ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2015
Deficiency of aldose reductase attenuates inner retinal neuronal changes in a mouse model of retinopathy of prematurity.
Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- Beyond Neovascularization: Light Response Deficits in Oxygen-Induced Retinopathy Models.Investigative ophthalmology & visual science · 2026Review
- Serine supplementation suppresses hypoxia-induced pathological retinal angiogenesis.Theranostics · 2025Article
- Localization of Calretinin, Parvalbumin, and S100 Protein inLife (Basel, Switzerland) · 2023Article
- Potential Neuroprotective Role of Calretinin-N18 and Calbindin-D28k in the Retina of Adult Zebrafish Exposed to Different Wavelength Lights.International journal of molecular sciences · 2023Article
- Article
- Neurosensory Alterations in Retinopathy of Prematurity: A Window to Neurological Impairments Associated to Preterm Birth.Biomedicines · 2022Review
- Anti-inflammatory α-Melanocyte-Stimulating Hormone Protects Retina After Ischemia/Reperfusion Injury in Type I Diabetes.Frontiers in neuroscience · 2022Article
- Müller glial responses compensate for degenerating photoreceptors in retinitis pigmentosa.Experimental & molecular medicine · 2021Article
- Metabolism in Retinopathy of Prematurity.Life (Basel, Switzerland) · 2021Review
- Autophagic Upregulation Is Cytoprotective in Ischemia/Reperfusion-Injured Retina and Retinal Progenitor Cells.International journal of molecular sciences · 2021Article
- Potential Effects of Nutraceuticals in Retinopathy of Prematurity.Life (Basel, Switzerland) · 2021Review
- Thyroid Activating Enzyme, Deiodinase II Is Required for Photoreceptor Function in the Mouse Model of Retinopathy of Prematurity.Investigative ophthalmology & visual science · 2020Article
- Targeting Neurovascular Interaction in Retinal Disorders.International journal of molecular sciences · 2020Review
- Stanniocalcin-1 is a Modifier of Oxygen-Induced Retinopathy Severity.Current eye research · 2020Article
- Metabolic Syndrome Triggered by Fructose Diet Impairs Neuronal Function and Vascular Integrity in ApoE-KO Mouse Retinas: Implications of Autophagy Deficient Activation.Frontiers in cell and developmental biology · 2020Article
- Vascular and Neuronal Protection in the Developing Retina: Potential Therapeutic Targets for Retinopathy of Prematurity.International journal of molecular sciences · 2019Review
- Lutein facilitates physiological revascularization in a mouse model of retinopathy of prematurity.Clinical & experimental ophthalmology · 2017Article
- Galectin-1 expression imprints a neurovascular phenotype in proliferative retinopathies and delineates responses to anti-VEGF.Oncotarget · 2017Article
- Review: adiponectin in retinopathy.Biochimica et biophysica acta · 2016Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinopathy of prematurity (ROP) is a leading cause of childhood blindness where vascular abnormality and retinal dysfunction are reported. We showed earlier that genetic deletion of aldose reductase (AR), the rate-limiting enzyme in the polyol pathway, reduced the neovascularization through attenuating oxidative stress induction in the mouse oxygen-induced retinopathy (OIR) modeling ROP. In this study, we further investigated the effects of AR deficiency on retinal neurons in the mouse OIR. Seven-day-old wild-type and AR-deficient mice were exposed to 75 % oxygen for 5 days and then returned to room air. Electroretinography was used to assess the neuronal function at postnatal day (P) 30. On P17 and P30, retinal cytoarchitecture was examined by morphometric analysis and immunohistochemistry for calbindin, protein kinase C alpha, calretinin, Tuj1, and glial fibrillary acidic protein. In OIR, attenuated amplitudes and delayed implicit time of a-wave, b-wave, and oscillatory potentials were observed in wild-type mice, but they were not significantly changed in AR-deficient mice. The morphological changes of horizontal, rod bipolar, and amacrine cells were shown in wild-type mice and these changes were partly preserved with AR deficiency. AR deficiency attenuated the Müller cell gliosis induced in OIR. Our observations demonstrated AR deficiency preserved retinal functions in OIR and AR deficiency could partly reduce the extent of retinal neuronal histopathology. These findings suggested a therapeutic potential of AR inhibition in ROP treatment with beneficial effects on the retinal neurons.
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