Serum hepcidin is associated with retinopathy of prematurity and modulates oxidative stress and angiogenic responses in retinal microvascular endothelial cells - Report - MDSpire
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Serum hepcidin is associated with retinopathy of prematurity and modulates oxidative stress and angiogenic responses in retinal microvascular endothelial cells
Hepcidin Levels Correlate with Retinopathy of Prematurity
Overview
This study investigates the relationship between hepcidin levels and retinopathy of prematurity (ROP) in preterm infants. It finds that lower hepcidin levels correlate with ROP and that hepcidin supplementation may mitigate oxidative stress and abnormal angiogenesis in retinal endothelial cells.
Background
Retinopathy of prematurity is a significant cause of blindness in preterm infants, driven by factors such as hypoxia and oxidative stress. Current treatments primarily target VEGF signaling, leaving a gap in addressing upstream oxidative injuries. Understanding the role of hepcidin in ROP could lead to novel therapeutic strategies.
Data Highlights
Parameter
ROP Infants
Non-ROP Controls
Gestational Age
Lower
Higher
Birth Weight
Lower
Higher
Serum Hepcidin
Numerically Lower
Higher
Key Findings
Infants with ROP had lower gestational age and birth weight compared to controls.
Serum hepcidin levels were numerically lower in ROP infants.
Hypoxia (1% O2) increased VEGFA and HIF-1α mRNA expression in hRMECs.
Hepcidin reduced intracellular ROS and suppressed hypoxia-induced tube formation in hRMECs.
Transcriptomic analysis indicated hepcidin's influence on hypoxia-responsive metabolic pathways.
Clinical Implications
The findings suggest that monitoring hepcidin levels could provide insights into ROP risk in preterm infants. Additionally, hepcidin supplementation may offer a novel therapeutic approach to mitigate oxidative stress and abnormal angiogenesis in ROP.
Conclusion
This study highlights the potential role of hepcidin in the pathogenesis of ROP and suggests avenues for further research into its therapeutic applications.
FOXC1 duplications were the second most common monogenic finding among genetically solved juvenile open-angle glaucoma cases in one registry, supporting the use of copy-number variant analysis in early-onset glaucoma testing.
