Cellular interplay in pulmonary arterial hypertension: Implications for new therapies

摘要: Pulmonary arterial hypertension (PAH) is a complex and multifactorial disease characterized by vascular remodeling, vasoconstriction, inflammation thrombosis. Although the available therapies have resulted in improvements morbidity survival, PAH remains severe devastating with poor prognosis high mortality, justifying need of novel therapeutic targets. An increasing number studies demonstrated that endothelial cells (ECs), smooth muscle (SMCs) fibroblasts pulmonary vessel wall, as well platelets inflammatory role pathogenesis. This review aims to integrate interplay among different types cells, during development progression, impact current cellular modulation. The present vessels regulated several mediators produced these contributing pathophysiologic features PAH. Current are mainly focused tone dysfunction. However, once they not been effective, targeting other features, such platelet dysfunction emerging. Further understanding cell involved progression can contribute find targets, decreasing mortality future.