ArticleMolecular biology reports2025
The role of miRNA-17-3p, oxidative stress, and trace elements in the pathogenesis of preeclampsia.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- MicroRNAs as Regulators of Reproductive Function: From Gametogenesis to Pregnancy.Journal of developmental biology · 2026Review
- MicroRNA-Mediated Placental Maladaptation in Preeclampsia Pathogenesis.FASEB bioAdvances · 2026Review
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Authors and funding
5 authors.
Funding
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Abstract
INTRODUCTION AND
aimsPreeclampsia (PE) is a multifactorial pregnancy disorder marked by hypertension and organ dysfunction. Emerging evidence suggests miRNAs, as epigenetic regulators, play a critical role. Since miR-17-3p is implicated in oxidative stress and vascular function, and considering the known roles of trace elements in redox homeostasis, we hypothesized that their interplay contributes to PE pathogenesis. This study examines the relationship between miRNA-17-3p expression, oxidative stress markers, and trace element levels (zinc and copper) in PE patients.
methodsA case-control study included 140 pregnant women (70 with PE and 70 controls). Placental tissue and serum samples were analyzed for miRNA-17-3p expression, oxidative stress markers [superoxide dismutase (SOD), total antioxidant capacity (TAC), total oxidative status (TOS)], and trace element levels. Statistical analyses explored associations among these variables.
resultsmiRNA-17-3p expression was significantly elevated in the placental tissue and serum of PE patients (P < 0.001). Serum zinc levels significantly decreased, while copper levels increased in the patient group (P < 0.05). SOD activity and TAC levels were reduced, whereas TOS was elevated in PE patients (P < 0.05).
conclusionmiRNA-17-3p is significantly dysregulated in PE, accompanied by increased oxidative stress and disrupted trace element balance. These findings provide insights into potential mechanisms and novel therapeutic targets for managing PE.
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