Why the study?
The paper aims to present methods for generating disturbed hemodynamics in chick embryos and summarize identified mechanosensitive genes to understand congenital heart defects.
The chick embryo model provides valuable insights into the mechanosensitive pathways and hemodynamic forces that govern embryonic heart development and the origins of congenital heart defects.
No immediate clinical application; leaves open translation of chick-derived mechanosensitive genes to human congenital heart defects.
The heart is the first organ that starts to function in a developing embryo. It continues to undergo dramatic morphological changes while pumping blood to the rest of the body. Genetic regulation of heart development is partly governed by hemodynamics. Chick embryo is a major animal model that has been used extensively in cardiogenesis research. To reveal mechanosensitive pathways, a variety of surgical interferences and chemical treatments can be applied to the chick embryo to manipulate the blood flow. Such manipulations alter expressions of mechanosensitive genes which may anticipate induction of morphological changes in the developing heart. This paper aims to present different approaches for generating clinically relevant disturbed hemodynamics conditions using this embryonic chick model and to summarize identified mechanosensitive genes using the model, providing insights into embryonic origins of congenital heart defects.
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Alser et al. (2021) studied this question.
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