ArticleInvestigative ophthalmology & visual science2024
Diabetes Renders Photoreceptors Susceptible to Retinal Ischemia-Reperfusion Injury.
Article in Investigative ophthalmology & visual science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Zero Warm Ischemia Time in Whole-Eye Transplantation through Retrograde Extracorporeal Perfusion.Ophthalmology science · 2026Article
- Retinoprotective Effects of Abscisic Acid in Ischemic Retinopathy Mouse Model.Antioxidants (Basel, Switzerland) · 2025Article
- Photoreceptor thickness in UK Biobank participants with and without diabetes mellitus.BMJ open ophthalmology · 2025Article
- Exosomal miR-450b-5p Secreted from Exendin-4-Stimulated Endothelial Cells Protects Retinal Ganglion Cells Against Ischemia Reperfusion Injury.International journal of nanomedicine · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Purpose: Studies have suggested that photoreceptors (PR) are altered by diabetes, contributing to diabetic retinopathy (DR) pathology. Here, we explored the effect of diabetes on retinal ischemic injury. Methods: Retinal ischemia-reperfusion (IR) injury was caused by elevation of intraocular pressure in 10-week-old BKS db/db type 2 diabetes mellitus (T2DM) mice or C57BL/6J mice at 4 or 12 weeks after streptozotocin (STZ)-induced type 1 diabetes mellitus (T1DM), and respective nondiabetic controls. Retinal neurodegeneration was evaluated by retinal layer thinning, TUNEL staining, and neuron loss. Vascular permeability was evaluated as retinal accumulation of circulating fluorescent albumin. The effects of pretreatment with a sodium-glucose co-transporter (SGLT1/2) inhibitor, phlorizin, were examined. Results: Nondiabetic control mice exhibited no significant outer retinal layer thinning or PR loss after IR injury. In contrast, db/db mice exhibited significant outer retina thinning (49%, P < 0.0001), loss of PR nuclei (45%, P < 0.05) and inner segment (IS) length decline (45%, P < 0.0001). STZ-induced diabetic mice at 4 weeks showed progressive thinning of the outer retina (55%, by 14 days, P < 0.0001) and 4.3-fold greater number of TUNEL+ cells in the outer nuclear layer (ONL) than injured retinas of control mice (P < 0.0001). After 12 weeks of diabetes, the retinas exhibited similar outer layer thinning and PR loss after IR. Diabetes also delayed restoration of the blood-retinal barrier after IR injury. Phlorizin reduced outer retinal layer thinning from 49% to 3% (P < 0.0001). Conclusions: Diabetes caused PR to become highly susceptible to IR injury. The ability of phlorizin pretreatment to block outer retinal thinning after IR suggests that the effects of diabetes on PR are readily reversible.
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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.