GPR34 and persistent truncus arteriosus: To examine the involvement of lysophosphatidylserine-dependent necrosis mediated by GPR34 in the pathogenesis of pressure overload-induced heart failure, control wild-type C57BL/6J mice (Gpr34+/+) and GPR34-deficient mice (Gpr34−/−) were subjected to TAC and then analyzed 5 days after TAC.