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Updated: Sep 14, 2025

Analysis of Congenital Heart Defects in Mouse Embryos Using Qualitative and Quantitative Histological Methods
Published on: March 10, 2020
Prenatal Alcohol Exposure and Congenital Heart Defects: Retinoic Acid Deficiency as a Potential Mechanism in
Roberto Paparella1, Carolina Putotto1, Marco Fiore2
1Department of Maternal Infantile and Urological Sciences, Sapienza University of Rome, 00185 Rome, Italy.
Insights
Fetal alcohol spectrum disorder (FASD) is a leading cause of developmental disabilities. Prenatal alcohol exposure may cause heart defects like d-TGA by interfering with retinoic acid, requiring further study.
Area of Science:
- Developmental Biology
- Teratology
- Cardiology
Background:
- Fetal alcohol spectrum disorder (FASD) is a preventable cause of developmental disabilities.
- Congenital heart defects (CHDs) are common in FASD, particularly dextro-type transposition of the great arteries (d-TGA).
- Prenatal alcohol exposure (PAE) is the primary risk factor for FASD.
Abstract:
Fetal alcohol spectrum disorder (FASD) is a preventable cause of developmental disabilities linked to prenatal alcohol exposure (PAE). Congenital heart defects (CHDs) are frequently observed in FASD, with a notable association between PAE and dextro-type transposition of the great arteries (d-TGA). A potential pathogenetic mechanism of d-TGA in FASD, involving retinoic acid (RA) deficiency due to the interference of ethanol with RA biosynthesis, is proposed. Further investigation is required to understand the timing and impact of alcohol exposure on congenital anomalies, particularly in the context of CHDs.
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