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A novel miR-338-3p/SLC1A5 axis has been identified as a key regulator of oxidative stress-induced ferroptosis in DR: high glucose significantly upregulates miR-338-3p expression in RPE cells, and miR-338-3p silencing reverses RPE cell death and ferroptosis ( Although studies have confirmed that the three components form a positive-feedback loop that drives DR progression and that antioxidant therapy can alleviate DR pathology, the key molecular triggers that initiate the loopsuch as the cell-specific mechanisms by which hyperglycemia induces excessive ROS production in different retinal cellsremain poorly defined
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