ArticleRedox biology2026
Quercetin improves retinal glycolysis to slow myopia progression through orchestrating the AKT/FOXO/HK2 axis.
Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Role of Autophagy in Scleral Remodeling During Form-Deprivation Myopia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Protective effect of Caftaric Acid against hepatic cold ischemia/reperfusion injury in the liver.Biology direct · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesMyopia is a major global public health issue. The retina relies on glycolysis to maintain its normal physiological functions and is vulnerable to oxidative damage. However, the effects of altered glycolysis on myopia progression remain poorly understood. This study aimed to explore how oxidative damage caused by changes in retinal glycolysis promotes myopia and evaluate the potential of quercetin in alleviating this process.
methodsWe used single-cell RNA sequencing to analyze the retinas of myopic guinea pigs, followed by proteomic and phosphoproteomic profiling to identify differentially expressed proteins. We investigated the regulatory role of the AKT/FOXO/HK2 pathway in glycolysis via coimmunoprecipitation and dual-luciferase assays. Additionally, we assessed the role of glycolysis in myopia by overexpressing HK2 and using 2-deoxy-d-glucose (2DG). The effects of neuronal injury on myopia progression were explored using Fos overexpression and knockdown. Finally, after quercetin intervention, we conducted metabolomic analysis and measured retinal mitochondrial pressure and glycolysis rate to evaluate their effects on retinal metabolism.
resultsMultiomics analysis showed that the AKT/FOXO/HK2 pathway suppresses glycolysis during myopia progression. Protein interaction and dual-luciferase assays confirmed that reduced glycolysis promotes oxidative phosphorylation, leading to retinal oxidative damage and accelerating the progression of myopia. Quercetin treatment inhibited the AKT/FOXO/HK2 axis, restored mitochondrial oxygen consumption and glycolysis rates, and mitigated oxidative damage, which subsequently suppressed the activation of stress-responsive Fos. Furthermore, Fos overexpression amplified retinal neuronal injury, apoptosis, and mitochondrial damage to drive myopia progression. Inhibiting Fos expression or quercetin treatment alleviated neuronal injury and apoptosis, thereby inhibiting myopia progression.
conclusionOur findings suggest that quercetin may attenuate myopia progression, at least in part, by modulating the AKT/FOXO/HK2 axis to restore retinal glycolysis, thereby reducing oxidative stress and mitigating retinal neuronal damage and apoptosis. This study lays the groundwork for further exploration metabolic reprogramming in myopia pathogenesis.
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.