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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

Genetic panels may identify tendencies, but they do not reliably establish whether a patient is currently undermethylated, overmethylated or functionally blocked

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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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