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Chronic hyperglycemia in DM disrupts normal mitochondrial function leading to excessive ROS generation, advanced glycation end-product (AGE) formation, and activation of pro-inflammatory pathways [29]

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[] Furthermore, BNIP3, a critical mitophagy receptor, is a known transcriptional target of FOXO3, which itself can stimulate PGC-1 expression

The results showed that the vast majority of apoptotic cells were neuronal cells, suggesting that sulindac exerts adverse effects on early neurodevelopment in zebrafish larvae