RAGE and Diaph1 deficiency affect retinal cytoarchitecture both in physiological and long-term hyperglycemic settings in diabetic mice - a preliminary study.

Retinal complications in diabetes are a leading cause of vision loss in adults. Long-term hyperglycemia triggers molecular changes that damage retinal neuronal tissues and blood vessels, leading to degeneration, inflammation, and vision impairment. Studies show that the Receptor for Advanced Glycation End-Products (RAGE) and its cytosolic ligand, Diaph1 are both implicated in the pathogenesis of diabetic complications; however, their role in the development of retinal damage is not yet clear. We hypothesized that the deletion of either RAGE or Diaph1 would be beneficial and prevent or delay damage to the retinal structure in diabetes. Wild-type, RAGE and Diaph1 knockout mice were used in the study. The mice were randomly selected and divided into control and diabetic groups. Diabetes was induced with Streptozotocin injections, and six months after diabetes induction all mice were sacrificed, samples collected and processed for morphometric analysis. Our analysis revealed a reduction in retinal depth across all layers between control and diabetic samples. The effect of RAGE or Diaph1 deletion on retinal structure differed, indicating that both proteins may play independent if not interchangeable roles in retina function and structure, highlighting their potential role in the pathogenesis of diabetic retinal complications.