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Under the iron-rich, ROS-prone conditions characteristic of lesions, this perturbation engages a coordinated program of RCD across intersecting pathways—not only ferroptosis but also necroptotic and pyroptotic signaling—while ferritin handling and mitophagy status further skew redox homeostasis toward irreversible injury in EESCs

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Essentially, it works by inhibiting the production of tyrosinase, an enzyme that triggers melanin production