ArticleInternational journal of molecular sciences2025
Acute Hyperglycemia-Induced Inflammation in MIO-M1 Cells: The Role of Aldose Reductase.
Article in International journal of molecular sciences, 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
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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
7 citing papers in PubMed.
- Beyond Glucose: Palmitic Acid Influences VEGFA-VEGFR2 Angiogenic Signaling in Müller Glial Cells.International journal of molecular sciences · 2026Article
- Metabolic Detoxification of Glucose and 4-Hydroxynonenal in Human Neuroblastoma Cell Models.Antioxidants (Basel, Switzerland) · 2026Article
- ExploringMolecules (Basel, Switzerland) · 2026Article
- Systemic Inflammation Mediates the Association Between Admission Hyperglycemia and Pulmonary Infection or Prognosis in Acute Ischemic Stroke.Mediators of inflammation · 2026Article
- Epigenetic dichotomy in florid vs. gliotic proliferative diabetic retinopathy: hypomethylation of EGLN1 and MMP9 drives divergent pathogenic pathways in angiogenesis and fibrosis.Frontiers in endocrinology · 2026Article
- Aldose Reductase Involvement in EMT: Emerging Insights and Current Proposed Molecular Mechanisms.Biology · 2025Review
- Hyperglycemia Modulates mTOR Signaling and Myelin Protein Expression in Schwann Cells.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Diabetic retinopathy (DR), traditionally considered a microvascular complication, is now recognized as a neuroinflammatory disorder involving retinal glial cells. Aldose reductase (AKR1B1), a key enzyme in the polyol pathway, has been implicated in the hyperglycemia-induced inflammatory response in various cell types, although its role in retinal Müller glial cells under acute glucose stress remains unclear. This study investigates AKR1B1 activity and its contribution to inflammatory signaling in MIO-M1 human Müller cells exposed to acute hyperglycemia. AKR1B1 expression and activity, as well as NF-κB activation and COX-2 expression, were evaluated. Sorbinil, a specific AKR1B1 inhibitor, was used to determine the enzyme's contribution to acute hyperglycemia-induced inflammation. Acute high-glucose treatment significantly increased AKR1B1 activity and sorbitol accumulation without affecting cell viability. In addition, activation of NF-κB and increased expression of cyclooxygenase-2 (COX-2) were observed, both of which were significantly reduced by Sorbinil. Our findings highlight the role of macroglia as active contributors to early inflammatory events in DR and suggest that transient hyperglycemic spikes are sufficient to trigger AKR1B1-dependent glial activation.
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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.