The outcomes of this research could help treat individuals experiencing congenital heart defects or myocardial infarction. By better characterizing the mechanism behind F1R1’s proliferative effect on cardiomyocytes, improved treatments targeting and upregulating this pathway could be used to repair and remodel heart tissue in disease states where there is cardiomyocyte loss. This would also add understanding to the field of cardiac regeneration, as the proliferative capabilities of fetal/neonatal heart cells are well known, but not well characterized in terms of the underlying biological mechanisms and environmental conditions.
Below is a design table that outlines the short-term, mid-term, and long-term needs and goals of our project.
Engineering Design Table
