Evidence map›Paper›PMID 25037585›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2014

Cardiac myocyte-specific AHR activation phenocopies TCDD-induced toxicity in zebrafish.

Kevin A Lanham, Jessica Plavicki, Richard E Peterson, Warren Heideman

Open access · greenAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Zebrafish Congenital Heart Disease Models: Opportunities and Challenges.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Article
  8. A Review of the Functional Roles of the Zebrafish Aryl Hydrocarbon Receptors.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Review
  9. Review
  10. Article
  11. Mechanisms of Developmental Toxicity of Dioxins and Related Compounds.International journal of molecular sciences · 2019
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  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

4 authors at 1 institution in 1 country.

Kevin A LanhamDepartment of Pharmaceutical Sciences, 777 Highland Avenue, University of Wisconsin, Madison, Wisconsin 53705-2222.
Jessica PlavickiDepartment of Pharmaceutical Sciences, 777 Highland Avenue, University of Wisconsin, Madison, Wisconsin 53705-2222.
Richard E PetersonDepartment of Pharmaceutical Sciences, 777 Highland Avenue, University of Wisconsin, Madison, Wisconsin 53705-2222.
Warren HeidemanDepartment of Pharmaceutical Sciences, 777 Highland Avenue, University of Wisconsin, Madison, Wisconsin 53705-2222 wheidema@wisc.edu.
University of Wisconsin–Madison · US

Funding

Molecular & Environmental Toxicology Pre-& Postdoctoral Training ProgramT32ES007015 · NIEHS · UNIVERSITY OF WISCONSIN-MADISON · PI CHRISTOPHER A BRADFIELD · 1985 to 2026
$11.5M
TCDD- INDUCED CARDIOTOXICITY IN DEVELOPING ZEBRAFISHR01ES012716 · NIEHS · UNIVERSITY OF WISCONSIN-MADISON · PI HEIDEMAN, WARREN NO MIDDLE NAME · 2005 to 2015
$2.7M
NIEHS NIH HHS R01 ES012716NIEHS NIH HHS T32 ES007015
6 · The paper itself

Abstract

Exposure of zebrafish embryos to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) activates the zebrafish aryl hydrocarbon receptor 2 (AHR) to produce developmental and cardiovascular toxicity. AHR is found in the heart; however, AHR activation by TCDD is not confined to the heart and occurs throughout the organism. In order to understand the cause of cardiotoxicity, we constructed a constitutively active AHR (caAHR) based on the zebrafish AHR2 and expressed it specifically in cardiomyocytes. We show that AHR activation within the cardiomyocytes can account for the heart failure induced by TCDD. Expression of the caAHR within the heart produced cardiac malformations, loss of circulation, and pericardial edema. The heart-specific activation of AHR reproduced several other well-characterized endpoints of TCDD toxicity outside of the cardiovascular system, including defects in swim bladder and craniofacial development. This work identifies a single cellular site of TCDD action, the myocardial cell, that can account for the severe cardiovascular collapse observed following early life stage exposure to TCDD, and contributes to other forms of toxicity.

Indexed as

ZebrafishAnimalsCardiotoxicityEmbryo, NonmammalianGene Expression Regulation, DevelopmentalHeart Defects, CongenitalMyocytes, CardiacPlasmidsPolychlorinated DibenzodioxinsPromoter Regions, GeneticReceptors, Aryl HydrocarbonRegional Blood FlowZebrafish ProteinsAHR2 protein, zebrafishPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonZebrafish Proteins

Identifiers

PMID25037585
PMCPMC4271120
OpenAlexW2315459591

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.