Reprogramming autologous skeletal myoblasts to express cardiomyogenic function. Challenges and possible approaches

Cell transplantation therapy is emerging as a promising mode of treatment following myocardial infarction. Of the various cell types that can potentially be used for transplantation, autologous skeletal myoblasts appear particularly attractive, because this would avoid issues of immunogenicity, tumo...

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Published in:International journal of cardiology 2005-04, Vol.100 (3), p.355-362
Main Authors: Heng, Boon Chin, Khawaja Haider, Husnain, Kwang-Wei Sim, Eugene, Cao, Tong, Qing Tong, Guo, Chye Ng, Soon
Format: Article
Language:English
Subjects:
Biological and medical sciences
Cardiology. Vascular system
Cardiomyocytes
Cell Differentiation - physiology
Cells, Cultured
Coronary heart disease
Heart
Heart Failure - physiopathology
Humans
Medical sciences
Myoblasts, Skeletal - metabolism
Myoblasts, Skeletal - transplantation
Myocardial ischemia
Myocarditis. Cardiomyopathies
Myocytes, Cardiac - physiology
Recovery of Function
Skeletal myoblasts
Transcription Factors - physiology
Transdifferentiation
Transplantation
Transplantation, Autologous
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Summary:Cell transplantation therapy is emerging as a promising mode of treatment following myocardial infarction. Of the various cell types that can potentially be used for transplantation, autologous skeletal myoblasts appear particularly attractive, because this would avoid issues of immunogenicity, tumorigenesis, ethics and donor availability. Additionally, skeletal myoblasts display much higher levels of ischemic tolerance and graft survival compared to other cell types. There is some evidence for improvement in heart function with skeletal myoblast transplantation. However, histological analysis revealed that transplanted myoblasts do not transdifferentiate into functional cardiomyocytes in situ. This is evident by the lack of expression of cardiac-specific antigens, and the absence of intercalated disc formation. Instead, there is differentiation into myotubes that are not electromechanically coupled to neighboring cardiomyocytes. This could in turn limit the clinical efficacy of treatment. This review would therefore examine the various challenges faced in attempting to reprogram autologous skeletal myoblast to express cardiomyogenic function, together with the various possible strategies that could be employed to achieve this objective.
ISSN:0167-5273
1874-1754
DOI:10.1016/j.ijcard.2004.06.009