Abstract
Study summary
Fetal hypoxia is a common complication of pregnancy that increases cardiovascular risk in offspring. This study tests whether miR-21-5p upregulation during developmental hypoxia protects embryonic growth and cardiac function. Using neonatal rat cardiomyocytes and hypoxic chicken embryos, the work shows that miR-21-5p dampens hypoxia-responsive gene expression, alters transcript isoform usage in key cardiac pathways, improves cardiomyocyte survival, and protects growth and cardiac performance during chronic hypoxia.