Abstract: Objective To investigate the roles of β-arrestin 1 in the collagen synthesis of pulmonary vessels in the pathogenesis of pulmonary hypertension induced by hypoxia, and illustrate the molecular mechanism of pulmonary vascular remodeling in pulmonary artery hypertension(PAH). Methods Twenty male Sprague-Dawley rats were randomly divided into control group and hypoxia group, with 10 rats in each group.Rats in hypoxia group were raised in a low oxygen chamber(oxygen concentration of 100 ml/L) for 3 weeks, while rats in normal control group were raised in the normal oxygen environment.Right cardiac catheterization procedure was used to detect mean pulmonary arterial pressure(mPAP), and the ratio of right ventricular mass to left ventricular plus septal massRV/LV+S was measured.Expressions of CollagenⅠand β-arrestin 1 in pulmonary vessel tissues were detected by immunohistochemistry assay and Western blot, while expressions of β-arrestin 1 and CollagenⅠin hypoxia-stimulated PASMCs were detected by Western blot and immunofluorence method after silencing the β-arrestin 1 gene. Results Compared with normoxic group, the mPAP(31.35±1.35 mmHg) and RV/(LV+S) (30.81%±0.81%) of rats in hypoxic group increased significantly(P< 0.01), and expression of β-arrestin1 and CollagenⅠ in pulmonary vascular tissues of rats raised in low oxygen condition also increased significantly.Hypoxia could upregulate the protein expression of β-arrestin1 and CollagenⅠ in PASMCs, and the collagen synthesis in PASMCs induced by hypoxia was inhibited by knockdown of β-arrestin 1. Conclusion β-arrestin 1 promotes the collagen synthesis of pulmonary vessels in PAH induced by hypoxia and pulmonary vascular remodeling, thus resulting in the development of PAH.