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After M1 polarization, macrophages release large amounts of Fe 2+ via ferritin autophagy mediated by nuclear receptor coactivator 4 (NCOA4), which not only promotes ferroptosis but also causes the further release of ferroptosis-promoting factors into the cornea, RPE, and RGCs, forming a vicious cycle in the ocular microenvironment

Quach HT, Johnson DB, LeBoeuf NR, Zwerner JP, Dewan AK

All patients gave informed consent for the anonymous use of their data

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Beyond its redox activity, GSH also plays a pivotal immunoregulatory role by reprogramming macrophages from the pro-inflammatory M1 phenotype toward the reparative M2 state, facilitating angiogenesis, ECM deposition, and tissue remodeling