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Studies with Tph1-KO mice have shown that maternal serotonin production is important for normal brain and heart development of the fetus [ 17, 28, 48].
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Taken together, the decrease of heart defects across samples indicates that Nkx2.7 and Nkx2.5 function redundantly during the heart development of zebrafish embryos.
Because of the increased pressure inside the ventricle during heart development, the weakest section of the ventricle wall may balloon out to form abnormal evaginations.
As with studies of heart development, the use of fluorescent reporters in zebrafish allows for direct visualization of vascular development in vivo, offering a complementary approach to in vitro endothelial cell sprouting experiments.
In this review, we discuss the mechanisms of zebrafish heart development and the utility of zebrafish for understanding syndromic CHDs, those cardiac abnormalities that occur in the context of multisystem disorders.
This is undoubtedly the case for later stages of heart development in the mouse where penetration of staining reagents into dense cardiac tissue can be problematic.
To date, most analysis of heart development in the mouse has focussed on qualitative comparisons of normal and mutant hearts, usually using selected 2D histological sections.
Canonical pathways enriched within our genes of interest have previously been implicated in heart development and some of the pathways appear to be interconnected.
Although these remain distant goals, studies of heart development are illuminating the path forward and suggest unique opportunities for heart regeneration, particularly in fetal and neonatal periods.
Heart development begins with the specification of myocardial and endocardial progenitor cells.
The homeobox transcription factors NKX2-5 and MEIS1 are essential for vertebrate heart development and normal physiology of the adult heart.
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