Epigenetic Regulation of Placental Function in Preeclampsia

Preeclampsia is a complex hypertensive disorder of pregnancy arising from defective placental development and function. Central to its pathophysiology is impaired trophoblast invasion and inadequate spiral artery remodelling, leading to placental hypoxia, oxidative stress and maternal endothelial dysfunction. Epigenetic mechanisms—including DNA methylation, DNA hydroxymethylation, histone modifications and non-coding RNA activity—fine-tune gene expression programmes that govern trophoblast differentiation, vascular development and immune tolerance at the maternal–foetal interface. In preeclampsia, widespread alterations of methylation patterns at gene promoters, enhancers and gene bodies disrupt expression of angiogenic factors, growth regulators and stress-response genes. Dysregulated activity of epigenetic enzymes such as DNA methyltransferases and TET dioxygenases contributes to an aberrant epigenomic landscape, with context-specific changes in enhancer methylation and chromatin accessibility. These insights have fostered interest in circulating epigenetic marks as early biomarkers and in targeting epigenetic modifiers to restore placental function, thereby offering new avenues for diagnosis and therapy.

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Epigenetic Regulation of Placental Function in Preeclampsia publication trend

The graph below shows the total number of articles in epigenetic regulation of placental function in preeclampsia across all publications each year (not limited to Nature Index journals).

Technical terms

DNA methylation: Addition of a methyl group to cytosine bases in DNA, influencing gene expression by altering transcription factor binding or chromatin structure.

DNA hydroxymethylation: Conversion of 5-methylcytosine to 5-hydroxymethylcytosine by TET enzymes, often representing an intermediate in active DNA demethylation and a regulatory epigenetic mark.

Enhancer: Regulatory DNA element that increases transcription of target genes, often through DNA–protein interactions and chromatin looping.

Trophoblast: Placental cell lineage responsible for embryo implantation, maternal tissue invasion and nutrient/gas exchange.

TET enzymes: Ten-Eleven Translocation dioxygenases that catalyse hydroxylation of 5-methylcytosine, modulating DNA demethylation and gene regulation.

References

1. Alpha 1,3 N-Acetylgalactosaminyl Transferase (GTA) Impairs Invasion Potential of Trophoblast Cells in Preeclampsia. International Journal of Molecular Sciences (2024).
2. The role of DNA hydroxymethylation and TET enzymes in placental development and pregnancy outcome. Clinical Epigenetics (2023).
3. DNA methylation landscape in pregnancy-induced hypertension: progress and challenges. Reproductive Biology and Endocrinology (2024).