ArticleClinical epigenetics2024
Methylation alterations of imprinted genes in different placental diseases.
Article in Clinical epigenetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- NewbornGenes · 2025Pooled it
- Article
- New Frontiers in the Pathophysiology of Hypertensive Pregnancy Disorders: A Systematic Review of Molecular Insights into Preeclampsia.Current issues in molecular biology · 2026Review
- Epigenetic Regulation of Imprinted Genes in the Neurodevelopment of Offspring Born to Women with Preeclampsia: A Review.International journal of women's health · 2026Review
- Placental DNA methylation key topics: sex- and cell-type specificity, mediation, multi-omics, and biomarker discovery.Epigenomics · 2025Review
- Identification of genetic and non-genetic modifiers of genomic imprinting through screening of imprinted DMR methylation in humans.Epigenetics & chromatin · 2025Article
- Dysregulation of Circadian Markers, HAT1 and Associated Epigenetic Proteins, and the Anti-Aging Protein KLOTHO in Placenta of Pregnant Women with Chronic Venous Disease.Journal of personalized medicine · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundImprinted genes play important functions in placentation and pregnancy; however, research on their roles in different placental diseases is limited. It is believed that epigenetic alterations, such as DNA methylation, of placental imprinting genes may contribute to the different pathological features of severe placental diseases, such as pre-eclampsia (PE) and placenta accreta spectrum disorders (PAS).
resultsIn this study, we conducted a comparative analysis of the methylation and expression of placental imprinted genes between PE and PAS using bisulfite sequencing polymerase chain reaction (PCR) and quantitative PCR, respectively. Additionally, we assessed oxidative damage of placental DNA by determining 8-hydroxy-2'-deoxyguanosine levels and fetal growth by determining insulin-like growth factor 2 (IGF2) and cortisol levels in the umbilical cord blood using enzyme-linked immunosorbent assay. Our results indicated that methylation and expression of potassium voltage-gated channel subfamily Q member 1, GNAS complex locus, mesoderm specific transcript, and IGF2 were significantly altered in both PE and PAS placentas. Additionally, our results revealed that the maternal imprinted genes were significantly over-expressed in PE and significantly under-expressed in PAS compared with a normal pregnancy. Moreover, DNA oxidative damage was elevated and positively correlated with IGF2 DNA methylation in both PE and PAS placentas, and cortisol and IGF2 levels were significantly decreased in PE and PAS.
conclusionsThis study suggested that DNA methylation and expression of imprinted genes are aberrant in both PE and PAS placentas and that PE and PAS have different methylation profiles, which may be linked to their unique pathogenesis.
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