Evidence map›Paper›PMID 31537853›Full record

ArticleScientific reports2019

Maternal cadmium exposure in the mouse leads to increased heart weight at birth and programs susceptibility to hypertension in adulthood.

Kathleen M Hudson, Scott M Belcher, Michael Cowley

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 63 citations in OpenAlex.

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  12. The imprinted gene Zac1 regulates steatosis in developmental cadmium-induced nonalcoholic fatty liver disease.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  13. Review
  14. LncRNAFrontiers in cell and developmental biology · 2023
    Article
  15. Review
  16. Cardiac Development in the Presence of Cadmium: AnEnvironmental health perspectives · 2022
    Article
  17. Article
  18. 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

3 authors at 1 institution in 1 country.

Kathleen M HudsonCenter for Human Health and the Environment, and Department of Biological Sciences, North Carolina State University, Raleigh, NC, 27695, USA.
Scott M BelcherCenter for Human Health and the Environment, and Department of Biological Sciences, North Carolina State University, Raleigh, NC, 27695, USA.
Michael CowleyCenter for Human Health and the Environment, and Department of Biological Sciences, North Carolina State University, Raleigh, NC, 27695, USA. macowley@ncsu.edu.ORCID http://orcid.org/0000-0001-8564-4224
North Carolina State University · US

Funding

Translational Research Support CoreP30ES025128 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI Kelly Sides · 2015 to 2026
$18.3M
Epigenetic mechanisms linking in utero cadmium exposure to hepatic steatosisK22ES027510 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI COWLEY, MICHAEL · 2017 to 2019
$485k
NIEHS NIH HHS K22 ES027510NIEHS NIH HHS P30 ES025128
6 · The paper itself

Abstract

Cadmium (Cd) is a toxic heavy metal ubiquitous in the environment. Maternal exposure to Cd is associated with fetal growth restriction, trace element deficiencies, and congenital malformations. Cd exposure during adulthood is associated with cardiovascular disease (CVD); however, the effects of maternal Cd exposure on offspring cardiovascular development and disease are not well-understood. Utilizing a mouse model of maternal Cd exposure, we show that offspring born to Cd-exposed mothers have increased heart weights at birth and susceptibility to hypertension during adulthood. Despite inefficient maternal-fetal transfer of Cd, maternal Cd alters fetal levels of essential trace elements including a deficiency in iron, which is required for cardiovascular system development, oxygen homeostasis, and cellular metabolism. RNA-seq on newborn hearts identifies differentially expressed genes associated with maternal Cd exposure that are enriched for functions in CVD, hypertension, enlarged hearts, cellular energy, and hypoxic stress. We propose that a maternal Cd exposure-induced iron deficiency leads to altered cellular metabolic pathways and hypoxic conditions during fetal development; this stress may contribute to increased heart weight at birth and the programming of susceptibility to hypertension in adulthood. These studies will give insights into potential mechanisms through which maternal Cd exposure impacts cardiovascular development and disease.

Indexed as

AnimalsAnimals, NewbornBody WeightCadmiumDisease Models, AnimalFemaleGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksHeartHypotensionMaternal ExposureMetabolic Networks and PathwaysMiceOrgan SizePregnancyCadmium

Identifiers

PMID31537853
PMCPMC6753073
OpenAlexW2974421437

What OpenQuestion holds

Textmetadata
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.