Evidence map›Paper›PMID 41689925›Full record

ArticlePlacenta2026

Characterizing placental dysfunction with DNA methylation profiling and placental histopathology.

Hannah J Illing, Alexa A Freedman, Ella O Beraldo, Lauren Keenan-Devlin, Gregory E Miller, Ann E Borders, Wendy P Robinson, Linda M Ernst

Abstract read
In one paragraph

Article in Placenta, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

  1. 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

8 authors.

Hannah J IllingDepartment of Medical Genetics, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada; British Columbia Children's Hospital Research Institute (BCCHR), Vancouver, British Columbia, Canada.
Alexa A FreedmanDepartment of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Ella O BeraldoBritish Columbia Children's Hospital Research Institute (BCCHR), Vancouver, British Columbia, Canada.
Lauren Keenan-DevlinDepartment of Obstetrics and Gynecology, Endeavor Health, Evanston, IL, USA; Department of Obstetrics and Gynecology, University of Chicago Pritzker School of Medicine, Evanston, IL, USA.
Gregory E MillerInstitute for Policy Research & Department of Psychology, Northwestern University, Evanston, Illinois, USA.
Ann E BordersDepartment of Obstetrics and Gynecology, Endeavor Health, Evanston, IL, USA; Department of Obstetrics and Gynecology, University of Chicago Pritzker School of Medicine, Evanston, IL, USA; Center for Healthcare Studies - Institute for Public Health and Medicine, Northwestern University, Evanston, IL, USA.
Wendy P RobinsonDepartment of Medical Genetics, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada; British Columbia Children's Hospital Research Institute (BCCHR), Vancouver, British Columbia, Canada. Electronic address: wrobinson@bcchr.ca.
Linda M ErnstDepartment of Pathology, Endeavor Health, Evanston, IL, USA; Department of Pathology, University of Chicago Pritzker School of Medicine, Evanston, IL, USA.

Funding

Understanding socioeconomic disparities in perinatal risk: The role of epigenetic and transcriptional regulation in the placentaR01MD011749 · NIMHD · NORTHWESTERN UNIVERSITY · PI BORDERS, ANN E.B., MILLER, GREGORY EVAN · 2017 to 2021
$3.9M
NIMHD NIH HHS R01 MD011749
6 · The paper itself

Abstract

backgroundPlacental pathology is associated with abnormal fetal growth and development. Altered placental DNA methylation (DNAme) has been associated with preeclampsia and fetal growth restriction but has not been well studied in the context of placental pathology, which likely underlies such changes. Our goal was thus to evaluate the association of DNAme with four major classes of placental pathology.

methodsWe utilized data from 484 placentas with both Illumina EPICv1 DNAme data and detailed histopathology information. Placental lesions were grouped as: acute inflammation (AI), chronic inflammation (CI), maternal vascular malperfusion (MVM), and fetal vascular malperfusion (FVM). We evaluated associations with DNAme based estimates of placental cell-types and epigenetic age acceleration, and used linear models to explore changes to autosome-wide DNAme with pathology.

resultsWe identified 281 and 56 CpGs that were differentially methylated (FDR<0.05, |Δβ|>0.05) in association with high-grade MVM and high-grade FVM respectively. High-grade MVM and high-grade FVM were associated with increased and decreased estimates of syncytiotrophoblast respectively. There were no CpGs differentially methylated in association with the inflammation pathologies. Epigenetic age acceleration was not associated with any pathology, suggesting the placental epigenetic clocks are robust at estimating gestational age in the presence of pathology.

conclusionsChanges in DNAme were associated with high-grade vascular pathologies, and DNAme may complement histopathologic placental examination. While changes largely reflected altered cell composition, altered gene regulation at the cellular level may also be present in these pathologies. Differential DNAme in high-grade MVM/FVM may contribute to or be a response to placental pathology.

Indexed as

DNA MethylationPlacentaPlacenta DiseasesEpigenesis, GeneticFemaleHumansPregnancyDNA methylationEpigeneticsPathologyPlacentaVascular malperfusion

Identifiers

PMID41689925
PMCPMC13251603

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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 OpenQuestion graph.