<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kumar S</submitter><funding>Impacting Research Innovation and Technology</funding><funding>Department of Science and Technology, Ministry of Science and Technology, India</funding><funding>DBT/Wellcome Trust India Alliance</funding><funding>Hyderabad Eye Research Foundation</funding><funding>Department of Biotechnology, Ministry of Science and Technology, India</funding><pagination>3171-3187</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7617615</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>168(9)</volume><pubmed_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 culture</pubmed_abstract><journal>Journal of neurochemistry</journal><pubmed_title>Arachidonic acid metabolism regulates the development of retinopathy of prematurity among preterm infants.</pubmed_title><pmcid>PMC7617615</pmcid><funding_grant_id>IMP/2018/001414</funding_grant_id><funding_grant_id>BT/PR32404/MED/30/2136/2019</funding_grant_id><funding_grant_id>IF190699</funding_grant_id><funding_grant_id>DBT/2020/LVPEI/1365</funding_grant_id><funding_grant_id>IA/E/22/1/506766</funding_grant_id><funding_grant_id>LEC02‐14‐029</funding_grant_id><funding_grant_id>LEC02-14-029</funding_grant_id><pubmed_authors>Sharma N</pubmed_authors><pubmed_authors>Mahajan A</pubmed_authors><pubmed_authors>Jalali S</pubmed_authors><pubmed_authors>Kaur I</pubmed_authors><pubmed_authors>Joshi MB</pubmed_authors><pubmed_authors>Kekunnaya R</pubmed_authors><pubmed_authors>Chakrabarti S</pubmed_authors><pubmed_authors>Kaur T</pubmed_authors><pubmed_authors>Kumar S</pubmed_authors><pubmed_authors>Patnaik S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Arachidonic acid metabolism regulates the development of retinopathy of prematurity among preterm infants.</name><description>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 culture</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Sep</publication><modification>2026-06-02T17:34:19.36Z</modification><creation>2025-07-12T03:04:36.445Z</creation></dates><accession>S-EPMC7617615</accession><cross_references><pubmed>39073120</pubmed><doi>10.1111/jnc.16190</doi></cross_references></HashMap>