Evidence map›Paper›PMID 34009372›Full record

ReviewToxicological sciences : an official journal of the Society of Toxicology2021

Converging Roles of the Aryl Hydrocarbon Receptor in Early Embryonic Development, Maintenance of Stemness, and Tissue Repair.

Hesbon A Zablon, Chia-I Ko, Alvaro Puga

Open access · bronzeAbstract readReview
In one paragraph

Review in Toxicological sciences : an official journal of the Society of Toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Toxics · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. AhR and Wnt/β-Catenin Signaling Pathways and Their Interplay.Current issues in molecular biology · 2023
    Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
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

3 authors at 1 institution in 1 country.

Hesbon A Zablon
Chia-I Ko
Alvaro PugaDepartment of Environmental and Public Health Sciences, Center for Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA.ORCID 0000-0002-1318-8909
University of Cincinnati Medical Center · US

Funding

REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY RESEARCHP30ES006096 · NIEHS · UNIVERSITY OF CINCINNATI · PI PINNEY, SUSAN MENGEL · 1992 to 2022
$35.4M
MOLECULAR MECHANISMS OF COMPLEX MIXTURE TOXICITYR01ES010807 · NIEHS · UNIVERSITY OF CINCINNATI · PI PUGA, ALVARO · 2001 to 2021
$8.0M
Gene-Environment Interactions in the Fetal Origin of Adult Cardiac DiseaseR01ES024744 · NIEHS · UNIVERSITY OF CINCINNATI · PI PUGA, ALVARO, RUBINSTEIN, JACK · 2015 to 2019
$2.4M
NIEHS NIH HHS P30 ES006096NIEHS NIH HHS R01 ES010807NIEHS NIH HHS R01 ES024744
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor well-known for its adaptive role as a sensor of environmental toxicants and mediator of the metabolic detoxification of xenobiotic ligands. In addition, a growing body of experimental data has provided indisputable evidence that the AHR regulates critical functions of cell physiology and embryonic development. Recent studies have shown that the naïve AHR-that is, unliganded to xenobiotics but activated endogenously-has a crucial role in maintenance of embryonic stem cell pluripotency, tissue repair, and regulation of cancer stem cell stemness. Depending on the cellular context, AHR silences the expression of pluripotency genes Oct4 and Nanog and potentiates differentiation, whereas curtailing cellular plasticity and stemness. In these processes, AHR-mediated contextual responses and outcomes are dictated by changes of interacting partners in signaling pathways, gene networks, and cell-type-specific genomic structures. In this review, we focus on AHR-mediated changes of genomic architecture as an emerging mechanism for the AHR to regulate gene expression at the transcriptional level. Collective evidence places this receptor as a physiological hub connecting multiple biological processes whose disruption impacts on embryonic development, tissue repair, and maintenance or loss of stemness.

Indexed as

Gene Expression RegulationReceptors, Aryl HydrocarbonCell DifferentiationEmbryonic DevelopmentEmbryonic Stem CellsHumansReceptors, Aryl HydrocarbonAh receptorembryonic developmentstemnesstissue repair

Identifiers

PMID34009372
PMCPMC8285021
OpenAlexW3160216513

What Socratic 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 Socratic graph.