S1PR2 and hydrops fetalis: Such augmented cerebrovascular S1PR2 signaling results from disturbances in S1P homeostasis during HF where an acquired cystic fibrosis transmembrane regulator (CFTR) dysfunction critically impairs the cerebrovascular S1P degradation, and hence increases S1P bioavailability for S1PR2 signaling on vascular smooth muscle cells (Meissner et al., 2012).