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The precise mechanism underlying ferroptosis is still unknown, but it is known that altered iron metabolism, glutathione (GSH) depletion, GPX4 inactivation, and increased PUFA peroxidation by ROS play key roles in its onset and progression [80, 81]

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It also pairs well with GHK-Cu in patients focused on skin, tissue repair, and systemic cellular regeneration alongside the longevity mechanisms Epithalon provides