SPHK1 and bronchopulmonary dysplasia: To date, the various findings in BPD in relation to sphingolipids can be summarized as follows: (i) preterm babies with increased ceramide and S1P levels in TAs are more likely to develop BPD; (ii) SPHK1 enzyme expression is increased both in patients with BPD and the murine hyperoxia model of BPD, and the Sphk1 knockout model offers protection; (iii) SPHK1 enzyme inhibitor, PF543, provides protection against hyperoxia-induced lung injury; and (iv) S1PR1 is upregulated in a mouse model of hyperoxia and promotes pathogenesis of BPD [27,29,30,31,41].