ABSTRACT
In considering the optimal strategy for cell therapy to treat myocardial dysfunction, the first issue to be resolved is the donor cell type. Implantation of proliferative skeletal myogenic precursor cells (MPCs; myoblasts) into the heart has yielded consistently beneficial functional results in both small and large animal models.1-5 Incontrast to the limited regenerative capacity of adult myocardium, these proliferative MPCs (derived from activated satellite cells) are normally responsible for the postnatal growth and repair of skeletal muscle. Although the precise mechanism of functional improvement following MPC transplantation to the heart remains uncertain, the cardiac microenvironment is permissive for differentiation of these cells – at least along the skeletal myogenic lineage.2,3 MPCs canbe harvested autologously from patients; they form stable vehicles for gene therapy; and they do not have the associated ethical implications of embryonic stem cells or fetal cardiac myocytes.4
