Besides, the present data proved that miR-34a-3p suppressed DUSP1 expression by binding to its 3′-UTR in PDGF-BB-induced PASMCs, which may attenuate the increase in cell viability, proliferation, and the protein expressions of NOR-1 and PCNA in PDGF-BB-induced PASMCs, thus confirming the role of miR-34a-3p as a potential biomarker and therapeutic target for APE. This evidence concerns the gene DUSP1 and apparent mineralocorticoid excess.