These results suggest that SeP, even without its selenium content, acts as an upstream negative regulator of antioxidative stress signaling, which induces both ROS generation through NADPH oxidases and stabilizes HIF-1α, providing a potential mechanism of SeP-mediated HIF-1α activation and resultant proliferation of PASMCs and their survival in PAH. This evidence concerns the gene HIF1A and pulmonary arterial hypertension.