In caveolin-1 (Cav-1) knockout mice subjected to chronic hypoxia the transition from RV hypertrophy to failure is accelerated compared to wild-type mice and caused by uncoupling of RV endothelial NOS and increased protein tyrosine nitration; all changes are prevented by re-expressing an endothelial-specific Cav-1 transgene (avoiding NOS uncoupling) or by NOS inhibition without modifying the extent of pulmonary hypertension (Cruz et al., 2012). Here, CAV1 is linked to pulmonary arterial hypertension.