Thymosin Beta 4 Protects Mice from Monocrotaline-Induced Pulmonary Hypertension and Right Ventricular Hypertrophy

摘要: Pulmonary hypertension (PH) is a progressive vascular disease of pulmonary arteries that impedes ejection blood by the right ventricle. As result there an increase in resistance and arterial pressure causing ventricular hypertrophy (RVH) RV failure. The pathology PAH involves cell remodeling including endothelial (PAEC) dysfunction smooth muscle (PASMC) proliferation. Current therapies are limited to reverse remodeling. Investigating key molecule required for development new therapeutic intervention. Thymosin beta-4 (Tβ4) ubiquitous G-actin sequestering protein with diverse biological function promotes wound healing modulates inflammatory responses. However, it remains unknown whether Tβ4 has any protective role PH. purpose this study evaluate can be used as vascular-protective agent. In monocrotaline (MCT)-induced PH mouse model, we showed mice treated significantly attenuated systolic RVH, compared MCT mice. Our data revealed first time selectively targets Notch3-Col 3A-CTGF gene axis preventing MCT-induced RVH. may provide pre-clinical evidence consider vasculo-protective agent treatment induced