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Fig. 7 | Respiratory Research

Fig. 7

From: CRISPR-mediated Bmpr2 point mutation exacerbates late pulmonary vasculopathy and reduces survival in rats with experimental pulmonary hypertension

Fig. 7

The impacts of Bmpr2 mutation on the phenotype of rats with monocrotaline-induced pulmonary hypertension with or without phosphodiesterase type 5 inhibitor treatment. Schematic representation for the impacts of Bmpr2 mutation on the course of monocrotaline (MCT) induced-pulmonary hypertension (PH) for the rats without treatment (top, natural course) and treated with a phosphodiesterase type 5 (PDE5) inhibitor (bottom) indicating survival, pulmonary vascular disease (PVD), pulmonary arterial pressure (PAP), right ventricular hypertrophy (RVH) and RV myocardial fibrosis in wild-type (WT, solid lines) and Bmpr2 mutation (+/44insG, dashed lines) rats. Disease stage of MCT-PH is classified into initial endothelial cell (EC) injury from day 0–7 of MCT injection showing baseline survival, PVD, PAP and RVH; early PVD without pulmonary hypertension (PH) from day 7–14; progressive PVD with PH from day 14–21 showing increase in both PAP and RVH; advanced PVD with severe PH after day 21. EC = endothelial cell; PVD = pulmonary vascular disease; PH = pulmonary hypertension; BMPR2 = bone morphogenetic protein receptor type 2; +/44insG = the Bmpr2 mutation generated in this study; WT = wild-type; PAP = pulmonary artery pressure; RVH = right ventricular hypertrophy; MCT = monocrotaline; PASMC = pulmonary artery smooth muscle cell; RV = right ventricle; PDE5 = phosphodiesterase type 5

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