Molecular and cellular defense against Retinopathy of Prematurity - Prevention, prediction, diagnosis and treatment

In preterm born infants, Retinopathy of Prematurity (ROP), a blinding disease, occurs due to loss of the intra-uterine environment.

Preterm born infants are exposed to factors usually absent in utero, such as bioenergetic failure, infections, and hypo- and hyperoxygenation, all contributing to oxidative stress.

We aim to identify molecular mechanisms based on this disruption and exposure to oxidative stress that underlie abnormal neurovascular development and translate these findings into studies of preventative treatment.

The project will 1) evaluate if combined metabolic activators (substrates promoting mitochondrial function) and fatty acids will prevent ROP and other CNS-related morbidities in preterm infants and evaluate the impact of these factors on biomarkers of inflammation, metabolism, and mitochondrial function, 2) evaluate effect of topical corticosteroid eyedrops on biomarkers of inflammation, metabolism and mitochondrial function, 3) evaluate mitochondrial respiration in preterm infants 4) evaluate in experimental studies the mechanisms of metabolic activators, corticosteroids and fatty acids on retinal inflammation, metabolism and mitochondrial function, 4) in large datasets use AI to personalize prediction to reduce unnecessary ROP examinations.

Our translational studies on the disease mechanisms have lead to possible strategies to promote normal retinal and brain development and will hopefully result in significant reduction in morbidities of preterm infants.