Review Article
Khiem Tran and You-Yang Zha
Abstract
Pulmonary hypertension is an unremitting disease characterized by progressive increase of pulmonary vascular resistance and vascular remodeling. Due to poor understanding of the molecular basis of the pathogenesis, there are currently limited options available for the treatment of this devastating disease. Recent studies with Cav1-/- mice and other genetically modified animal models as well as experimental animal models of pulmonary hypertension have demonstrated the critical role of Caveolin-1 deficiency in the pathogenesis of pulmonary hypertension. Here, we will review the current knowledge about the role of Caveolin-1 signaling in the mechanisms of pulmonary hypertension focusing on protein kinase G nitration and STAT3 activation and provide insights into the molecular basis of the pathogenesis of human pulmonary hypertension.