ArticleHeliyon2025
Enhancing NADPH to restore redox homeostasis and lysosomal function in G6PD-deficient microglia.
Article in Heliyon, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Disulfidptosis: Mechanisms, evidence boundaries, and translational opportunities.Redox biology · 2026Review
- Microglial Immunometabolic Remodeling After Ischemic Stroke: The Interplay Between Mitochondrial Stress and the Ischemic Microenvironment.Translational stroke research · 2026Review
- Redox Molecules in Aging and Neurodegenerative Disorders.International journal of molecular sciences · 2026Review
- NADPH Dehydrogenase Gene Regulates Energy Distribution and Fatty Acid Metabolism During Fruiting Body Formation in the Filamentous Fungus Podospora anserina.Microbial biotechnology · 2026Article
- LDHA protects vascular endothelial cells from oxidative stress‑induced mitochondrial damage via HIF‑1α activation and glycolytic reprogramming.Molecular medicine reports · 2026Article
- G6PD deficiency as a underrecognized genetic risk factor for rare neurological disorders: evidence from a population-based genetic analysis.Frontiers in genetics · 2026Article
- The research progress on the role of glucose-6-phosphate dehydrogenase in immune regulation.PeerJ · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglia, the immune cells of the central nervous system (CNS), play key roles in neurogenesis, myelination, synaptic transmission, immune surveillance, and neuroinflammation. Inflammatory responses in microglia can lead to oxidative stress and neurodegeneration, contributing to diseases like Parkinson's and Alzheimer's. The enzyme glucose-6-phosphate dehydrogenase (G6PD) is essential for producing nicotinamide adenine dinucleotide phosphate hydrogen (NADPH), which neutralizes oxidative stress. G6PD deficiency has been linked to several disorders, including neurological conditions. Our study shows that G6PD deficiency in microglia reduces NADPH levels, disrupting redox balance and lysosomal function. To address this, we explored alternative metabolic pathways by targeting enzymes like isocitrate dehydrogenase 1 (IDH1) and malic enzyme 1 (ME1), both crucial for NADPH production. Supplementing metabolites such as citric and malic acid improved NADPH levels, while small molecules like dieckol and resveratrol enhanced IDH1 and ME1 expression. The combination of these approaches restored redox homeostasis and lysosomal function, offering potential therapeutic strategies for G6PD deficiency.
Indexed as
Identifiers
What Socratic 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 Socratic graph.