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They act on overlapping wound-healing pathways but through different receptor mechanisms

At the metabolic interface, oxidative stress impairs the Nrf2 antioxidant defense system and compromises mitochondrial membrane integrity [113, 114], while emerging non-apoptotic cell death pathwayssuch as ferroptosis (GPX4/ACSL4) and necroptosis (RIPK1/3MLKL)drive follicular demise in toxin-exposed or inflamed ovaries [79, 115]

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