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Moreover, oxidative stress upregulates adhesion molecules like intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on orbital fibroblasts and endothelial cells, facilitating immune cell recruitment and adhesion to inflamed orbital tissue (88, 89)

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GHK-Cu and reactive oxygen species modulation An in vitro study [9] examined the role of the tripeptide glycyl-L-histidyl-L-lysine in the regulation of intracellular reactive oxygen species observed in mammalian models

NRF2/HO-1 signaling pathway activation effectively mitigates oxidative stress and scavenges ROS by decreasing the ferroptosis of MC3T3-E1 cells, and in increasing bone formation [105]