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Although few studies have directly examined autophagy in the context of testicular regeneration, available evidence suggests that transient induction is protective, whereas chronic overactivation is detrimental

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by increasing or decreasing doses of medication, or by changing the particular type of mimic that is administered, or by changing the frequency of dosing or the route of administration, etc

Similarly, it has also been shown that GPX4 is degraded by interacting with different autophagic receptors after Fin56 (type 3 ferroptosis inducer) or excessive copper treatment, triggering ferroptosis [205, 206]

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