We next assessed the efficacy of SecinH3 treatment in the monocrotaline rat model of PAH, a nongenetic model of disease in which activation of NF-κB and reduction of BMPRII expression play a central role.30,31 The treatment regime started 8 days after a single injection of monocrotaline, when the pathological processes leading to vascular remodeling are already established.32 Increase in CLIC4 expression and Arf6 activation were noted from day 3, while significant rise in mean pulmonary artery pressure was noted later—14 days post-monocrotaline injection (Online Figure XVIII). Here, BMPR2 is linked to pulmonary arterial hypertension.