Cardiovascular Research

[Cardiomyocyte transplantation--a cell replacement for repair of myocardial infarction?].

Authors: E R Schwarz|||M Patterson|||R A Kloner

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Abstract

Cardiomyocytes lose the ability to proliferate after birth. Subsequently, irreversible cellular damage, e.g., during myocardial infarction, causes loss of functional properties and cell replacement by fibrotic tissue. It is, therefore, not surprising that cell replacement strategies such as cardiomyocyte transplantation in damaged myocardium or scar tissue has gained widespread interest. In other species such as mice, rats, and dogs, the technical feasibility of skeletal myoblast-, satellite cell-, and fetal cardiomyocyte engraftment into normal and diseased myocardium has been demonstrated by simple injection methods. Repeatedly, it has been shown that transplanted cells may survive for weeks within host myocardium and build intercellular connections such as gap junctions and desmosomes. In contrast, grafthost connections have not, as yet, been convincingly demonstrated. Hypothetically, cell transplants might exhibit the following functional properties: stabilization of diseased tissue to prevent structural remodeling; carrier for recombinant proteins, growth factors or drugs to induce molecular alterations of host myocardium; and improvement of regional and global myocardial function due to active contractility. However, clear evidence of coordinated contractility of transplanted cells, and, thus, of a clinically relevant therapeutical use of cardiomyocyte transplantation as a replacement strategy for damaged host cardiac cells, remains to be demonstrated.