Fig. 9

Schematic figure of the current study. The expression of eIF3a was significantly increased in MCT-induced pulmonary hypertension rat, double-labeled immunofluorescence showed eIF3a was mostly co-localized with CD31, indicated that the development of MCT-induced PAH was related to the regulation of pulmonary artery endothelial cell function. After knockdown of eIF3a expression by AAV1-shRNA-eIF3a, the expression of TGFβ1 was significantly down-regulated, and SMAD2/3 as a downstream molecule of TGFβ1 regulation, its phosphorylation level was significantly reduced, thus improving extracellular matrix deposition and EndMT in lung tissue of PAH rats, and improving vascular remodeling in pulmonary arteries of MCT-induced PAH rats. Moreover, in rat pulmonary artery endothelial cells incubated in a hypoxic environment, following the knockdown of eIF3a expression by si-eIF3a, we observed results consistent with the in vitro experiments