ArticleGenome biology2024
Disruption of maternal vascular remodeling by a fetal endoretrovirus-derived gene in preeclampsia.
Article in Genome biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Epigenetic alterations in preeclampsia: a systematic review of current mechanisms and biomarker potential.Journal of medicine and life · 2026Pooled it
- Paradigms, innovations, and biological applications of RNA velocity: a comprehensive review.Briefings in bioinformatics · 2025Review
- TET1-mediated DNA demethylation suppresses migration of goat placental trophoblast cells.Journal of animal science · 2025Article
- Bioinformatic Analysis of Apoptosis-Related Genes in Preeclampsia Using Public Transcriptomic and Single-Cell RNA Sequencing Datasets.Journal of inflammation research · 2025Article
- Disruption of maternal vascular remodeling by a fetal endoretrovirus-derived gene in preeclampsia.Genome biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors.
Funding
Abstract
backgroundPreeclampsia, one of the most lethal pregnancy-related diseases, is associated with the disruption of uterine spiral artery remodeling during placentation. However, the early molecular events leading to preeclampsia remain unknown.
resultsBy analyzing placentas from preeclampsia, non-preeclampsia, and twin pregnancies with selective intrauterine growth restriction, we show that the pathogenesis of preeclampsia is attributed to immature trophoblast and maldeveloped endothelial cells. Delayed epigenetic reprogramming during early extraembryonic tissue development leads to generation of excessive immature trophoblast cells. We find reduction of de novo DNA methylation in these trophoblast cells results in selective overexpression of maternally imprinted genes, including the endoretrovirus-derived gene PEG10 (paternally expressed gene 10). PEG10 forms virus-like particles, which are transferred from the trophoblast to the closely proximate endothelial cells. In normal pregnancy, only a low amount of PEG10 is transferred to maternal cells; however, in preeclampsia, excessive PEG10 disrupts maternal vascular development by inhibiting TGF-beta signaling.
conclusionsOur study reveals the intricate epigenetic mechanisms that regulate trans-generational genetic conflict and ultimately ensure proper maternal-fetal interface formation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.