Therefore using monocrotaline (MCT)-induced PH rat model and derived PASMCs with salusin-β knockdown or overexpression, we evaluated the roles of salusin-β in regulating the proliferation, migration, fibrosis, and calcification of PASMCs, and the roles of it in regulating the imbalance of vasomotor function, vascular remodeling, and the development and progression of pulmonary hypertension, as well as its down-steam mechanisms. Here, PPIB is linked to pulmonary hypertension.