J Thorac Cardiovasc Surg 2007;134:20-22
© 2007 The American Association for Thoracic Surgery
In vivo tissue engineering an autologous semilunar biovalve: Can we get what we want?
Hans-Hinrich Sievers, MD*
Department of Cardiac Surgery, University of Schleswig-Holstein, Campus Luebeck, Luebeck, Germany.
Received for publication March 12, 2007; revisions received March 21, 2007; accepted for publication March 29, 2007.
* Address for reprints: Hans-Hinrich Sievers, MD, University of Schleswig-Holstein, Campus Luebeck, Department of Cardiac Surgery, Ratzeburger Allee 160, Luebeck D-23538 Germany. (Email: herzchir@medinf.mu-luebeck.de).
| The first 20% of the full text of this article appears below. |
Since the 1950s, conventional bioprosthetic and mechanical heart valve substitutes have significantly improved survival and quality of life for millions of patients. Nevertheless, these replacement devices are subject to serious, still unsurmounted, shortcomings, among others macroembolic and microembolic events, anticoagulation, premature degeneration and failure, functional imperfection, and lack of growth. Thus, there is an undoubted need for better prostheses. Tissue engineering has evolved during the last 20 years as an appealing alternative with great promise, bringing into play the application of principles and methods of engineering and life science.E1
Understandably, the ultimate goal is to construct a living aortic valve substitute equal to the patients own native valve. This makes sense, because the native valve is the optimal solution as a valve mechanism for that particular position that has developed in an evolutionary process over millions of years, an inconceivable period for human beings. For tissue engineering, a thorough understanding of developmental processes, as well as of relationships of structure to function, is indispensable. Some issues are touched on in the present study with regard to semilunar heart valves.
The heart and the valves are the first organs to form during a complex morphogenetic process harmonizing with evolving hemodynamic forces.1
In addition to transition of endothelial to mesenchymal cells and migration of these cells to form the endocardial cushions, numerous genes, molecules, signals, and proteins are involved.E2,E3
Of most interest, multipotent neural crest cells migrate to the outflow tract2
(Figure 1) and semilunar valves,E4,E5
contributing to development.E4
This process follows a finely tuned, albeit vulnerable,E6-E8
biologic concert not yet completely known, which is also true for the molecular mechanisms to maintain structural integrity, regeneration, aging, and remodeling in response to dynamic environmental factors.3
How do cells differentiate at the right time, . . . [Full Text of this Article]
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Copyright © 2007 by The American Association for Thoracic Surgery.