Underlying mechanisms of Tregs in PAH. Tregs repair injured PAECs and endothelium integrity by secreting interleukin‐10 and upregulating BMPR2 expression. Tregs inhibit excessive PASMC proliferation and apoptosis resistance by suppressing the Akt and ERK pathway, reducing cyclin D1 and CDK expression, and restraining the RhoA/ROCK pathway. Tregs regulate abnormal fibroblast proliferation and activation by suppressing TGF‐β and FGF‐9 production, inhibiting the CXCL12–CXCR4 axis, suppressing leukotriene B4 production, and directly secreting interleukin‐10 and interferon‐γ. BMPR2 indicates bone morphogenetic protein receptor type 2; CDK, cyclin‐dependent kinase; CXCL12–CXCR4, chemokine (C‐X‐C motif) ligand 12—CXC receptor 4; ERK, extracellular signal‐regulated kinase; FGF‐9, fibroblast growth factor‐9; LTB4, leukotriene B4; PAEC, pulmonary arterial endothelial cell; PASMC, pulmonary arterial smooth muscle cell; TGF‐β, transforming growth factor‐β.