Serum hepcidin is associated with retinopathy of prematurity and modulates oxidative stress and angiogenic responses in retinal microvascular endothelial cells - Scorecard - 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
Clinical Scorecard: Hepcidin Levels Correlate with Retinopathy of Prematurity and Influence Oxidative Stress and Angiogenic Activity in Retinal Microvascular Endothelial Cells
At a Glance
Category
Detail
Condition
Retinopathy of Prematurity (ROP)
Key Mechanisms
Impaired vascular development, hypoxia, oxidative stress, and pathological angiogenesis
Target Population
Preterm infants with gestational age <36 weeks
Care Setting
Neonatal intensive care
Key Highlights
ROP is a leading cause of blindness in premature infants.
Hepcidin may modulate oxidative stress and angiogenic activation.
Lower gestational age and birth weight are associated with ROP.
Hepcidin reduced VEGFA levels and intracellular ROS in vitro.
Current treatments primarily target VEGF signaling.
Guideline-Based Recommendations
Diagnosis
Clinical assessment of gestational age, birth weight, and ROP stage.
Management
Current treatments include laser photocoagulation and anti-VEGF therapy.
Monitoring & Follow-up
Monitor serum hepcidin levels and ROP progression.
Risks
High recurrence rates and potential adverse effects of current treatments.
Patient & Prescribing Data
Preterm infants with ROP
Hepcidin supplementation may mitigate oxidative stress and abnormal angiogenesis.
Clinical Best Practices
Consider hepcidin-related signaling in ROP research.
Evaluate the role of oxidative stress in ROP pathogenesis.