Evidence map›Paper›PMID 38301654›Full record

ArticleCell reports. Medicine2024

Epigenetic programming mediates abnormal gut microbiota and disease susceptibility in offspring with prenatal dexamethasone exposure.

Xiaoqian Lu, Beidi Chen, Dan Xu, Wen Hu, Xia Wang, Yongguo Dai, Qian Wang, Yu Peng, Kaiqi Chen, Dongchi Zhao and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.8field-weighted citation impact, top 10% of its field
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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Rethinking corticosteroids use in oncology.Frontiers in pharmacology · 2025
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  6. Review
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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

11 authors at 3 institutions in 1 country.

Xiaoqian LuDepartment of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, China.
Beidi ChenDepartment of Rheumatology and Immunology, Peking University Third Hospital, Beijing 100191, China.
Dan XuDepartment of Obstetrics and Gynaecology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Wen HuHubei Provincial Key Laboratory of Developmentally Originated Diseases, Wuhan 430071, China.
Xia WangDepartment of Pediatrics, Children's Digital Health, and Data Center, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Yongguo DaiDepartment of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, China.
Qian WangDepartment of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, China.
Yu PengDepartment of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, China.
Kaiqi ChenDepartment of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, China.
Dongchi ZhaoHubei Provincial Key Laboratory of Developmentally Originated Diseases, Wuhan 430071, China; Department of Pediatrics, Children's Digital Health, and Data Center, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Hui WangDepartment of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, China; Department of Obstetrics and Gynaecology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China; Hubei Provincial Key Laboratory of Developmentally Originated Diseases, Wuhan 430071, China. Electronic address: wanghui19@whu.edu.cn.
Wuhan University · CNHubei Provincial Center for Disease Control and Prevention · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prenatal dexamethasone exposure (PDE) can lead to increased susceptibility to various diseases in adult offspring, but its effect on gut microbiota composition and the relationship with disease susceptibility remains unclear. In this study, we find sex-differential changes in the gut microbiota of 6-month-old infants with prenatal dexamethasone therapy (PDT) that persisted in female infants up to 2.5 years of age with altered bile acid metabolism. PDE female offspring rats show abnormal colonization and composition of gut microbiota and increased susceptibility to cholestatic liver injury. The aberrant gut microbiota colonization in the PDE offspring can be attributed to the inhibited Muc2 expression caused by decreased CDX2 expression before and after birth. Integrating animal and cell experiments, we further confirm that dexamethasone could inhibit Muc2 expression by activating GR/HDAC11 signaling and regulating CDX2 epigenetic modification. This study interprets abnormal gut microbiota and disease susceptibility in PDT offspring from intrauterine intestinal dysplasia.

Indexed as

Gastrointestinal MicrobiomePrenatal Exposure Delayed EffectsAnimalsDexamethasoneDisease SusceptibilityEpigenesis, GeneticFemaleHumansInfantPregnancyRatsRats, WistarDexamethasoneepigenetic modificationgut microbiotaintrauterine programmingmucin-2prenatal dexamethasone therapy

Identifiers

PMID38301654
PMCPMC10897547
OpenAlexW4391385335

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.