Evidence map›Paper›PMID 29119010›Full record

ArticleEnvironmental epigenetics2017

Epigenetic impact of endocrine disrupting chemicals on lipid homeostasis and atherosclerosis: a pregnane X receptor-centric view.

Robert N Helsley, Changcheng Zhou

Open access · goldAbstract read
In one paragraph

Article in Environmental epigenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

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  8. Adipocyte-Derived PXR Signaling Is Dispensable for Diet-Induced Obesity and Metabolic Disorders in Mice.Drug metabolism and disposition: the biological fate of chemicals · 2023
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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

2 authors at 1 institution in 1 country.

Robert N HelsleyDepartment of Pharmacology and Nutritional Sciences, Center for Metabolic Disease Research, University of Kentucky, Lexington, KY 40536, USA.
Changcheng ZhouDepartment of Pharmacology and Nutritional Sciences, Center for Metabolic Disease Research, University of Kentucky, Lexington, KY 40536, USA.
University of Kentucky · US

Funding

Endocrine disruptor mediated activation of PXR causes dyslipidemia and atherosclerosisR01ES023470 · NIEHS · UNIVERSITY OF KENTUCKY · PI ZHOU, CHANGCHENG · 2013 to 2022
$2.7M
TRAINING PROGRAM IN OXIDATIVE STRESS AND NUTRITIONT32DK007778 · NIDDK · UNIVERSITY OF KENTUCKY · PI WEBB, NANCY R · 2000 to 2019
$2.5M
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 HL131925NIDDK NIH HHS T32 DK007778NIEHS NIH HHS R01 ES023470NIEHS NIH HHS R21 ES022745
6 · The paper itself

Abstract

Despite the major advances in developing diagnostic techniques and effective treatments, atherosclerotic cardiovascular disease (CVD) is still the leading cause of mortality and morbidity worldwide. While considerable progress has been achieved to identify gene variations and environmental factors that contribute to CVD, much less is known about the role of "gene-environment interactions" in predisposing individuals to CVD. Our chemical environment has significantly changed in the last few decades, and there are more than 100,000 synthetic chemicals in the market. Recent large-scale human population studies have associated exposure to certain chemicals including many endocrine disrupting chemicals (EDCs) with increased CVD risk, and animal studies have also confirmed that some EDCs can cause aberrant lipid homeostasis and increase atherosclerosis. However, the underlying mechanisms of how exposure to those EDCs influences CVD risk remain elusive. Numerous EDCs can activate the nuclear receptor pregnane X receptor (PXR) that functions as a xenobiotic sensor to regulate host xenobiotic metabolism. Recent studies have demonstrated the novel functions of PXR in lipid homeostasis and atherosclerosis. In addition to directly regulating transcription, PXR has been implicated in the epigenetic regulation of gene transcription. Exposure to many EDCs can also induce epigenetic modifications, but little is known about how the changes relate to the onset or progression of CVD. In this review, we will discuss recent research on PXR and EDCs in the context of CVD and propose that PXR may play a previously unrealized role in EDC-mediated epigenetic modifications that affect lipid homeostasis and atherosclerosis.

Indexed as

cardiovascular disease (CVD)endocrine disrupting chemicals (EDCs)epigeneticsnuclear receptorspregnane X receptor (PXR)

Identifiers

PMID29119010
PMCPMC5672952
OpenAlexW2767075292

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.