Fig. 3From: Bioactivities and mechanisms of natural medicines in the management of pulmonary arterial hypertensionPathogenesis of PAH in genetic and cellular levels. The main pathogenesis involves in genetic mutations (BMPR2, ACVRL1, KCNK3, Smad1/4/9 and EIF2AK4), dysregulation of vascular cells (HPAECs and PASMc), epigenetic factors (miRNA and lncRNA), metabolic dysfunction (oestrogen, mitochondrial and glucose metabolism), inflammation and immunity (NF-κB and complement cascade). PAH pulmonary arterial hypertension, NO nitric oxide, ET-1 endothelin-1, PASMCs pulmonary arterial smooth muscle cells, HPAECs human pulmonary arterial endothelial cells, EndMT endothelial–mesenchymal transition, PECAM1 platelet endothelial cell adhesion molecule 1, α-SMA α-smooth muscle actin, HIF hypoxia-inducible factor, SOD superoxide dismutase, PFKFB3 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3, IgG immunoglobulin GBack to article page