ABSTRACT
Introduction Adult cardiac muscle lacks significant capacity to regenerate, and therefore any significant heart cell loss such as occurs during myocardial infarction is mostly irreversible and may result in permanent impairment of myocardial performance and the development of progressive heart failure. The recent advances in molecular and stem cell biology and in tissue engineering have paved the way to the development of a new biomedicine discipline: regenerative medicine. This approach seeks to circumvent the low regenerative capacity of certain organs by using cell replacement strategies to restore the function of diseased or absent tissues. The hope is that these emerging strategies will enable the development of future cures for a variety of devastating disease states such as Parkinson’s disease, stroke, heart failure, and diabetes. The heart represents an attractive candidate for these emerging technologies, and much attention has been directed in recent years to utilize cell therapy and tissue engineering to ameliorate cardiac injury.1-3
The overall objective of cell replacement therapy is to repopulate postinfarction scar tissue with a new pool of functional cells that can restore the mechanical properties of this compromised region. Although several cell types have been suggested as possible candidates for myocardial repair (as outlined in the different
chapters and in a number of excellent reviews1-3), the inherent structural, electrophysiological, and contractile properties of cardiomyocytes strongly suggest that they may be the ideal donor cell type. In early studies, fetal cardiomyocytes transplanted into healthy mice hearts were demonstrated to survive, align, and form cell-to-cell contacts with host myocardium.4 Cardiomyocyte transplantation in rodent models of myocardial infarction was associated with smaller infarcts, prevented cardiac dilatation and remodeling,5
and also resulted in function improvements in some of these studies.6 Despite these encouraging results, the clinical utility of this approach is significantly hampered by the paucity of cell sources for human cardiomyocytes.
