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Finally, knockdown of Gln transporters (SLC38A1 and SLC1A5) or pharmacological inhibition of SLC1A5 also significantly blocked cysteine starvation-mediated ferroptosis [85, 86]

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The dual role of ROS underscores the need for controlled redox modulation while excessive ROS disrupts healing, physiological levels drive angiogenesis, fibroblast activation, and cell migration