The Role of Hepcidin in Hypoxic Human Retinal Microvascular Endothelial Cells
Retinopathy of prematurity (ROP), a leading blinding disease in preterm infants, is associated with immature retinal vascular development and hypoxia-induced pathological neovascularization. Hepcidin, a hepatic iron-regulatory hormone, maintains systemic iron homeostasis by modulating iron absorption, release, and storage. Emerging evidence indicates hepcidin alleviates oxidative stress and inflammation through iron metabolism-related gene regulation. To investigate the potential therapeutic role of hepcidin in ROP, we performed RNA sequencing on three groups of human retinal microvascular endothelial cells (hRMECs):Normoxia-cultured hRMECs (21% oxygen).Hypoxia-exposed hRMECs (1% oxygen for 24 hours).Hypoxia-exposed hRMECs with hepcidin treatment (1% oxygen with hepcidin for 24 hours).This study aimed to elucidate the molecular mechanisms by which hepcidin modulates pathological angiogenesis in ROP.