Loss of Akt2 also inhibited diabetes-induced elevation of RNA and protein levels of the EMT markers Snail/Slug and Twist1 in the RPE as compared to Akt2 fl/fl diabetic mice. Diabetes induction in the floxed control mice decreased levels of the RPE tight junction protein ZO-1 and adherens junction proteins occludin and E-cadherin these decreases were rescued in Akt2 cKO diabetic mice.
After an 8-month duration of diabetes (10 months of age), the mice were euthanized and expression of tight junction proteins, epithelial–mesenchymal transition (EMT), and fibrosis markers were examined in the RPE. Therefore, to investigate the potential role of Akt2 in the diabetes-induced retinal fibrosis process, we generated RPE-specific Akt2 conditional knockout (cKO) mice and induced diabetes in these mice and Akt2 fl/fl control mice by intraperitoneal injection of streptozotocin. While anti-VEGF agents and invasive laser treatments are the primary treatments for PDR, retinal fibrosis has received minimal attention as a potential target for therapeutic intervention. Clinical studies have shown that fibrotic membranes exhibit uncontrolled growth in PDR and contribute to retinal detachment from RPE cells, ultimately leading to vision loss. Retinal fibrosis is closely associated with developing proliferative diabetic retinopathy (PDR). Diabetic Retinopathy (DR) is a complication of diabetes that causes blindness in adults.
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