Abstract
Tightly-regulated levels of retinoic acid (RA) are critical for promoting normal vertebrate development. The extensive history of research on RA has shown that its proper regulation is essential for cardiac progenitor specification and organogenesis. Here, we discuss the roles of RA signaling and its establishment of networks that drive both early and later steps of normal vertebrate heart development. We focus on studies that highlight the drastic effects alternative levels of RA have on early cardiomyocyte (CM) specification and cardiac chamber morphogenesis, consequences of improper RA synthesis and degradation, and known effectors downstream of RA. We conclude with the implications of these findings to our understanding of cardiac regeneration and the etiologies of congenital heart defects.
Highlights
The vertebrate heart is the first organ to form and function in all vertebrates
retinoic acid (RA) signaling is necessary for normal vertebrate heart development, it is critical that the levels of embryonic RA are maintained within an appropriate range as both decreases and increases in RA signaling can result in congenital heart malformations [3,4]
A mutagenesis screen in mice first showed that Retinol dehydrogenase 10 (Rdh10), which is required for the conversion from retinol to retinal has localized expression that helps generate the RA gradient [85]
Summary
The vertebrate heart is the first organ to form and function in all vertebrates. Its ability to function properly during embryogenesis and postnatal life is vital for both the normal development of other organs and an embryo’s long-term survival. Understanding the mechanisms that promote normal and aberrant vertebrate heart development is critical for generating preventative and therapeutic strategies for the broad etiologies of CHDs. Retinoic acid (RA) is the most active metabolic product of Vitamin A (retinol) within vertebrate embryos. RA signaling is necessary for normal vertebrate heart development, it is critical that the levels of embryonic RA are maintained within an appropriate range as both decreases and increases in RA signaling can result in congenital heart malformations [3,4]. At least in animal models, Vitamin A deficiency (VAD) can result in a variety of severe congenital heart abnormalities, J. A) is teratogenic in humans and can result in transposition of the great vessels (TGV), tetralogy ofhighly.
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