Circulating soluble fms-like tyrosine kinase-1 (sFlt-1) induces widespread endothelial dysfunction by binding to and competitively inhibiting vascular endothelial growth factor (VEGF) and placental growth factor (PlGF); sFlt-1-loaded exosomes (sFlt-1-Exo) markedly suppress cell proliferation, migration, and tube formation [34]. Here, PGF is linked to endothelial dysfunction.