Abstract
Abnormalities in the arterial valves are some of the commonest congenital malformations, with bicuspid aortic valve (BAV) occurring in as many as 2% of the population. Despite this, most of what we understand about the development of the arterial (semilunar; aortic and pulmonary) valves is extrapolated from investigations of the atrioventricular valves in animal models, with surprisingly little specifically known about how the arterial valves develop in mouse, and even less in human. In this review, we summarise what is known about the development of the human arterial valve leaflets, comparing this to the mouse where appropriate.
Highlights
Edited by: Michel Puceat, Institut National de la Santé et de la Recherche Médicale (INSERM), France
Most of what we understand about the development of the arterial valves is extrapolated from investigations of the atrioventricular valves in animal models, with surprisingly little known about how the arterial valves develop in mouse, and even less in human
We summarise what is known about the development of the human arterial valve leaflets, comparing this to the mouse where appropriate
Summary
The first and probably best understood process required for the development of the cardiac valves is the process of endocardial to mesenchyme transition (EndMT). It is accepted that NCCs are crucial for human outflow tract development as they are in birds and mice [reviewed in [24, 25]], there is limited information available, at least in part because of the difficulty in labelling this progenitor cell population in the human heart. It has been shown, using AP2α as a marker, that NCCs are found within the distal outflow cushions at 33 dpc [CS15; [32]]. The characteristic condensed mesenchyme within the outflow cushions, which is shown to be made up of NCCs in the mouse, is apparent in the human outflow cushions from approximately 32 dpc (CS14) [33]
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