The proliferation and migration of pulmonary artery endothelial cells are the pathological basis of pulmonary vascular remodeling with pulmonary hypertension. Recent studies have shown that circular RNA (circRNA) regulates biological processes in various vascular diseases, including pulmonary arterial hypertension (PAH). It has been reported that CircRNA regulates the vascular endothelial cells’ function. Therefore, circRNA may have crucial roles in pulmonary artery endothelial cells (hPAECs) proliferation, migration, and tube formation in PAH. In this study, we aimed to discover the role and mechanism of circHIPK3 in the proliferation and migration of pulmonary hypertension hPAECs. First, we used platelet-derived growth factor (PDGF) –stimulated hPAECs as a cellular model of PAH. The results showed that PDGF promoted hPAECs proliferation, migration, and tube formation. Notably, PDGF upregulated the expression of circHIPK3 in hPAECs and regulated their proliferation, migration, and angiogenesis. Mechanistically, we confirmed miR-328-3p was copiously pulled down by circHIPK3 in hPAECs. Luciferase reporter and RNA immunoprecipitation assays further indicated the cytoplasmic interactions between circHIPK3 and miR-328-3p. Subsequently, we found that circHIPK3 might increase the expression of STAT3 by sponging miR-328-3p. Collectively, our results demonstrated that the circHIPK3-miR-328-3p-STAT3 axis contributed to the pathogenesis of PAH by stimulating hPAECs proliferation, migration, and angiogenesis. The circHIPK3 has an accelerated role in PAH development, implicating the potential values of circHIPK3 in PAH therapy.