PIN1 and idiopathic pulmonary arterial hypertension: The model we propose (Fig. 6) is based on our observations that (i) Pin1 expression is up-regulated in both pulmonary MVECs and lungs of iPAH patients; (ii) lack of Pin1 inhibits EC dysfunction and PA-SMC proliferation; (iii) inhibition of Pin1 by juglone as well as Pin1 knock-down attenuates inflammation through inhibition of the NFκB pathway; (iv) juglone inhibits MVEC dysfunction, inhibits TGF-β signalling, and potently augments BMP/SMAD signalling in MVECs in vitro and rat lungs in vivo.