Evidence map›Paper›PMID 26555816›Full record

ArticlePloS one2015

Disruption of Ah Receptor Signaling during Mouse Development Leads to Abnormal Cardiac Structure and Function in the Adult.

Vinicius S Carreira, Yunxia Fan, Hisaka Kurita, Qin Wang, Chia-I Ko, Mindi Naticchioni, Min Jiang, Sheryl Koch, Xiang Zhang, Jacek Biesiada and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
12.1field-weighted citation impact, top 2% 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

23 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
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  8. Dioxin Disrupts Dynamic DNA Methylation Patterns in Genes That Govern Cardiomyocyte Maturation.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article
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  12. Review
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  15. Structural hierarchy controlling dimerization and target DNA recognition in the AHR transcriptional complex.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  16. Review
  17. Article
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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

14 authors at 1 institution in 1 country.

Vinicius S CarreiraDepartment of Environmental Health and Center for Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
Yunxia FanDepartment of Environmental Health and Center for Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
Hisaka KuritaDepartment of Environmental Health and Center for Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
Qin WangDepartment of Environmental Health and Center for Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
Chia-I KoDepartment of Environmental Health and Center for Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
Mindi NaticchioniDepartment of Internal Medicine, Division of Cardiovascular Health and Disease, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
Min JiangDepartment of Internal Medicine, Division of Cardiovascular Health and Disease, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
Sheryl KochDepartment of Internal Medicine, Division of Cardiovascular Health and Disease, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
Xiang ZhangDepartment of Environmental Health and Center for Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
Jacek BiesiadaDepartment of Environmental Health and Center for Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
Mario MedvedovicDepartment of Environmental Health and Center for Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
Ying XiaDepartment of Environmental Health and Center for Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
Jack RubinsteinDepartment of Internal Medicine, Division of Cardiovascular Health and Disease, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
Alvaro PugaDepartment of Environmental Health and Center for Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, United States of America.
University of Cincinnati Medical Center · US

Funding

REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY RESEARCHP30ES006096 · NIEHS · UNIVERSITY OF CINCINNATI · PI YADAV, JAGJIT S · 1992 to 2022
$35.4M
MOLECULAR MECHANISMS OF COMPLEX MIXTURE TOXICITYR01ES010807 · NIEHS · UNIVERSITY OF CINCINNATI · PI PUGA, ALVARO · 2001 to 2021
$8.0M
MOLECULAR MECHANISMS OF DIOXIN ACTIONR01ES006273 · NIEHS · UNIVERSITY OF CINCINNATI · PI PUGA, ALVARO · 1993 to 2015
$4.6M
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
Gene-Environment Interactinos Training ProgramT32ES016646 · NIEHS · UNIVERSITY OF CINCINNATI · PI PUGA, ALVARO · 2008 to 2014
$2.1M
NIEHS NIH HHS P30 ES006096NIEHS NIH HHS P30 ES06096NIEHS NIH HHS R01 ES006273NIEHS NIH HHS R01 ES010807NIEHS NIH HHS R01 ES024744NIEHS NIH HHS R01 ES06273NIEHS NIH HHS R01 ES10807NIEHS NIH HHS T32 ES016646
6 · The paper itself

Abstract

The Developmental Origins of Health and Disease (DOHaD) Theory proposes that the environment encountered during fetal life and infancy permanently shapes tissue physiology and homeostasis such that damage resulting from maternal stress, poor nutrition or exposure to environmental agents may be at the heart of adult onset disease. Interference with endogenous developmental functions of the aryl hydrocarbon receptor (AHR), either by gene ablation or by exposure in utero to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a potent AHR ligand, causes structural, molecular and functional cardiac abnormalities and altered heart physiology in mouse embryos. To test if embryonic effects progress into an adult phenotype, we investigated whether Ahr ablation or TCDD exposure in utero resulted in cardiac abnormalities in adult mice long after removal of the agent. Ten-months old adult Ahr-/- and in utero TCDD-exposed Ahr+/+ mice showed sexually dimorphic abnormal cardiovascular phenotypes characterized by echocardiographic findings of hypertrophy, ventricular dilation and increased heart weight, resting heart rate and systolic and mean blood pressure, and decreased exercise tolerance. Underlying these effects, genes in signaling networks related to cardiac hypertrophy and mitochondrial function were differentially expressed. Cardiac dysfunction in mouse embryos resulting from AHR signaling disruption seems to progress into abnormal cardiac structure and function that predispose adults to cardiac disease, but while embryonic dysfunction is equally robust in males and females, the adult abnormalities are more prevalent in females, with the highest severity in Ahr-/- females. The findings reported here underscore the conclusion that AHR signaling in the developing heart is one potential target of environmental factors associated with cardiovascular disease.

Indexed as

Signal TransductionAnimalsFemaleHeart Defects, CongenitalHomeostasisMaternal ExposureMiceMice, Inbred C57BLMice, TransgenicMitochondria, HeartPregnancyReceptors, Aryl HydrocarbonReceptors, Aryl Hydrocarbon

Identifiers

PMID26555816
PMCPMC4640841
OpenAlexW2172661774

What OpenQuestion holds

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LicenceCC BY
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.