S1P receptors (S1PRs) have been implicated in mediating S1P-dependent protection against cardiomyocyte cell death following hypoxia and rexoygenation, although different receptors have been implicated in HDL-dependent protection under different conditions; S1PR3 is reportedly required for HDL-mediated protection against myocardial infarction in mice in vivo [32], whereas mouse cardiomyocytes subjected to hypoxia/reoxygenation required both S1PR1 and S1PR3 [31], and doxorubicin-treated cultured rat cardiomyocytes required S1PR2 but not S1PR1 or S1PR3 [28] for HDL/S1P-mediated cytoprotection. This evidence concerns the gene S1PR3 and myocardial infarction.