Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.ijcard.2004.06.009
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dc.titleReprogramming autologous skeletal myoblasts to express cardiomyogenic function. Challenges and possible approaches
dc.contributor.authorHeng, B.C.
dc.contributor.authorQing, Tong G.
dc.contributor.authorNg, S.C.
dc.contributor.authorHaider, H.K.
dc.contributor.authorSim, E.K.-W.
dc.contributor.authorCao, T.
dc.date.accessioned2013-04-10T04:41:27Z
dc.date.available2013-04-10T04:41:27Z
dc.date.issued2005
dc.identifier.citationHeng, B.C., Qing, Tong G., Ng, S.C., Haider, H.K., Sim, E.K.-W., Cao, T. (2005). Reprogramming autologous skeletal myoblasts to express cardiomyogenic function. Challenges and possible approaches. International Journal of Cardiology 100 (3) : 355-362. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ijcard.2004.06.009
dc.identifier.issn01675273
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/37413
dc.description.abstractCell 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. © 2004 Elsevier Ireland Ltd. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.ijcard.2004.06.009
dc.sourceScopus
dc.subjectCardiomyocytes
dc.subjectMyocardial ischemia
dc.subjectSkeletal myoblasts
dc.subjectTransdifferentiation
dc.subjectTransplantation
dc.typeReview
dc.contributor.departmentOBSTETRICS & GYNAECOLOGY
dc.contributor.departmentSURGERY
dc.contributor.departmentDEAN'S OFFICE (DENTISTRY)
dc.description.doi10.1016/j.ijcard.2004.06.009
dc.description.sourcetitleInternational Journal of Cardiology
dc.description.volume100
dc.description.issue3
dc.description.page355-362
dc.description.codenIJCDD
dc.identifier.isiut000228814600002
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