Evidence map›Paper›PMID 39606093›Full record

ArticleEnvironmental epigenetics2024

Epigenetic biomarker for preeclampsia-associated preterm birth and potential preventative medicine.

Eric E Nilsson, Paul Winchester, Cathy Proctor, Daniel Beck, Michael K Skinner

Abstract read
In one paragraph

Article in Environmental epigenetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Stability of epigenetic transgenerational inheritance of adult-onset disease and parturition abnormalities.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Review
  4. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Eric E NilssonCenter for Reproductive Biology, School of Biological Sciences, Washington State University, Pullman, WA 99164-4236, United States.ORCID https://orcid.org/0000-0001-8894-4054
Paul WinchesterDepartment of Pediatrics, St. Franciscan Hospital, School of Medicine, Indiana University, Indianapolis, IN 46202-5201, United States.
Cathy ProctorDepartment of Pediatrics, St. Franciscan Hospital, School of Medicine, Indiana University, Indianapolis, IN 46202-5201, United States.
Daniel BeckCenter for Reproductive Biology, School of Biological Sciences, Washington State University, Pullman, WA 99164-4236, United States.
Michael K SkinnerCenter for Reproductive Biology, School of Biological Sciences, Washington State University, Pullman, WA 99164-4236, United States.ORCID https://orcid.org/0000-0001-8224-2078

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preterm birth (PTB) has dramatically increased within the population (i.e. >10%) and preeclampsia is a significant sub-category of PTB. Currently, there are no practical clinical parameters or biomarkers which predict preeclampsia induced PTB. The current study investigates the potential use of epigenetic (DNA methylation) alterations as a maternal preeclampsia biomarker. Non-preeclampsia term births were compared to preeclampsia PTBs to identify DNA methylation differences (i.e. potential epigenetic biomarker). Maternal buccal cell cheek swabs were used as a marker cell for systemic epigenetic alterations in the individuals, which are primarily due to environmentally induced early life or previous generations impacts, and minimally impacted or associated with the disease etiology or gestation variables. A total of 389 differential DNA methylation regions (DMRs) were identified and associated with the presence of preeclampsia. The DMRs were genome-wide and were predominantly low CpG density (<2 CpG/100 bp). In comparison with a previous PTB buccal cell epigenetic biomarker there was a 15% (60 DMR) overlap, indicating that the majority of the DMRs are unique for preeclampsia. Few previously identified preeclampsia genes have been identified, however, the DMRs had gene associations in the P13 K-Akt signaling pathway and metabolic gene family, such as phospholipid signaling pathway. Preliminary validation of the DMR use as a potential maternal biomarker used a cross-validation analysis on the samples and provided 78% accuracy. Although prospective expanded clinical trials in first trimester pregnancies and clinical comparisons are required, the current study provides the potential proof of concept a preeclampsia epigenetic biomarker may exist. The availability of a preeclampsia PTB maternal susceptibility biomarker may facilitate clinical management and allow preventative medicine approaches to identify and treat the preeclampsia condition prior to its occurrence.

Indexed as

environmental inducedepigeneticmaternal biomarkerpreeclampsiapregnancypreterm birthpreventative medicinesystemic biomarker

Identifiers

PMID39606093
PMCPMC11602036

What Socratic holds

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LicenceCC BY-NC
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Registered trials

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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.