ArticleBiomolecules2025
Folic Acid Supplementation Inhibits Proliferative Retinopathy of Prematurity.
Article in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Loss of Kv8.2 in the Mouse Retina Is Associated With Altered One-Carbon Metabolism.Journal of neurochemistry · 2026Article
- The controversial role of nutraceuticals vs. drugs in proliferative retinopathies.Frontiers in neuroscience · 2025Review
- Circulating micronutrients as protective factors for the retinal structure and vasculature: Mendelian randomization analyses.Advances in ophthalmology practice and researchArticle
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
backgroundRetinopathy of prematurity (ROP) is the major cause of blindness in children. It is a biphasic disease with retinal vessel growth cessation and loss (Phase I) followed by uncontrolled retinal vessel growth (Phase II). Folate is an essential nutrient for fetal development and growth. Premature infants have a high risk for folate deficiency. However, the contribution of folate to ROP risk remains unknown.
methodsIn mouse oxygen-induced retinopathy (OIR), the nursing dams were fed with a folic acid-deficient or control diet after delivery until the end of hyperoxia. Alternatively, pups received direct injection of either folic acid or vehicle during Phase I hyperoxia. Genes involved in the folate cycle and angiogenic responses were examined using real-time PCR. Total retinal folate levels were measured with the
resultsMaternal folic acid deficiency in early life exacerbated pathological retinal vessel growth, while supplementation with folic acid suppressed it. Genes involved in the folate cycle were downregulated in Phase I OIR retinas and were highly expressed in Müller glia. Folic acid reduced pro-angiogenic signaling in cultured rat retinal Müller glia in vitro.
conclusionsAppropriate supplementation of folic acid might be a new and safe treatment for ROP at an early stage.
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Registered trials
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