Cardiovascular System - Heart Valve Development
Introduction
The heart valves form between the atria and ventricles and between the atria and blood vessels. The cardiac cushions in the atrioventricular (AV) canal contain cells that are the primordia of the cardiac valves.
Textbooks
- Human Embryology (2nd ed.) Larson Ch7 p151-188 Heart
- The Developing Human: Clinically Oriented Embryology (6th ed.) Moore and Persaud Ch14: p304-349
- Before we Are Born (5th ed.) Moore and Persaud Ch12; p241-254
- Essentials of Human Embryology Larson Ch7 p97-122 Heart
- Human Embryology Fitzgerald and Fitzgerald Ch13-17: p77-111
Recent References
Transcriptional Regulation of Heart Valve Progenitor Cells PEDIATRIC CARDIOLOGY Volume 31, Number 3, 414-421, DOI: 10.1007/s00246-009-9616-x
"The development and normal function of the heart valves requires complex interactions among signaling molecules, transcription factors and structural proteins that are tightly regulated in time and space. Here we review the roles of critical transcription factors that are required for specific aspects of normal valve development. The early progenitors of the heart valves are localized in endocardial cushions that express transcription factors characteristic of mesenchyme, including Twist1, Tbx20, Msx1 and Msx2. As the valve leaflets mature, they are composed of complex stratified extracellular matrix proteins that are regulated by the transcriptional functions of NFATc1, Sox9, and Scleraxis. Each of these factors has analogous functions in differentiation of related connective tissue lineages. Together, the precise timing and localized functions of specific transcription factors control cell proliferation, differentiation, elongation, and remodeling processes that are necessary for normal valve structure and function. In addition, there is increasing evidence that these same transcription factors contribute to congenital, as well as degenerative, valve disease."
Molecular
Scleraxis (Scx) - basic helix–loop–helix transcription factor expressed in the progenitors and cells of all tendon tissues (mouse).[1]
Periostin - regulates lineage commitment of valve precursor cells (chicken).[2]
Gata4 and Gata6
Tbx5
Abnormalities
Noonan syndrome
An autosomal dominant single-gene cause of congenital heart disease. Patients also have proportionate short stature, facial abnormalities, and an increased risk of myeloproliferative disease. About half the patients have mutations in PTPN11, encoding the protein tyrosine phosphatase SHP2. A recent study in mice has identified PTPN11 acting in endocardium to enhance endocardial-mesenchymal transformation.[3]
References
Reviews
<pubmed>20809794</pubmed> <pubmed>20201901</pubmed> <pubmed>14567955</pubmed> <pubmed>12768658</pubmed>
Articles
<pubmed>17549728</pubmed>
Search PubMed
Search Pubmed: heart valve development | heart valve morphogenesis | Valvulogenesis
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Cite this page: Hill, M.A. (2024, April 26) Embryology Cardiovascular System - Heart Valve Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Cardiovascular_System_-_Heart_Valve_Development
- © Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G