S1PR2 is a G protein-coupled receptor that serves as a primary receptor for sphingosine-1-phosphate (S1P), a bioactive lysophospholipid signaling molecule 1. In hepatoma cells, S1PR2 mediates S1P-induced cell proliferation and suppression of apoptosis 2. S1PR2 also functions as a receptor for the chemokine-like protein FAM19A5, mediating inhibitory effects on vascular smooth muscle cell proliferation and migration 3. In lymphoid follicles, S1PR2 couples S1P binding to GNA13 activation, leading to downstream inhibition of AKT and suppression of germinal center B cell growth [UniProt]. Mechanistically, S1PR2 regulates cell trafficking, vascular autophagy, and inflammatory responses through multiple signaling pathways including p38 MAPK and YAP 45. S1PR2 plays critical roles in cardiovascular physiology, regulating endothelial function, vascular tone, and lymphocyte trafficking 1. In pathological contexts, S1PR2 activation promotes hepatic stellate cell activation and liver fibrosis through the S1PR2/p38 MAPK/YAP axis 4, while S1PR2 inhibition shows potential therapeutic benefit in colorectal cancer chemoresistance 6. S1PR2 dysfunction is associated with autosomal recessive deafness 68, highlighting its role in sensory organ function.