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Targeting this windowe.g., via specific activation of the AMPK-SIRT3 axis, inhibition of Drp1 hyperactivation-induced fission, or enhancement of PINK1/Parkin-mediated mitophagyholds promise for restoring mitochondrial metabolic homeostasis and halting OA progression at its initial stages (87, 88)

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In PCOS, rebound could plausibly compromise the stability of metabolic and reproductive gains during the preconception interval, particularly where restoration of ovulatory function appears to depend on sustained improvement in adiposity and insulin resistance