In animal models of myocardial infarction (MI), transplantation of various types of progenitor cells has been reported to (i) improve left ventricular (LV) function, (ii) decrease LV remodeling, (iii) limit fibrosis of noninfarcted LV regions, and (iv) in some cases, reduce infarct scar size. Moreover, in some reports these beneficial effects were present despite very low rates of long-term engraftment and transdifferentiation of transplanted cells into cardiomyocytes. In contrast, in other reports, significant numbers of transplanted cells do appear to have transdifferentiated into cardiomyocytes and vascular cells. Paracrine signals emanating from transplanted cells also appear to be very important because they protect injured cardiomyocytes and may activate endogenous cardiac progenitor cells (CPCs) to generate cardiomyocytes and vascular cells. Herein, we review evidence that transplanted bone-marrow- or cardiac-derived CPCs and/or in situ CPCs can be stimulated to propagate, differentiate, and partially replace cardiomyocytes damaged during AMI. The possibility that preexisting cardiomyocytes can be induced to reenter the cell cycle and regenerate replacement cardiomyocytes is also discussed.
|Original language||English (US)|
|Title of host publication||Progress in Molecular Biology and Translational Science|
|Number of pages||21|
|State||Published - 2012|
|Name||Progress in Molecular Biology and Translational Science|
Bibliographical noteFunding Information:
This work was supported by U.S. Public Health Service Grants HL50470, HL67828, and HL95077, and by National Centers for Research Resources (NCRR), National Institutes of Health Grant P41RR08079. X. W. was supported AHA Greater Midwest Grant-in-Aid.
- bone marrow
- heart failure
- myocyte regeneration
- stem cell