Evidence map›Paper›PMID 40089607›Full record

ArticlePediatric research2026

Maternal di(2-ethylhexyl) phthalate exposure increases the risk of congenital heart disease in mice offspring.

Haiqun Shi, Zehua Zhang, Anna Shen, Tong Ding, Rui Zhao, Yan Shi, Jianyuan Zhao, Ke Cai, Feng Wang

Abstract read
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In one paragraph

Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

9 authors.

Haiqun Shi *Pediatric Heart Center, NHC Key Laboratory of Neonatal Diseases, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, 201102, China.
Zehua Zhang *Pediatric Heart Center, NHC Key Laboratory of Neonatal Diseases, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, 201102, China.
Anna ShenPediatric Heart Center, NHC Key Laboratory of Neonatal Diseases, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, 201102, China.
Tong DingPediatric Heart Center, NHC Key Laboratory of Neonatal Diseases, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, 201102, China.
Rui ZhaoInstitute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200092, China.
Yan ShiInstitute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200092, China.
Jianyuan ZhaoInstitute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200092, China.
Ke CaiInstitute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200092, China. kcai1994@163.com.
Feng WangPediatric Heart Center, NHC Key Laboratory of Neonatal Diseases, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, 201102, China. fmwong@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

abstrctBACKGROUD: Epidemiological data suggest that maternal occupational exposure to mixed phthalates comprising di(2-ethylhexyl) phthalate (DEHP) increases the risk of congenital heart disease (CHD). In this study, we used mice as an animal model to validate impact of first-trimester DEHP exposure on the risk of CHD in offspring, to elucidate the possible mechanisms and to provide a potential feasible intervention. METHODS AND

resultsEight-week-old C57BL/6J pregnant mice were randomly divided into standard and DEHP diet groups. The incidence of CHD in DEHP diet group offspring was up to 14.41% observed via Hematoxylin-eosin (HE) staining. Quantitative PCR analysis revealed that expression of key genes involved in cardiogenesis were suppressed at the transcriptional level, which may be due to decreased nuclear translocation of p65. The inhibition of DEHP on key genes was rescued to some extent by choline through driving p65 into nuclear. In the mice, supplementation of choline during DEHP exposure reduced the incidence of CHD in offspring from 14.41% to 4.63%.

conclusionsOur study demonstrates that mice first-trimester DEHP exposure significantly increases the risk of CHD in the offspring via inhibiting mRNA levels of key genes in cardiogenesis, and choline could protect against the pathogenesis. IMPACT: Our study provides key mechanistic insights into the risk of CHD by DEHP exposure during early pregnancy, and provides choline as a potentially effective intervention. DEHP suppressed the expression of key genes involved in embryonic cardiac septum development at the transcriptional level via inhibiting nuclear translocation of p65. Choline can play a role in rescuing the inhibition of DEHP on cardiogenesis genes via driving p65 translocate into the nuclear.

Indexed as

Diethylhexyl PhthalateHeart Defects, CongenitalMaternal ExposurePrenatal Exposure Delayed EffectsAnimalsDisease Models, AnimalFemaleMaleMiceMice, Inbred C57BLPregnancyDiethylhexyl Phthalate

Identifiers

PMID40089607

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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.