This study demonstrated that microvesicles can be interrogated as a source of miRNAs released into the circulation with HF, that there is an inverse relationship between levels of miR129-5p in circulating microvesicles and the degree of HF in pediatric patients with univentricular heart disease, that miR129-5p is similarly downregulated in cultured human cardiomyocytes and cardiomyocytes derived from hESCs exposed to oxidative stress, and that BMPR2 expression is likely regulated by miR129-5p in the setting of cardiomyocyte stress. The gene discussed is BMPR2; the disease is hydrops fetalis.