ArticleToxicological sciences : an official journal of the Society of Toxicology2011
Perspectives on the potential involvement of the AH receptor-dioxin axis in cardiovascular disease.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Environmental Toxins and Oxidative Stress: The Link to Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Elevated congenital heart disease birth prevalence rates found in Central Vietnam and dioxin TCDD residuals from the use of 2, 4, 5-T herbicides (Agent Orange) in the Da Nang region.PLOS global public health · 2022Article
- Review
- Developmental and lifelong dioxin exposure induces measurable changes in cardiac structure and function in adulthood.Scientific reports · 2021Article
- Dioxin Disrupts Dynamic DNA Methylation Patterns in Genes That Govern Cardiomyocyte Maturation.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- AHR Signaling Interacting with Nutritional Factors Regulating the Expression of Markers in Vascular Inflammation and Atherogenesis.International journal of molecular sciences · 2020Article
- The aryl hydrocarbon receptor as a target of environmental stressors - Implications for pollution mediated stress and inflammatory responses.Redox biology · 2020Review
- Cardiovascular Effects of PCB 126 (3,3',4,4',5-Pentachlorobiphenyl) in Zebrafish Embryos and Impact of Co-Exposure to Redox Modulating Chemicals.International journal of molecular sciences · 2019Article
- Ah Receptor Activation by Dioxin Disrupts Activin, BMP, and WNT Signals During the Early Differentiation of Mouse Embryonic Stem Cells and Inhibits Cardiomyocyte Functions.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Ah Receptor Signaling Controls the Expression of Cardiac Development and Homeostasis Genes.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- Disruption of Ah Receptor Signaling during Mouse Development Leads to Abnormal Cardiac Structure and Function in the Adult.PloS one · 2015Article
- Toxic effects of polychlorinated biphenyls on cardiac development in zebrafish.Molecular biology reports · 2014Article
- Article
- Dioxin inhibits zebrafish epicardium and proepicardium development.Toxicological sciences : an official journal of the Society of Toxicology · 2013Article
- Treatment of mice with 2,3,7,8-Tetrachlorodibenzo-p-dioxin markedly increases the levels of a number of cytochrome P450 metabolites of omega-3 polyunsaturated fatty acids in the liver and lung.The Journal of toxicological sciences · 2013Article
- TCDD disrupts hypural skeletogenesis during medaka embryonic development.Toxicological sciences : an official journal of the Society of Toxicology · 2012Article
- Polychlorinated biphenyl 77 augments angiotensin II-induced atherosclerosis and abdominal aortic aneurysms in male apolipoprotein E deficient mice.Toxicology and applied pharmacology · 2011Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the induction of the CYP1 family of cytochrome P450s and of several phase II detoxification enzymes. Although induction of these genes is the best characterized AHR function, it does not adequately explain the diversity of AHR-mediated effects. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the prototypical AHR ligand and dioxin congener and a model for many environmentally relevant organochlorinated compounds. Research over the course of the last 30 years has made it evident that AHR activation in response to TCDD and other xenobiotic agonists directly affects multiple metabolic pathways, leading to the identification of many AHR-directed effects of dioxin involved in regulation of growth factor signaling, cell cycle proliferation, differentiation, arrest, and apoptosis. There is ample evidence that TCDD causes persistent cardiac defects in zebrafish, chickens, mice, and likely humans and is associated with human cardiovascular disease. The question that I address here is whether exposure to TCDD during early development perturbs the concerted differentiation patterns of cardiovascular cell lineages and tissues and leads to cardiac malformations and long-term cardiovascular disease. Research to define the mechanisms responsible for the lifelong cardiovascular malformations resulting from TCDD exposure during embryonic development will be highly significant to the prevention of environmental cardiovascular injury.
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Registered trials
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.