As the need for whole heart transplantation to treat heart failure grows faster than the supply, alternative methods are in increasing demand. Transplantation of cardiomyocytes to replace injured myocardium after MI has shown promise. Myocardium is notoriously ineffective at proliferating after switching from hyperplastic to hypertrophic growth. FOXM1 has been established as having a strong role in cell cycle regulation in cancerous tumors and cardiomyocytes, and these experiments show the relationship between FOXM1 and iPSC-derived cardiomyocyte proliferation and attempt to improve a treatment option for heart failure through manipulation of this gene. Our experiment concludes that FOXM1 knockdown increases iPSC-CM cell proliferation, and can be further explored to better increase cardiomyocyte proliferation.

As the need for whole heart transplantation to treat heart failure grows faster than the supply, alternative methods are in increasing demand. Transplantation of cardiomyocytes to replace injured myocardium after MI has shown promise. Myocardium is notoriously ineffective at proliferating after switching from hyperplastic to hypertrophic growth. FOXM1 has been established as having a strong role in cell cycle regulation in cancerous tumors and cardiomyocytes, and these experiments show the relationship between FOXM1 and iPSC-derived cardiomyocyte proliferation and attempt to improve a treatment option for heart failure through manipulation of this gene. Our experiment concludes that FOXM1 knockout increases iPSC-CM cell proliferation, and can be further explored to better increase cardiomyocyte proliferation.