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[Cardiomyocyte transplantation--a cell replacement for repair of myocardial infarction?]
E R Schwarz1, M Patterson, R A Kloner
1Heart Institute Good Samaritan Hospital, Los Angeles, California 90017, USA.
Insights
Cardiomyocyte transplantation shows potential for cardiac repair, with transplanted cells surviving and forming connections. However, coordinated contractility and clinical relevance for replacing damaged heart cells require further demonstration.
Area of Science:
- Cardiovascular Biology
- Regenerative Medicine
- Cell Biology
Context:
- Adult cardiomyocytes lack proliferation capacity, leading to irreversible damage and fibrosis after events like myocardial infarction.
- Cell replacement strategies, particularly cardiomyocyte transplantation, are being explored to restore cardiac function.
- Previous studies in animal models demonstrate the feasibility of transplanting various cell types into the myocardium.
Purpose:
- To review the current state and potential of cardiomyocyte transplantation as a therapeutic strategy for damaged myocardium.
- To assess the survival, integration, and functional capabilities of transplanted cells within the host heart.
- To identify the limitations and future research directions for clinical application of cardiac cell therapy.
Summary:
- Transplanted cells, including skeletal myoblasts and fetal cardiomyocytes, can survive in the host myocardium for weeks and form intercellular connections like gap junctions and desmosomes.
- While hypothetical benefits include tissue stabilization and drug delivery, convincing evidence of graft-host functional integration and coordinated contractility is lacking.
- The clinical utility of cardiomyocyte transplantation for replacing damaged cardiac cells remains to be definitively proven, necessitating further research.
Impact:
- Highlights the need for robust evidence of functional integration for clinical translation of cardiac cell therapies.
- Identifies key research gaps in demonstrating coordinated contractility and therapeutic efficacy of cardiomyocyte transplantation.
- Provides a critical overview for researchers and clinicians in the field of cardiac regenerative medicine.
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.