Proposed model of the mechanistic link between low birth weight (LBW) due to preterm birth and adult developmentally programmed hypertension. Ligi et al demonstrate that endothelial progenitors in the cord blood of LBW infants have increased expression levels of antiangiogenic molecules, including thrombospondin 1 (THBS1), endostatin (COL18A1), and platelet factor 4 (PF4), and decreased levels of phosphorylated AKT (pAKT). This angiostatic profile was associated with substantially decreased angiogenic properties, which—if persistent—could explain the vascular abnormalities found in former LBW infants with developmentally programmed hypertension in adulthood. It remains unclear whether and how the premature transition from the intrauterine to the extrauterine (oxygen-rich) environment affects the angiogenic properties of LBW endothelial progenitors, how long the angiogenic defects persist, and how events and interventions during early neonatal life influence this process. Professional illustration by Alice Y. Chen.