Rewiring the heart: stem cell therapy to restore normal cardiac excitability and conduction.
The regenerative capacity of the mammalian heart is insufficient to recover from myocardial infarction. Stem cells are currently considered as a promising and valuable tool to replace the, often large, loss of contractile tissue. One of the bottlenecks hampering fast clinical application is the large amount of cells required to replace a single damaged region combined with an appropriate strategy to succeed in homogeneous repair. A second class of major cardiac disorders for which stem cell therapy might be fruitful and would require less cells for repair, are chronic rhythm disorders. In this area, most research has been focused on stem-cell based biological pacemakers, but increasing amounts of data on AV nodal repair appear in literature. Both therapies, in principle, could eventually replace current instrumentation with electronic pacemakers. Finally, an emerging field of interest explores transplantation of stem cells expressing specific ion channels aiming at suppression of focal arrhythmias, providing an alternative strategy for surgical and catheter-mediated ablation. Since in this second class of applications the number of transplanted cells required may be relatively low, effective clinical therapy may be within close range. Here, we will review recent achievements in the fields of stem-cell based biological pacemakers, AV nodal repair and biological ablation.
Blank
A Christian
AC
Department of Medical Physiology, Division Heart & Lungs, University Medical Center Utrecht, Yalelaan 50, Utrecht, The Netherlands.
van Veen
Toon A B
TA
Jonsson
Malin K B
MK
Zelen
Jirre S J
JS
Strengers
Jan L
JL
de Boer
Teun P
TP
van der Heyden
Marcel A G
MA
D000818:Animals; D001145:Arrhythmias, Cardiac; D001683:Biological Clocks / Q000502:physiology*; D002465:Cell Movement; D005818:Genetic Engineering; D006329:Heart Conduction System / Q000502:physiology / Q000503:physiopathology*; D006801:Humans; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D020127:Recovery of Function; D033581:Stem Cell Transplantation
D007473:Ion Channels