Developmental anatomy of the heart: a tale of mice and man

Abstract

Because of the increasing availability of tools for genetic manipulation, the mouse has become the most popular animal model for studying normal and abnormal cardiac development. However, despite the enormous advances in mouse genetics, which have led to the production of numerous mutants with cardiac abnormalities resembling those seen in human congenital heart disease, relatively little comparative work has been published to demonstrate the similarities and differences in the developmental cardiac anatomy in both species. In this review we discuss some aspects of the comparative anatomy, with emphasis on the atrial anatomy, the valvuloseptal complex, and ventricular myocardial development. From the data presented it can be concluded that, apart from the obvious differences in size, the mouse and human heart are anatomically remarkably similar throughout development. The partitioning of the cardiac chambers (septation) follows the same sequence of events, while also the maturation of the cardiac valves and myocardium is quite similar in both species. The major anatomical differences are seen in the venous pole of the heart. We conclude that, taking note of the few anatomical “variations,” the use of the mouse as a model system for the human heart is warranted. Thus the analysis of mouse mutants with impaired septation will provide valuable information on cellular mechanisms involved in valvuloseptal morphogenesis (a process often disrupted in congenital heart disease), while the study of embryonic lethal mouse mutants that present with lack of compaction of ventricular trabeculae will ultimately provide clues on the etiology of this abnormality in humans.

The TGFβ type II receptor plays a critical role in the endothelial cells during cardiac development

“…The cushion fusion defects may indicate a role for TGFb signalling in delamination of endothelial cells and eventual fusion of the atrioventricular and outflow cushions to close the interventricular communication. On the other hand, the larger VSDs are more likely to be due to failures in gross remodelling of the cushion mesenchyme across the atrioventricular junction, an essential step during formation of the membranous portion of the ventricular septum (Wessels and Sedmera, 2003). Such remodelling is likely to involve signalling in endothelial/endocardial cells.…”

Cardiovascular Assessment of Fetal Mice by In Utero Echocardiography

“…As mice are air breathing mammals with four chamber hearts, they have proven to be an excellent model system for studying human congenital heart disease (Wessels and Sedmera 2003). In fact, most of the major congenital heart anomalies seen clinically can be found in mutant mouse models (Yu et al 2004;Shen et al 2005).…”

Cardiopulmonary resuscitation in a swine model of cardiac arrest

“…Τέλος, η καρδιακή συ χνότητα σε ηρεμία στο χοίρο προσομοιάζει με αυτήν του ανθρώπου, σε αντίθεση με το μυ ο οποίος έχει συ χνότητα τριπλάσια από αυτήν του ανθρώπου και η ανε-ρέθιστη περίοδος του είδους είναι εξαιρετικά μικρή (Kofier et al 2004) (Wessels and Sedmera 2003). Εκτός από τις ανατομικές και φυσιολογικές ομοιότητες, οι 240 Θ. ΞΑΝΘΟΣ, Ε. ΜΠΑΣΙΑΚΟΥ, Δ. ΠΑΠΑΔΗΜΗΤΡΙΟΥ, Ε. ΚΟΥΔΟΥΝΑ, Π. ΛΕΛΟΒΑΣ, Λ. ΠΑΠΑΔΗΜΗΤΡΙΟΥ χοίροι απαιτούν λιγότερη ανθρώπινη φροντίδα, ενώ ταυτόχρονα οι ερευνητές αποδέχονται περισσότερο ψυχολογικά τους πειραματισμούς στο είδος αυτό (White 1996).…”

“…In addition, after induction of myocardial ischaemia, the porcine myo cardium responds biochemically and metabolically in the same way as the human heart (Weaver et al 1986) (White et al 1992). The swine model has a resting heart rate which averages that of the human, whereas, the mouse model has a high resting heart rate that approxi mates 500bpm and its refractory period is extremely short (Kofier et al 2004) (Wessels and Sedmera 2003). Furthermore, pigs require less human care and resear chers find experimentation on the species more accep table (White 1996).…”