ArticleChemico-biological interactions2019
Role of aldose reductase in diabetes-induced retinal microglia activation.
Article in Chemico-biological interactions, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Effects of diabetes on microglial physiology: a systematic review of in vitro, preclinical and clinical studies.Journal of neuroinflammation · 2023Pooled it
- Aldose reductase as a regulator of ocular pathology: Mechanisms and therapeutic potential.Histology and histopathology · 2026Review
- The NFAT5-AR Axis Is Associated with Hyperosmolarity, Renal Dysfunction, and Neutrophil-Related Inflammatory Markers in Diabetic Retinopathy.International journal of molecular sciences · 2026Article
- Investigating the role of the ALPK1 signaling pathway in the pathogenesis of diabetic retinopathy.Scientific reports · 2025Article
- Efficacy and Safety of Femtosecond Laser-Assisted Cataract Surgery with the Catalys Platform in Patients with Type 2 Diabetes and Cataract: A Prospective Cohort Study.Ophthalmology and therapy · 2025Article
- "ArmedFrontiers in cell and developmental biology · 2025Review
- TargetingFrontiers in bioinformatics · 2025Article
- Redefining our vision: an updated guide to the ocular immune system.Nature reviews. Immunology · 2024Review
- Nicotinamide and Nicotinoyl-Gamma-Aminobutyric Acid as Neuroprotective Agents Against Type 1 Diabetes-Induced Nervous System Impairments in Rats.Neurochemical research · 2024Article
- Müller Cells Harboring Exosomal lncRNA OGRU Modulate Microglia Polarization in Diabetic Retinopathy by Serving as miRNA Sponges.Diabetes · 2024Article
- Macrophage activation contributes to diabetic retinopathy.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Aldose reductase is a potential therapeutic target for neurodegeneration.Chemico-biological interactions · 2024Review
- Article
- Updating the Pharmacological Effects of α-Mangostin Compound and Unraveling Its Mechanism of Action: A Computational Study Review.Drug design, development and therapy · 2024Review
- Inhibition of the polyol pathway byFrontiers in pharmacology · 2024Article
- Elucidating glial responses to products of diabetes-associated systemic dyshomeostasis.Progress in retinal and eye research · 2023Review
- The Role of Aldose Reductase in Beta-Amyloid-Induced Microglia Activation.International journal of molecular sciences · 2022Article
- Stem cell therapy for central nervous system disorders: Metabolic interactions between transplanted cells and local microenvironments.Neurobiology of disease · 2022Review
- Reducing host aldose reductase activity promotes neuronal differentiation of transplanted neural stem cells at spinal cord injury sites and facilitates locomotion recovery.Neural regeneration research · 2022Article
- PPARɣ2, aldose reductase, and TCF7L2 gene polymorphisms: relation to diabetes mellitus.Journal of diabetes and metabolic disorders · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Diabetes-induced hyperglycemia plays a key pathogenic role in degenerative retinal diseases. In diabetic hyperglycemia, aldose reductase (AR) is elevated and linked to the pathogenesis of diabetic retinopathy (DR) and cataract. Retinal microglia (RMG), the resident immune cells in the retina, are thought to contribute to the proinflammatory phenotype in the diabetic eye. However, we have a limited understanding of the potential role of AR expressed in RMG as a mediator of inflammation in the diabetic retina. Glycated proteins accumulate in diabetes, including Amadori-glycated albumin (AGA) which has been shown to induce a proinflammatory phenotype in various tissues. In this study, we investigated the ability of AGA to stimulate inflammatory changes to RMG and macrophages, and whether AR plays a role in this process. In macrophages, treatment with an AR inhibitor (Sorbinil) or genetic knockdown of AR lowered AGA-induced TNF-α secretion (56% and 40%, respectively) as well as cell migration. In a mouse RMG model, AR inhibition attenuated AGA-induced TNF-α secretion and cell migration (67% and 40%, respectively). To further mimic the diabetic milieu in retina, we cultured RMG under conditions of hypoxia and observed the induction of TNF-α and VEGF protein expression. Downregulation of AR in either a pharmacological or genetic manner prevented hypoxia-induced TNF-α and VEGF expression. In our animal study, increased numbers of RMG observed in streptozotocin (STZ)-induced diabetic retina was substantially lower when diabetes was induced in AR knockout mice. Thus, in vitro and in vivo studies demonstrated that AR is involved in diabetes-induced RMG activation, providing a rationale for targeting AR as a therapeutic strategy for DR.
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