Fetal Alcohol Spectrum Disorder: Embryogenesis Under Reduced Retinoic Acid Signaling Conditions

Abraham Fainsod*, Liat Bendelac-Kapon, Yehuda Shabtai

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

11 Scopus citations


Fetal Alcohol Spectrum Disorder (FASD) is a complex set of developmental malformations, neurobehavioral anomalies and mental disabilities induced by exposing human embryos to alcohol during fetal development. Several experimental models and a series of developmental and biochemical approaches have established a strong link between FASD and reduced retinoic acid (RA) signaling. RA signaling is involved in the regulation of numerous developmental decisions from patterning of the anterior–posterior axis, starting at gastrulation, to the differentiation of specific cell types within developing organs, to adult tissue homeostasis. Being such an important regulatory signal during embryonic development, mutations or environmental perturbations that affect the level, timing or location of the RA signal can induce multiple and severe developmental malformations. The evidence connecting human syndromes to reduced RA signaling is presented here and the resulting phenotypes are compared to FASD. Available data suggest that competition between ethanol clearance and RA biosynthesis is a major etiological component in FASD.

Original languageAmerican English
Title of host publicationSubcellular Biochemistry
Number of pages29
StatePublished - 2020

Publication series

NameSubcellular Biochemistry
ISSN (Print)0306-0225

Bibliographical note

Publisher Copyright:
© 2020, Springer Nature Switzerland AG.


  • Acetaldehyde
  • Alcohol clearance
  • Biosynthesis
  • Birth Defects
  • Development
  • Embryogenesis
  • Ethanol
  • FAS
  • FASD
  • Fetal alcohol spectrum disorder
  • Fetal alcohol syndrome
  • Human
  • Malformations
  • Metabolism
  • Retinoic acid
  • Retinol
  • Signaling
  • Teratology
  • Vitamin A deficiency
  • Xenopus


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