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In addition, long-term hyperglycemia (glucotoxicity) and hyperlipidemia (lipotoxicity) synergistically amplify inflammatory responses, accelerate the functional failure of cells, and ultimately lead to the inability of insulin secretion to compensate for IR, thereby triggering T2DM [26]

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Furthermore, Nox2 activation has been identified as an early event in DR, with cytosolic ROS progressively damaging mitochondria, leading to their dysfunction (73)