Evidence map›Paper›PMID 26924429›Full record

ReviewBiochimica et biophysica acta2016

Novel functions of PXR in cardiometabolic disease.

Changcheng Zhou

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. 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
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. 4Frontiers in pharmacology · 2020
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

1 author at 1 institution in 1 country.

Changcheng ZhouDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY 40536, USA; Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY 40536, USA. Electronic address: c.zhou@uky.edu.
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
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 ES022745
6 · The paper itself

Abstract

Cardiometabolic disease emerges as a worldwide epidemic and there is urgent need to understand the molecular mechanisms underlying this chronic disease. The chemical environment to which we are exposed has significantly changed in the past few decades and recent research has implicated its contribution to the development of many chronic human diseases. However, the mechanisms of how exposure to chemicals contributes to the development of cardiometabolic disease are poorly understood. Numerous chemicals have been identified as ligands for the pregnane X receptor (PXR), a nuclear receptor functioning as a xenobiotic sensor to coordinately regulate xenobiotic metabolism via transcriptional regulation of xenobiotic-detoxifying enzymes and transporters. In the past decade, the function of PXR in the regulation of xenobiotic metabolism has been extensively studied by many laboratories and the role of PXR as a xenobiotic sensor has been well-established. The identification of PXR as a xenobiotic sensor has provided an important tool for the study of new mechanisms through which xenobiotic exposure impacts human chronic diseases. Recent studies have revealed novel and unexpected roles of PXR in modulating obesity, insulin sensitivity, lipid homeostasis, atherogenesis, and vascular functions. These studies suggest that PXR signaling may contribute significantly to the pathophysiological effects of many known xenobiotics on cardiometabolic disease in humans. The discovery of novel functions of PXR in cardiometabolic disease not only contributes to our understanding of "gene-environment interactions" in predisposing individuals to chronic diseases but also provides strong evidence to inform future risk assessment for relevant chemicals. This article is part of a Special Issue entitled: Xenobiotic nuclear receptors: New Tricks for An Old Dog, edited by Dr. Wen Xie.

Indexed as

AnimalsAtherosclerosisBlood VesselsChronic DiseaseGene-Environment InteractionGene Expression RegulationHumansInactivation, MetabolicInsulin ResistanceIntestinal MucosaIntestinesLipid MetabolismLiverObesityPregnane X ReceptorReceptors, SteroidPregnane X ReceptorReceptors, SteroidXenobioticsCardiovascular diseaseEndocrine disrupting chemicalsLipid homeostasisMetabolic disordersObesityXenobiotic receptor

Identifiers

PMID26924429
PMCPMC4975627
OpenAlexW2289365417

What OpenQuestion holds

Textmetadata
LicenceTDM
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.