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<p>In normal pregnancy, systemic inflammation, oxidative stress, and angiogenic balance are tightly regulated. However, in preeclampsia, excessive oxidative and nitrosative stress disrupt vascular function, alter angiogenic signaling and promote the release of cell-free fetal DNA (cffDNA) into maternal circulation. In the current prospective observational study, we investigated the role of oxidative stress and angiogenic imbalance in preeclampsia by including 31 women with preeclampsia, 31 age-matched normotensive pregnant and 26 non-pregnant women based on feasibility within the study period. Biochemical parameters, oxidative stress markers, angiogenic/anti-angiogenic factors, and cffDNA (via hypermethylated RASSF1A gene expression) were investigated. We found that preeclamptic patients showed significantly higher BMI and blood pressure, reduced hemoglobin and platelet counts, and elevated liver enzymes, while no change in the renal and glucose profiles. Oxidative stress markers show decreased glutathione and glutathione-related enzymes, increased malondialdehyde, and altered nitric oxide levels. On the otherhand, a marked imbalance between angiogenic (VEGF, PlGF) and anti-angiogenic factors (sFlt-1, soluble endoglin) was observed. Importantly, cffDNA levels were markedly present in preeclamptic women. In conclusion, oxidative stress, angiogenic imbalance, and increased cffDNA are interrelated in preeclampsia. These findings support a combination biomarker strategy incorporating oxidative stress markers, angiogenic profiles, and fetal-specific cffDNA to improve early prediction and risk stratification of preeclampsia.</p>

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Oxidative Stress–Mediated Endothelial Dysfunction and Cell-Free Fetal DNA Release in Preeclampsia

  • 期刊论文

  • 发表日期：

    2026年2月16日

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  • Sayanica Dutta,
  • Soubhik Bhattacharya,
  • Mriganka Mouli Saha,
  • Sukanya Dhar,
  • Amit Pal,
  • Utpal Basu,
  • Subir Kumar Das

摘要

In normal pregnancy, systemic inflammation, oxidative stress, and angiogenic balance are tightly regulated. However, in preeclampsia, excessive oxidative and nitrosative stress disrupt vascular function, alter angiogenic signaling and promote the release of cell-free fetal DNA (cffDNA) into maternal circulation. In the current prospective observational study, we investigated the role of oxidative stress and angiogenic imbalance in preeclampsia by including 31 women with preeclampsia, 31 age-matched normotensive pregnant and 26 non-pregnant women based on feasibility within the study period. Biochemical parameters, oxidative stress markers, angiogenic/anti-angiogenic factors, and cffDNA (via hypermethylated RASSF1A gene expression) were investigated. We found that preeclamptic patients showed significantly higher BMI and blood pressure, reduced hemoglobin and platelet counts, and elevated liver enzymes, while no change in the renal and glucose profiles. Oxidative stress markers show decreased glutathione and glutathione-related enzymes, increased malondialdehyde, and altered nitric oxide levels. On the otherhand, a marked imbalance between angiogenic (VEGF, PlGF) and anti-angiogenic factors (sFlt-1, soluble endoglin) was observed. Importantly, cffDNA levels were markedly present in preeclamptic women. In conclusion, oxidative stress, angiogenic imbalance, and increased cffDNA are interrelated in preeclampsia. These findings support a combination biomarker strategy incorporating oxidative stress markers, angiogenic profiles, and fetal-specific cffDNA to improve early prediction and risk stratification of preeclampsia.