Administration of the SOD analog, MnTBAP, regresses PAH in FHRs. (a) MnTBAP reduces mean PA pressure measured by Doppler (lengthens PA acceleration time [PAAT]) and decreases right ventricular (RV) thickness in FHRs treated for 4 weeks (n=5 per group). *P<0.05. (b) MnTBAP therapy reduces mean pulmonary artery pressure (PAP) and total pulmonary resistance (TPR). (c) FHRs treated with MnTBAP exercise longer on a graded treadmill (n=15 per group). (d) Lung sections were stained for von Willebrand factor (vWF; red), a-smooth muscle cell (SMC) actin (green), and DAPI (blue). Note the fully muscularized (white arrows), partially muscularized (yellow arrows), and nonmuscularized blood vessels (red arrows). Bottom, A representative fully muscularized PA in a vehicle-treated FHR (left) vs MnTBAP (right). The percent medial thickness of precapillary resistance PAs was reduced and the number of nonmuscularized resistance PAs was increased by MnTBAP. **P<0.01 vs control. Reproduced with permission from Archer et al ; (1)Archer SL,Marsboom G,Kim GH,Zhang HJ,Toth PT,Svensson EC,Dyck JRB,Gomberg-Maitland M,Thbaud B,Husain AN, et al.Epigenetic attenuation of mitochondrial superoxide dismutase 2 in pulmonary arterial hypertension: a basis for excessive cell proliferation and a new therapeutic target.Circulation. 2010 ;121(24):2661-71.
Additional keywords: SOD2,methylation,PASMC,fawn hooded rat,pulmonary vascular remodeling