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Published on: July 13, 2014
Prenatal alcohol exposure induced congenital heart diseases: From bench to bedside
Zhiyan Chen1,2, Sheng Li1,2, Linghong Guo3
1Department of Basic Medical Sciences, Sichuan Vocational College of Health and Rehabilitation, Zigong, Sichuan, China.
Insights
Prenatal alcohol exposure (PAE) can cause congenital heart disease (CHD) in infants. Early diagnosis and interventions like drug supplements may prevent these serious birth defects.
Area of Science:
- Cardiology
- Developmental Biology
- Public Health
Background:
- Alcohol consumption during pregnancy is a global concern.
- Congenital heart disease (CHD) is the most prevalent birth defect worldwide.
- Prenatal alcohol exposure (PAE) is a significant teratogenic factor for CHD.
Purpose of the Study:
- To review the mechanisms linking PAE to CHD phenotypes.
- To highlight potential preventative strategies for PAE-induced CHDs.
Main Methods:
- Review of animal experiments and clinical retrospective studies on PAE and CHD.
- Analysis of molecular and cellular pathways involved in PAE-induced teratogenesis.
Main Results:
- PAE is linked to specific CHD phenotypes, including septal, valvular, and great artery defects.
- Key mechanisms involve altered retinoic acid and Wntβ-catenin signaling, disrupted cardiac neural crest cell function, and suppressed BMP signaling.
- Epigenetic factors also contribute to PAE-induced cardiac malformations.
Conclusions:
- PAE is a critical cause of congenital heart defects.
- Interventions such as drug supplements and early diagnosis are crucial for preventing PAE-induced CHDs.
Abstract:
Alcohol consumption is increasing worldwide. Many child-bearing-aged women consume alcohol during pregnancy, intentionally or unintentionally, thereby increasing the potential risk for severe congenital diseases. Congenital heart disease (CHD) is the most common birth defect worldwide and can result from both hereditary and acquired factors. Prenatal alcohol exposure (PAE) is considered a key factor that leads to teratogenesis in CHD and its specific phenotypes, especially defects of the cardiac septa, cardiac valves, cardiac canals, and great arteries, adjacent to the chambers, both in animal experiments and clinical retrospective studies. The mechanisms underlying CHD and its phenotypes caused by PAE are associated with changes in retinoic acid biosynthesis and its signaling pathway, apoptosis and defective function of cardiac neural crest cells, disturbance of the Wntβ-catenin signaling pathway, suppression of bone morphogenetic protein (BMP) signaling, and other epigenetic mechanisms. Drug supplements and early diagnosis can help prevent PAE from inducing CHDs.
