This paper explores the potential mechanism of microRNA-143–5p regulation effects on pulmonary arterysmooth muscle cells (PASMCs) functions in hypoxic pulmonary hypertension (HPH) via targeting HIF-1α,which may offer a new idea for HPH therapy. PASMCs were transfected with mimics control/miR-143–5pmimics or inhibitor control/miR-143–5p inhibitor. We used Western blotting and RT-qPCR to detect the proteinand mRNA expressions, CCK-8 assay to detect cellular viability, Annexin V-FITC/PI staining and caspase-3/cleaved caspase-3 protein to evaluate cellular apoptosis, transwell migration experiment for cellularmigration measurement and Dual luciferase reporter gene assay to prove the target of miR-143–5p. Cells underhypoxic condition presented the decreased protein and mRNA expressions of a-smooth muscle actin (SM-α-actin),Myocardin, smooth muscle myosin heavy chain (SMMHC), and smooth muscle-22α (SM22α),Calponin1 and Hypoxia-inducible factor-1α (HIF-1α), the increased cell viability and miR-143–5p level; Overexpressionof miR-143–5p obviously reduced vascular smooth muscle-specific contraction marker proteinlevels and cellular apoptosis, increased cellular migration of PASMCs with hypoxia stimulation; Low-expressionof miR-143–5p caused the opposite changes, while co-transfected with Si HIF-1a blocked thebeneficial effects of miR-143–5p inhibition on PASMCs under hypoxia. MicroRNA-143–5p can promote thephenotype conversion, proliferation and migration of pulmonary artery smooth muscle cells under hypoxiccondition through direct targeting of HIF-1α.