Lázár et al. (2020) study have shown that the decreased expression or dysfunction of endothelial nitric oxide synthase (eNOS) can eliminate the NO signal transduction in PAH. It can be seen that targeted inhibition of eNOS degradation may repair mitochondrial function, thereby reducing the occurrence and development of PAH. Another study also has shown that miR-1226-3p can target Profilin-1 to increase the content of eNOS and NO in PAH rats, thereby protecting rats from PAH induced injury (Jian and Xia, 2021). Here, PFN1 is linked to pulmonary arterial hypertension.