Getting to the Heart of Cardiac Morphogenesis

Kirby, Margaret L.

doi:10.1161/01.res.88.4.370

Cited by 4 publications

(5 citation statements)

References 20 publications

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“…In this model the atrium is not connected to the right ventricle and the left ventricle not to the outflow tract. The conversion of such a serial arrangement of segments into the proper parallel arrangement has remained one of the most difficult concepts of heart development (156), for it seems illogical first to make a serial arrangement of cardiac segments and then a parallel one. Based on morphological and flow direction considerations, Steding and Seidl (292) described this concept as "one of the most fatal assumptions."…”

Section: A Scopementioning

confidence: 99%

“…Anatomically this is not entirely true either: when describing developing cardiac morphology one is confronted with the changing position of the organ within the body and of the cardiac component parts in relation to each other. This easily results in confusion: people with a medical background tend to use the body axes as the points of reference and those with a biological background use the axes of the organ, while often terminology is used indifferently (156).…”

Section: B Cardiac Looping Changing Blood Flows and Chamber Formationmentioning

confidence: 99%

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Cardiac Chamber Formation: Development, Genes, and Evolution

Moorman

Christoffels

2003

Physiological Reviews

641

526

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Moorman, Antoon F. M., and Vincent M. Christoffels. Cardiac Chamber Formation: Development, Genes, and Evolution. Physiol Rev 83: 1223-1267, 2003; 10.1152/physrev.00006.2003.—Concepts of cardiac development have greatly influenced the description of the formation of the four-chambered vertebrate heart. Traditionally, the embryonic tubular heart is considered to be a composite of serially arranged segments representing adult cardiac compartments. Conversion of such a serial arrangement into the parallel arrangement of the mammalian heart is difficult to understand. Logical integration of the development of the cardiac conduction system into the serial concept has remained puzzling as well. Therefore, the current description needed reconsideration, and we decided to evaluate the essentialities of cardiac design, its evolutionary and embryonic development, and the molecular pathways recruited to make the four-chambered mammalian heart. The three principal notions taken into consideration are as follows. 1) Both the ancestor chordate heart and the embryonic tubular heart of higher vertebrates consist of poorly developed and poorly coupled “pacemaker-like” cardiac muscle cells with the highest pacemaker activity at the venous pole, causing unidirectional peristaltic contraction waves. 2) From this heart tube, ventricular chambers differentiate ventrally and atrial chambers dorsally. The developing chambers display high proliferative activity and consist of structurally well-developed and well-coupled muscle cells with low pacemaker activity, which permits fast conduction of the impulse and efficacious contraction. The forming chambers remain flanked by slowly proliferating pacemaker-like myocardium that is temporally prevented from differentiating into chamber myocardium. 3) The trabecular myocardium proliferates slowly, consists of structurally poorly developed, but well-coupled, cells and contributes to the ventricular conduction system. The atrial and ventricular chambers of the formed heart are activated and interconnected by derivatives of embryonic myocardium. The topographical arrangement of the distinct cardiac muscle cells in the forming heart explains the embryonic electrocardiogram (ECG), does not require the invention of nodes, and allows a logical transition from a peristaltic tubular heart to a synchronously contracting four-chambered heart. This view on the development of cardiac design unfolds fascinating possibilities for future research.

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Section: A Scopementioning

confidence: 99%

Section: B Cardiac Looping Changing Blood Flows and Chamber Formationmentioning

confidence: 99%

Cardiac Chamber Formation: Development, Genes, and Evolution

Moorman

Christoffels

2003

Physiological Reviews

641

526

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“…The formation of the four chambered heart requires a series of septations in the atrioventricular canal, the atrium and the ventricle (Kirby, 2001). The first septation in the atrioventricular canal involves a process called epithelial-to-mesencyhmal transition (EMT) where endocardial cells migrate into the cardiac jelly, proliferate, and form valve leaflets (Armstrong and Bischoff, 2004).…”

Section: Introductionmentioning

confidence: 99%

Gene expression profiling in the fetal cardiac tissue after folate and low‐dose trichloroethylene exposure

Caldwell

Manziello

Howard

et al. 2009

Birth Defects Research

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Background Previous studies show gene expression alterations in rat embryo hearts and cell lines that correspond to the cardio-teratogenic effects of trichloroethylene (TCE) in animal models. One potential mechanism of TCE teratogenicity may be through altered regulation of calcium homeostatic genes with a corresponding inhibition of cardiac function. It has been suggested that TCE may interfere with the folic acid/methylation pathway in liver and kidney and alter gene regulation by epigenetic mechanisms. According to this hypothesis, folate supplementation in the maternal diet should counteract TCE effects on gene expression in the embryonic heart. Approach To identify transcriptional targets altered in the embryonic heart after exposure to TCE, and possible protective effects of folate, we used DNA microarray technology to profile gene expression in embryonic mouse hearts with maternal TCE exposure and dietary changes in maternal folate. Results Exposure to low doses of TCE (10ppb) caused extensive alterations in transcripts encoding proteins involved in transport, ion channel, transcription, differentiation, cytoskeleton, cell cycle and apoptosis. Exogenous folate did not offset the effects of TCE exposure on normal gene expression and both high and low levels of folate produced additional significant changes in gene expression. Conclusions A mechanism where TCE induces a folate deficiency does not explain altered gene expression patterns in the embryonic mouse heart. The data further suggest that use of folate supplementation, in the presence of this toxin, may be detrimental and non-protective of the developing embryo.

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“…This has been to explain how an initially solitary tube, with laminar flow through a single lumen, can transform into a 4-chambered heart in which the pulmonary and systemic circulations work in parallel (Kirby, 2001). The solution to this problem was difficult to understand when it was presumed that the primordiums for all cardiac chambers were already present in a linear array of transverse segments within the initial heart tube, as in the concept advanced by Anderson and Becker in their atlas of 1980.…”

Section: Localized Differentiation Of Working Myocardium Formation Ofmentioning

confidence: 99%

Can recent insights into cardiac development improve our understanding of congenitally malformed hearts?

et al. 2008

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Congenital cardiac malformations account for one-quarter of all human congenital abnormalities. They are caused by environmental and genetic factors. Despite increasing efforts in fundamental research, as yet, the morphogenesis of only a limited number of malformations has been elucidated. Over the last decades, new genetic modifications have made it possible to manipulate the mammalian embryo. Evidence provided using these transgenic techniques has, over the past decade, necessitated re-evaluation of several developmental processes, important in the understanding of normal as opposed to abnormal cardiac development. In this review, we discuss current understanding of the patterning of the initial heart tube, new insights into formation of the atrial and ventricular chambers, and novel information on the origin of the cells that are added to the heart after formation of the initial tube. All of these advances modify our appreciation of malformations involving the venous and arterial poles. As we demonstrate, this new information sheds light not only on normal cardiac development, but also explains the structure of several previously controversial lesions seen in malformed human hearts.

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Getting to the Heart of Cardiac Morphogenesis

Cited by 4 publications

References 20 publications

Cardiac Chamber Formation: Development, Genes, and Evolution

Cardiac Chamber Formation: Development, Genes, and Evolution

Gene expression profiling in the fetal cardiac tissue after folate and low‐dose trichloroethylene exposure

Can recent insights into cardiac development improve our understanding of congenitally malformed hearts?

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