Evidence map›Paper›PMID 29425287›Full record

ArticleEndocrinology2018

Perinatal Bisphenol A Exposure Increases Atherosclerosis in Adult Male PXR-Humanized Mice.

Yipeng Sui, Se-Hyung Park, Fang Wang, Changcheng Zhou

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Review
  3. Physiological Functions and Pathological Roles of PXR.Journal of the Endocrine Society · 2025
    Review
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  5. 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

4 authors at 1 institution in 1 country.

Yipeng SuiDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky.
Se-Hyung ParkDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky.
Fang WangDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky.
Changcheng ZhouDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky.
University of Kentucky · US

Funding

The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI MORRIS, ANDREW J · 2012 to 2017
$13.7M
Endocrine disruptor mediated activation of PXR causes dyslipidemia and atherosclerosisR01ES023470 · NIEHS · UNIVERSITY OF KENTUCKY · PI ZHOU, CHANGCHENG · 2013 to 2022
$2.7M
Role of IKKβ in obesity and atherosclerosisR01HL131925 · NHLBI · UNIVERSITY OF KENTUCKY · PI ZHOU, CHANGCHENG · 2016 to 2019
$1.5M
A novel mechanism for ART-associated dyslipidemia and atherosclerosisR01HL123358 · NHLBI · UNIVERSITY OF KENTUCKY · PI ZHOU, CHANGCHENG · 2015 to 2018
$1.5M
Mechanisms of atherogenic effects of bisphenol AR21ES022745 · NIEHS · UNIVERSITY OF KENTUCKY · PI ZHOU, CHANGCHENG · 2014 to 2015
$413k
NHLBI NIH HHS R01 HL123358NHLBI NIH HHS R01 HL131925NIEHS NIH HHS R01 ES023470NIEHS NIH HHS R21 ES022745NIGMS NIH HHS P20 GM103527
6 · The paper itself

Abstract

Bisphenol A (BPA) is a base chemical used extensively in numerous consumer products, and human exposure to BPA is ubiquitous. Higher BPA exposure has been associated with an increased risk of atherosclerosis and cardiovascular disease (CVD) in multiple human population-based studies. However, the underlying mechanisms responsible for the associations remain elusive. We previously reported that BPA activates the xenobiotic receptor pregnane X receptor (PXR), which has proatherogenic effects in animal models. Because BPA is a potent agonist for human PXR but does not affect rodent PXR activity, a suitable PXR-humanized apolipoprotein E-deficient (huPXR•ApoE-/-) mouse model was developed to study BPA's atherogenic effects. Chronic BPA exposure increased atherosclerosis in the huPXR•ApoE-/- mice. We report that BPA exposure can also activate human PXR signaling in the heart tubes of huPXR•ApoE-/- embryos, and perinatal BPA exposure exacerbated atherosclerosis in adult male huPXR•ApoE-/- offspring. However, atherosclerosis development in female offspring was not affected by perinatal BPA exposure. Perinatal BPA exposure did not affect plasma lipid levels but increased aortic and atherosclerotic lesional fatty acid transporter CD36 expression in male huPXR•ApoE-/- offspring. Mechanistically, PXR epigenetically regulated CD36 expression by increasing H3K4me3 levels and decreasing H3K27me3 levels in the CD36 promoter in response to perinatal BPA exposure. The findings from the present study contribute to our understanding of the association between BPA exposure and increased atherosclerosis or CVD risk in humans, and activation of human PXR should be considered for future BPA risk assessment.

Indexed as

AnimalsAortaApolipoproteins EAtherosclerosisBenzhydryl CompoundsBisphenol A CompoundsCD36 AntigensCholesterolEnvironmental PollutantsGene Expression RegulationMaleMiceMice, KnockoutPhenolsPregnane X ReceptorReceptors, SteroidApolipoproteins EBenzhydryl Compoundsbisphenol ABisphenol A CompoundsCD36 AntigensCholesterolEnvironmental PollutantsPhenolsPregnane X ReceptorReceptors, Steroid

Identifiers

PMID29425287
PMCPMC5939635
OpenAlexW2790510014

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.