# Association Between Genetic Polymorphisms in the Prostaglandin Pathway and the Development of Patent Ductus Arteriosus in Preterm Infants

**Authors:** Marcin Minta, Grażyna Kurzawińska, Zuzanna-Banach Minta, Agnieszka Seremak Mrozikiewicz, Dawid Szpecht

PMC · DOI: 10.3390/ijms26199274 · 2025-09-23

## TL;DR

This study explores how genetic variations in the prostaglandin pathway may increase the risk of patent ductus arteriosus in preterm infants.

## Contribution

The study identifies specific genetic polymorphisms in the prostaglandin pathway associated with PDA development in preterm infants.

## Key findings

- Selected polymorphisms in the prostaglandin pathway genes were significantly associated with increased PDA risk.
- The study suggests genetic variability may contribute to PDA pathogenesis in preterm neonates.

## Abstract

Patent ductus arteriosus (PDA) constitutes a significant clinical condition, frequently associated with a spectrum of complications that may profoundly compromise the health status of neonates, particularly those born preterm. Multiple predisposing factors—including prematurity, low birth weight, and respiratory insufficiency—have been consistently documented in the scientific literature. In this study, we investigated the influence of genetic polymorphisms in genes associated with the arachidonic acid–prostaglandin metabolic pathway. Specifically, we analyzed polymorphisms in genes encoding phospholipase A2 (rs10798059, rs1549637, rs4375, rs1805017, rs1051931), cyclooxygenase-1 (rs1236913), prostaglandin synthase 2 (rs13283456), and the prostaglandin E2 receptor EP4 (rs4613763). The study cohort comprised 99 preterm neonates born between 24 and 32 weeks of gestation. Genetic analyses were performed to identify polymorphisms in the aforementioned genes. Statistical evaluation demonstrated that selected polymorphic were significantly associated with an increased risk of patent ductus arteriosus development. This study represents a preliminary step toward elucidating the contribution of genetic variability to the pathogenesis of patent ductus arteriosus. Improved understanding of these molecular mechanisms may facilitate the early identification of neonates at increased risk and support the implementation of targeted monitoring and preventive strategies in this high-risk population.

## Linked entities

- **Diseases:** patent ductus arteriosus (MONDO:0011827)

## Full-text entities

- **Genes:** PTGS1 (prostaglandin-endoperoxide synthase 1) [NCBI Gene 5742] {aka COX1, COX3, PCOX1, PES-1, PGG/HS, PGHS-1}, PLA2G1B (phospholipase A2 group IB) [NCBI Gene 5319] {aka PLA2, PLA2A, PPLA2}, PTGER4 (prostaglandin E receptor 4) [NCBI Gene 5734] {aka EP4, EP4R}
- **Diseases:** prematurity (MESH:C536271), PDA (MESH:D004374), respiratory insufficiency (MESH:D012131)
- **Chemicals:** arachidonic acid (MESH:D016718), Prostaglandin (MESH:D011453)
- **Mutations:** rs1805017, rs1236913, rs13283456, rs4375, rs1051931, rs4613763, rs10798059, rs1549637

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12524655/full.md

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Source: https://tomesphere.com/paper/PMC12524655