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Several mechanisms contributing to increased oxidative stress in the diabetic milieu have been proposed, including glucose auto-oxidation, weakened antioxidant defense systems, metabolic abnormalities, and mitochondrial damage [45,46,47]

Reducing exposure while maintaining effectiveness represents a reasonable risk reduction strategy for those concerned about theoretical cancer risk

Current scientific investigations continue exploring intracellular signaling pathways associated with AOD9604

Research suggests it can upregulate genes involved in: Tissue repair Anti-inflammatory responses Cellular regeneration At the same time, it may downregulate genes associated with oxidative stress and tissue breakdown