Evidence map›Paper›PMID 21168493›Full record

ReviewThe Journal of steroid biochemistry and molecular biology2011

Molecular targets that link dioxin exposure to toxicity phenotypes.

Wataru Yoshioka, Richard E Peterson, Chiharu Tohyama

Abstract readReview
In one paragraph

Review in The Journal of steroid biochemistry and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.8field-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

26 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. An Overview of Adverse Outcome Pathway Links between PMEnvironment & health (Washington, D.C.) · 2024
    Review
  4. Article
  5. Article
  6. A Review of the Functional Roles of the Zebrafish Aryl Hydrocarbon Receptors.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Review
  7. Dioxin Disrupts Dynamic DNA Methylation Patterns in Genes That Govern Cardiomyocyte Maturation.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article
  8. Article
  9. Mechanisms of Developmental Toxicity of Dioxins and Related Compounds.International journal of molecular sciences · 2019
    Review
  10. Article
  11. Article
  12. Article
  13. Ah Receptor Signaling Controls the Expression of Cardiac Development and Homeostasis Genes.Toxicological sciences : an official journal of the Society of Toxicology · 2015
    Article
  14. Article
  15. Male reproductive cancers and infertility: a mutual relationship.International journal of molecular sciences · 2015
    Review
  16. Article
  17. Inhibition of cathepsin B activity by 2,3,7,8-tetrachlorodibenzo-p-dioxin.Environmental science and pollution research international · 2015
    Article
  18. Article
  19. Intersection of AHR and Wnt signaling in development, health, and disease.International journal of molecular sciences · 2014
    Review
  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

3 authors at 2 institutions in 2 countries.

Wataru YoshiokaLaboratory of Environmental Health Sciences, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Richard E Peterson
Chiharu Tohyama
The University of Tokyo · JPUniversity of Wisconsin–Madison · US

Funding

REPRODUCTIVE AND DEVELOPMENTAL TOXICITY OF DIOXINR01ES001332 · NIEHS · UNIVERSITY OF WISCONSIN-MADISON · PI PETERSON, RICHARD EUGENE, VEZINA, CHAD M. · 1985 to 2021
$5.3M
REPRODUCTIVE AND DEVELOPMENTAL TOXICITY OF DIOXINR37ES001332 · NIEHS · UNIVERSITY OF WISCONSIN-MADISON · PI PETERSON, RICHARD EUGENE · 2000 to 2009
$3.9M
NIEHS NIH HHS ES01332NIEHS NIH HHS R01 ES001332NIEHS NIH HHS R37 ES001332
6 · The paper itself

Abstract

Many toxicology studies have elucidated health effects associated with exposure to various chemicals, but few have identified the molecular targets that cause specific endpoints of toxicity. Our understanding of the toxicity of dioxins, a group of chemicals capable of causing toxicity at environmentally relevant levels of exposure, is no exception. Dioxins are unique compared to most chemicals that we are exposed to in the environment because they activate a high affinity receptor, aryl hydrocarbon receptor (AhR), that was identified more than three decades ago. In recent years, several lines of experimental evidence have provided clues for opening the "black box" that contains the molecular mechanisms of dioxin action. These clues have emerged by toxicologists beginning to identify the molecular targets that link AhR signaling to tissue-specific toxicity phenotypes. Endpoints of dioxin toxicity for which downstream molecular targets have begun to be elucidated are observed in developmental or tissue regeneration processes, and include impaired prostate development and hydronephrosis in mouse fetuses and pups, reduced midbrain blood flow and jaw malformation in zebrafish embryos, and impaired fin regeneration in larval and adult zebrafish. Significant progress in identifying molecular targets for dioxin-induced hepatotoxicity in adult mice also has occurred. Misregulation of AhR downstream pathways, such as conversion of arachidonic acid to prostanoids via cyclooxygenase-2, and altered Wnt/β-catenin signaling downregulating Sox9, and signaling by receptors for inflammatory cytokines have been implicated in tissue-specific endpoints of dioxin toxicity. These findings may not only begin to clarify the molecular targets of dioxin action but shed light on new molecular events associated with development and disease.

Indexed as

Animal FinsAnimalsbeta CateninCyclooxygenase 2DioxinsFemaleHumansInflammation MediatorsJaw AbnormalitiesLiverMaleMesencephalonMiceReceptors, Aryl HydrocarbonReceptors, SteroidSignal Transductionbeta CateninCyclooxygenase 2DioxinsInflammation MediatorsReceptors, Aryl HydrocarbonReceptors, SteroidSOX9 Transcription Factor

Identifiers

PMID21168493
PMCPMC3433800
OpenAlexW1984281715

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.