In the present study, the data demonstrated that arteriovenous shunt-induced PAH was associated with exacerbation of inflammation, apoptosis, and extracellular matrix accumulation in lung tissues, whereas overexpression of CTRP9 mitigated the pathological progression of PAH by activating the AKT and MAPK pathways. This evidence concerns the gene AKT1 and pulmonary arterial hypertension.