ArticleJournal of neurochemistry2024
Arachidonic acid metabolism regulates the development of retinopathy of prematurity among preterm infants.
Article in Journal of neurochemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- In situ bioactive nanocoating enables transocular delivery of permeable drug for dual-location intervention of ocular surface and fundus disorders.Bioactive materials · 2027Article
- Enzymatic Degumming of Arachidonic Acid Oil Using Immobilized Phospholipase A1 on Hollow Double-Layer Mesoporous Silica Nanoparticles.Molecules (Basel, Switzerland) · 2026Article
- Development of a Disposable Chemiresistive Biochip for Tear-Based Retinopathy of Prematurity Diagnosis: Early Screening and Risk Prediction.IEEE sensors journal · 2026Article
- Proinflammatory state and metabolic dysregulation linking delayed feeding progression to extrauterine restricted head growth in extremely preterm infants.BMC medicine · 2025Article
- Potential of Pterostilbene as an Antioxidant Therapy for Delaying Retinal Damage in Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2025Article
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10 authors.
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Abstract
Extremely preterm infants are at risk of developing retinopathy of prematurity (ROP), characterized by neovascularization and neuroinflammation leading to blindness. Polyunsaturated fatty acid (PUFA) supplementation is recommended in preterm infants to lower the risk of ROP, however, with no significant improvement in visual acuity. Reasonably, this could be as a result of the non-consideration of PUFA metabolizing enzymes. We hypothesize that abnormal metabolism of the arachidonic acid (AA) pathway may contribute to severe stages of ROP. The present study investigated the AA-metabolizing enzymes in ROP pathogenesis by a targeted gene expression analysis of blood (severe ROP = 70, No/Mild = 56), placenta (preterm placenta = 6, full term placenta = 3), and human primary retinal cell cultures and further confirmed at the protein level by performing IHC in sections of ROP retina. The lipid metabolites were identified by LC-MS in the vitreous humor (VH; severe ROP = 15, control = 15). Prostaglandins D2 (p = 0.02), leukotrienes B5 (p = 0.0001), 11,12-epoxyeicosatrienoic acid (p = 0.01), and lipid-metabolizing enzymes of the AA pathway such as CYP1B1, CYP2C8, COX2, and ALOX15 were significantly upregulated while EPHX2 was significantly (0.04) downregulated in ROP cases. Genes involved in hypoxic stress, angiogenesis, and apoptosis showed increased expression in ROP. An increase in the metabolic intermediates generated from the AA metabolism pathway further confirmed the role of these enzymes in ROP, while metabolites for EPHX2 activity were low in abundance. Inflammatory lipid intermediates were higher compared to anti-inflammatory lipids in VH and showed an association with enzyme activity. Both the placenta of preterm infants who developed ROP and hypoxic retinal cultures showed a reduced expression of EPHX2. These findings suggested a strong involvement of EPHX2 in regulating retinal neovascularization and inflammation. The study results underscore the role of arachidonic acid metabolism in the development of ROP and as a potential target for preventing vision loss among preterm-born infants.
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