Evidence map›Paper›PMID 40863927›Full record

ArticleToxics2025

LDLR H3K27ac in PBMCs: An Early Warning Biomarker for Hypercholesterolemia Susceptibility in Male Newborns Treated with Prenatal Dexamethasone.

Kexin Liu, Can Ai, Dan Xu, Wen Hu, Guanghui Chen, Jinzhi Zhang, Ning Zhang, Dongfang Wu, Hui Wang

Abstract read
In one paragraph

Article in Toxics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Kexin LiuDepartment of Pharmacology, School of Basic Medical Science, Wuhan University, Wuhan 430071, China.ORCID 0009-0007-4856-3899
Can AiDepartment of Pharmacology, School of Basic Medical Science, Wuhan University, Wuhan 430071, China.ORCID 0009-0004-4581-3520
Dan XuDepartment of Pharmacology, School of Basic Medical Science, Wuhan University, Wuhan 430071, China.
Wen HuDepartment of Pharmacy, Zhongnan Hospital of Wuhan University, Wuhan 430072, China.
Guanghui ChenDepartment of Pharmacology, School of Basic Medical Science, Wuhan University, Wuhan 430071, China.
Jinzhi ZhangDepartment of Pharmacology, School of Basic Medical Science, Wuhan University, Wuhan 430071, China.
Ning ZhangDepartment of Pharmacology, School of Basic Medical Science, Wuhan University, Wuhan 430071, China.
Dongfang WuDepartment of Pharmacy, Zhongnan Hospital of Wuhan University, Wuhan 430072, China.
Hui WangDepartment of Pharmacology, School of Basic Medical Science, Wuhan University, Wuhan 430071, China.ORCID 0000-0001-5300-8661

Funding

Fundamental Research Funds for the Central Universities 2042023kf0066Hubei Province Health and Family Planning Scientific Research Project WJ2017C0003Hubei Province's Outstanding Medical Academic Leader programMedical Sciences Advancement Program (Basic Medical Sciences) of Wuhan University TFJC2018001National Key Research and Development Program of China 2020YFA0803900National Natural Science Foundation of China 32300973National Natural Science Foundation of China 82030111
6 · The paper itself

Abstract

Dexamethasone, widely used as an exogenous glucocorticoid in clinical and animal practice, has recently been recognized as an environmental contaminant of concern. Existing evidence documents its ability to induce persistent dyslipidemia in adult offspring. In this study, plasma cholesterol levels in male rats exposed to dexamethasone prenatally (PDE) were increased. Meanwhile, developmental tracking revealed a reduction in hepatic low-density lipoprotein receptor (LDLR) promoter H3K27 acetylation (H3K27ac) and corresponding transcriptional activity across gestational-to-postnatal stages. Mechanistic investigations established glucocorticoid receptor/histone deacetylase2 (GR/HDAC2) axis-mediated epigenetic programming of LDLR through H3K27ac modulation in PDE offspring, potentiating susceptibility to hypercholesterolemia. Additionally, in peripheral blood mononuclear cells (PBMC) of PDE male adult offspring, LDLR H3K27ac level and expression were also decreased and positively correlated with those in the liver. Clinical studies further substantiated that male newborns prenatally treated with dexamethasone exhibited increased serum cholesterol levels and consistent reductions in LDLR H3K27ac levels and corresponding transcriptional activity in PBMC. This study establishes a complete evidence chain linking PDE with epigenetic programming and cholesterol metabolic dysfunction, proposing PBMC epigenetic biomarkers as a novel non-invasive monitoring tool for assessing the developmental toxicity of chemical exposures during pregnancy. This has significant implications for improving environmental health risk assessment systems.

Indexed as

dexamethasoneepigenetic inheritancehypercholesterolemiaperipheral blood mononuclear cellswarning biomarker

Identifiers

PMID40863927
PMCPMC12390111

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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.