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Prenatal alcohol exposure induced congenital heart diseases: From bench to bedside
Author(s) -
Chen Zhiyan,
Li Sheng,
Guo Linghong,
Peng Xu,
Liu Yin
Publication year - 2021
Publication title -
birth defects research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.845
H-Index - 17
ISSN - 2472-1727
DOI - 10.1002/bdr2.1743
Subject(s) - medicine , wnt signaling pathway , heart disease , epigenetics , phenotype , heart development , teratology , pregnancy , neural tube , retinoic acid , fetus , bioinformatics , physiology , embryonic stem cell , signal transduction , biology , embryo , genetics , gene
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.