As observed in the Su/Hx model, inhibition of HDAC6 with TubA significantly improved RVSP, mPAP, CO, TPR, RV hypertrophy, vascular remodeling (as assessed by medial wall thickness and percentage of occluded vessels) and cell proliferation/apoptosis imbalance in the MCT rat model (Supplementary Figure S9) reinforcing the view that HDAC6 is an essential component of vascular remodeling in PAH. Here, HDAC6 is linked to pulmonary arterial hypertension.