Specifically, in PASMCs from PAH patients with BMPR2 mutations and Bmpr2+/− mice, chronic BMPR2 deficiency inhibits the expression of SOD3, increases ROS production, enhances lipopolysaccharide-induced IL-6 expression and secretion, and promotes proliferation via activated STAT3.56 Elevated IL-6 levels in rat lung tissues with MCT-PAH have been shown to downregulate BMPR2 and activate STAT3, creating a vicious cycle that further stimulates the proliferation of PASMCs.57 Here, STAT3 is linked to pulmonary arterial hypertension.