Overexpressing FSTL1 for heart repair

Abstract

Myocardial infarction (MI), a major cause of death worldwide, further impairs the inherently low regenerative capacity of cardiomyocytes, with barely 1% of cardiomyocytes per year undergoing cell division [1]. While this low division rate increases in response to MI, it does not compensate for the loss of cardiomyocytes; thus, the area of scarred (fibrotic) tissue expands and such unfavorable tissue remodeling further deteriorates cardiac contractile capacity, ultimately leading to heart failure (HF).