Serum hepcidin is associated with retinopathy of prematurity and modulates oxidative stress and angiogenic responses in retinal microvascular endothelial cells.

Introduction: Retinopathy of prematurity (ROP) is a vasoproliferative retinal disorder in preterm infants driven by impaired vascular development, hypoxia, oxidative stress, and pathological angiogenesis. Current treatments mainly target VEGF signaling but do not directly address upstream oxidative injury. Hepcidin, a key iron-homeostasis regulator, may modulate redox balance and angiogenic activation. However, whether hepcidin is reduced in ROP and whether supplementation mitigates hypoxia-induced oxidative stress and abnormal angiogenesis in retinal endothelial cells remain unclear. Objective: To investigate the effects of hepcidin on human retinal microvascular endothelial cells (hRMECs) under oxidative stress and assess its translational potential in ROP. Methods: Clinical data were collected from 35 preterm infants with gestational age <36 weeks, including 24 non-ROP controls and 11 ROP infants. Gestational age, birth weight, ROP stage, and serum hepcidin were analyzed. hRMECs were exposed to 1% O Results: Infants with ROP had lower gestational age and birth weight than controls, and gestational age differed across ROP stage groups. Serum hepcidin-related signals were numerically lower in ROP infants, but no significant stage-dependent decrease was observed. In hRMECs, 1% O Conclusion: This study provides preliminary clinical and experimental evidence supporting a potential role of hepcidin-related signaling in ROP. Although the clinical findings are exploratory, the