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Embryonic development of bicuspid aortic valves.
María Teresa Soto-Navarrete1, Miguel Ángel López-Unzu1, Ana Carmen Durán1
1Departamento de Biología Animal, Facultad de Ciencias, Universidad de Málaga, Málaga, Spain; Instituto de Investigación Biomédica de Málaga (IBIMA), Málaga, Spain.
Progress in Cardiovascular Diseases
|June 28, 2020
Summary
Bicuspid aortic valve (BAV), a congenital heart defect, arises from embryonic developmental issues. Animal models reveal how genetic and cellular defects, particularly involving cardiac neural crest cells, lead to various BAV morphologies.
Area of Science:
- Developmental Biology
- Congenital Heart Disease
- Genetics
Background:
- Bicuspid aortic valve (BAV) is the most prevalent congenital cardiac malformation.
- BAV is frequently linked to aortopathies and valvulopathies, with suspected impacts from its congenital origin on adult disease progression.
- Recent advancements in embryonic heart development research have significantly enhanced understanding of BAV etiology.
Purpose of the Study:
- To synthesize information on developmental defects causing BAV in animal models.
- To elucidate the morphogenetic origins of the diverse BAV morphologies observed in humans.
- To propose a unified hypothesis for BAV formation based on cardiac neural crest cell function.
Main Methods:
- Review of studies on embryonic development of congenital heart disease, focusing on animal models (hamster, genetically modified mice).
- Analysis of molecular, cellular, and morphological defects associated with BAV formation.
- Examination of genetic pathways, including the NOTCH pathway, implicated in BAV development.
Main Results:
- Alterations in genes associated with BAV affect key cellular mechanisms: endocardial-to-mesenchymal transformation, cardiac neural crest (CNC) cell behavior, and valve cushion mesenchymal cell differentiation.
- Defective cellular functions impact morphogenetic processes: outflow tract endocardial cushion formation, outflow tract septation, and valve cushion excavation.
- Specific defects correlate with BAV types: cushion abnormalities often lead to latero-lateral BAVs, septation defects to antero-posterior BAVs, and excavation alterations to both.
Conclusions:
- BAV arises from disruptions in fundamental embryonic heart development processes.
- Cardiac neural crest cell (CNC) behavior plays a crucial inductive role in BAV development.
- A unified hypothesis suggests that alterations in CNC cell behavior during key valvulogenic processes explain the spectrum of BAV morphologies.
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