ArticleToxicology letters2022
In ovo exposure to cadmium causes right ventricle hyperplasia due to cell proliferation of cardiomyocytes.
Article in Toxicology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Cardiotoxicity of Cadmium and Its Effects on Heart Efficiency During Early and Late Chick Embryogenesis.Cardiovascular toxicology · 2024Article
- Prenatal exposure to air pollutants and the risk of congenital heart disease: a Korean national health insurance database-based study.Scientific reports · 2024Article
- Exposure to essential and non-essential trace elements and risks of congenital heart defects: A narrative review.Frontiers in nutrition · 2023Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Cadmium (Cd) is an environmental and occupational pollutant inhaled through smoking or ingested through contaminated food. Yet, little is known about its teratogenicity. In this study, the effects of Cd on embryonic heart development were investigated by exposing Cd to chicken embryos in ovo. Fertilized eggs were treated with Cd at Hamburger-Hamilton Stage (HH)16 and collected at HH35 for histological evaluation of the heart. Cd treatment of 100 μM at HH16 increased embryo mortality at HH35. Specific structural heart defects were not observed in any Cd treatment group, but the relative myocardial tissue area of the right ventricle was increased with Cd exposure. When the HH31 hearts were stained with p-H3S10, the right ventricle had an increased number of cells undergoing proliferation, which was associated with upregulation of Cdk1, Cdk6, CycA, CycD, and CycE detected by qPCR. These findings suggest that Cd exposure from HH16 upregulates proliferation genes and drives overgrowth of the right ventricle. These results grant further attention to Cd teratogenicity on embryonic heart development. Such morphological changes in the heart can potentially affect cardiac function and increase the risk for future cardiovascular diseases, such as heart failure.
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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.