed functional assays.Genome biology · 2026Article
- Cellular Signalling Networks in High Altitude Pulmonary Hypertension: From Canonical Pathways to Emerging Targets.Cell proliferation · 2026Review
- Pentose phosphate pathway fuels cGAS-STING signalling to boost function of intratumoral conventional dendritic cells.Nature communications · 2026Article
- Post-irradiation dietary restriction impairs hematopoiesis via inhibition of the pentose phosphate pathway in hematopoietic stem and progenitor cells.Cell death & disease · 2026Article
- Metabolic changes during cardiac regeneration in the axolotl.Developmental dynamics : an official publication of the American Association of Anatomists · 2026Article
- Insights into Neutrophil Dysfunction in Inherited Metabolic Disorders.Journal of innate immunity · 2026Review
- Evidence forbioRxiv : the preprint server for biology · 2025Article
- Giving an Enzyme Scissors: Serotonin Derivatives as Potent Organocatalytic Switches for DNA Repair Enzyme OGG1.Journal of medicinal chemistry · 2025Article
- A sensory and motor neuropathy caused by a genetic variant ofScience advances · 2025Article
- A live bacteria enzyme assay for identification of human disease mutations and drug screening.Nature biomedical engineering · 2025Article
- Integrated Approach for Biochemical and Functional Characterization of Six Clinical Variants of Glucose-6-Phosphate Dehydrogenase.International journal of molecular sciences · 2025Article
- Precise correction of G6PD Viangchan mutation in iPSCs by prime editing strategy.Scientific reports · 2025Article
- Lactate dehydrogenase B facilitates disulfidptosis and exhaustion of tumour-infiltrating CD8Nature cell biology · 2025Article
- A hidden cysteine in Fis1 targeted to prevent excessive mitochondrial fission and dysfunction under oxidative stress.Nature communications · 2025Article
- NRF2 activation in the heart induces glucose metabolic reprogramming and reduces cardiac dysfunction via upregulation of the pentose phosphate pathway.Cardiovascular research · 2025Article
- Enhancing NADPH to restore redox homeostasis and lysosomal function in G6PD-deficient microglia.Heliyon · 2025Article
- p53-dependent crosstalk between DNA replication integrity and redox metabolism mediated through a NRF2-PARP1 axis.Nucleic acids research · 2024Article
- Histone deacetylase 7 activates 6-phosphogluconate dehydrogenase via an enzyme-independent mechanism that involves the N-terminal protein-protein interaction domain.The Biochemical journal · 2024Article
6 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
10 authors at 5 institutions in 1 country.
Funding
Abstract
Glucose-6-phosphate dehydrogenase (G6PD) deficiency, one of the most common human genetic enzymopathies, is caused by over 160 different point mutations and contributes to the severity of many acute and chronic diseases associated with oxidative stress, including hemolytic anemia and bilirubin-induced neurological damage particularly in newborns. As no medications are available to treat G6PD deficiency, here we seek to identify a small molecule that corrects it. Crystallographic study and mutagenesis analysis identify the structural and functional defect of one common mutant (Canton, R459L). Using high-throughput screening, we subsequently identify AG1, a small molecule that increases the activity of the wild-type, the Canton mutant and several other common G6PD mutants. AG1 reduces oxidative stress in cells and zebrafish. Furthermore, AG1 decreases chloroquine- or diamide-induced oxidative stress in human erythrocytes. Our study suggests that a pharmacological agent, of which AG1 may be a lead, will likely alleviate the challenges associated with G6PD deficiency.
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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.