Similarly, our experiments revealed that TGF-β1 expression and Smad2/3 phosphorylation were significantly increased in the MCT-induced pulmonary hypertension rat model, and the same results were observed in pulmonary arterial endothelial cells exposed to hypoxia, whereas eIF3a knockdown inhibited TGF-β1 expression, thereby inhibiting the phosphorylation of Smad 2/3. This evidence concerns the gene SMAD2 and pulmonary arterial hypertension.