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Pulmonary hypertension (PH) is a progressive and devastating disease of various causes that is associated with structural and functional disorder and inappropriately increased pressure of pulmonary small-to medium-sized vasculature.Extensive pulmonary vascular remodeling with narrowing lumen is well characterized in all forms of PH,which is hemodynamically defined by a mean pulmonary artery pressure exceeding 25 mmHg at rest (Schermuly et al., 2011;Mehari et al., 2014).The morbidity and mortality of PH continues to increase due to no cure (Mehari et al.,2014);however, our understanding of the mechanism and therapeutics underlying PH remains far from complete.There are many competing hypotheses for how PH develops in a genetic or sporadic way (Schermuly et al., 2011).One of them is that the endothelial-to-mesenchymal transition (EndMT) could be implicated in initiation and progression of human PH (Arciniegas et al., 2007).Notably, this point is further emphasized by two recent papers, which provide direct evidence linking EndMT to PH (Good et al., 2015;Ranchoux et al., 2015).