Evidence map›Paper›PMID 29024604›Full record

ReviewBiochemistry and cell biology = Biochimie et biologie cellulaire2018

The avian embryo as a model for fetal alcohol spectrum disorder.

George R Flentke, Susan M Smith

Open access · greenAbstract readReview
In one paragraph

Review in Biochemistry and cell biology = Biochimie et biologie cellulaire, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. The Role of the Hedgehog Pathway in Alcohol-Induced Birth Defects.Advances in experimental medicine and biology · 2026
    Review
  3. Animal Models of Prenatal Alcohol Exposure.Advances in experimental medicine and biology · 2026
    Review
  4. Review
  5. The avian embryo as a time-honoured animal model in developmental, biomedical and agricultural research.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. The m6A methylation regulates gonadal sex differentiation in chicken embryo.Journal of animal science and biotechnology · 2022
    Article
  11. Review
  12. Article
  13. Embryonic Chicken (Comparative medicine · 2019
    Review
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

2 authors at 1 institution in 1 country.

George R FlentkeUNC-Nutrition Research Institute and Department of Nutrition, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA.
Susan M SmithUNC-Nutrition Research Institute and Department of Nutrition, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA.
David H. Murdock Research Institute · US

Funding

Craniofacial Morphogenesis in Prenatal Alcohol ExposureR01AA011085 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SMITH, SUSAN M. · 2001 to 2025
$6.3M
Craniofacial Morphogenesis in Prenatal Alcohol ExposureR37AA011085 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SMITH, SUSAN M. · 2007 to 2016
$3.3M
Prenatal alcohol exposure disrupts maternal-fetal iron metabolism in FASDR01AA022999 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KLING, PAMELA J, SMITH, SUSAN M. · 2014 to 2018
$1.6M
NIAAA NIH HHS R01 AA011085NIAAA NIH HHS R01 AA022999NIAAA NIH HHS R37 AA011085
6 · The paper itself

Abstract

Prenatal alcohol exposure (PAE) remains a leading preventable cause of structural birth defects and permanent neurodevelopmental disability. The chicken (Gallus gallus domesticus) is a powerful embryological research model, and was possibly the first in which the teratogenicity of alcohol was demonstrated. Pharmacologically relevant exposure to alcohol in the range of 20-70 mmol/L (20-80 mg/egg) disrupt the growth of chicken embryos, morphogenesis, and behavior, and the resulting phenotypes strongly parallel those of mammalian models. The avian embryo's direct accessibility has enabled novel insights into the teratogenic mechanisms of alcohol. These include the contribution of IGF1 signaling to growth suppression, the altered flow dynamics that reshape valvuloseptal morphogenesis and mediate its cardiac teratogenicity, and the suppression of Wnt and Shh signals thereby disrupting the migration, expansion, and survival of the neural crest, and underlie its characteristic craniofacial deficits. The genetic diversity within commercial avian strains has enabled the identification of unique loci, such as ribosome biogenesis, that modify vulnerability to alcohol. This venerable research model is equally relevant for the future, as the application of technological advances including CRISPR, optogenetics, and biophotonics to the embryo's ready accessibility creates a unique model in which investigators can manipulate and monitor the embryo in real-time to investigate the effect of alcohol on cell fate.

Indexed as

ChickensDisease Models, AnimalEmbryonic DevelopmentOrganogenesisSignal TransductionTeratogenesisAnimalsChick EmbryoFetal Alcohol Spectrum DisordersHumanscardiac developmentchickencraniofacial developmentcrête neuraledéveloppement cardiaquedéveloppement cranio-facialfetal alcohol spectrum disorderneural crestpoulettroubles du spectre de l’alcoolisation fœtale

Identifiers

PMID29024604
PMCPMC5914177
OpenAlexW2764182400

What OpenQuestion holds

Textmetadata
LicenceTDM
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.