The objective of this project is to identify relevant mechanisms associated to maladaptive right ventricular hypertrophy (RV) in pulmonary hypertension (PH), beyond pressure overload. For that, we analyzed plasma samples from PH pig models by high-throughput proteomics. Four different experimental models in 48 Yucatan pigs were developed: chronic postcapillary PH by pulmonary vein banding (M1); chronic PH by aorto-pulmonary shunting (M2); RV pressure overload by pulmonary artery banding, thus without PH (M3); and a sham procedure (M0). Animals were evaluated at months 1, and 8 after surgery with right heart catheterization, cardiac magnetic resonance (CMR), and blood sampling, and myocardial tissue was analyzed with histology and molecular biology. Unbiased proteomic and metabolomic analyses were performed and compared among experimental groups and related to the severity of PH and RV dysfunction through integrative interactome networking.