Moreover, we have previously revealed that CTRP9 mitigates the progression of arteriovenous shunt-induced pulmonary artery hypertension (PAH) in rats, including suppressed inflammation, apoptosis and extracellular matrix injury by increased the phosphorylation of Akt and p38-MAPK in the lung tissues of shunt-operated animals, suggesting that CTRP9 maintains the pulmonary vascular homeostasis during the pathogenesis of PAH (Guan et al., 2021). This evidence concerns the gene C1QTNF9 and pulmonary arterial hypertension.