Abstract
Pulmonary arterial hypertension (PAH) is a vasculopathy characterized by enhanced pulmonary artery smooth muscle cells (PASMC) proliferation and suppressed apoptosis. This results in both increase in pulmonary arterial pressure and pulmonary vascular remodeling. Recent studies have shown the implication of different transcription factors and proteins such as signal of transducer and activator of transcription 3 (STAT3), bone morphogenetic protein receptor 2 (BMPR2) and peroxisome proliferator-activated receptor gamma (PPARã) in the etiology of PAH.
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