These data altogether suggest that CSE induces an imbalanced prostanoid release characterized by the reduced PGI2/TXA2 ratio, likely as a result of an imbalanced expression of PGIS and TXAS in PASMCs and PAECs, and that this imbalance may promote proliferation of both cell types, thereby contributing to pulmonary vascular remodelling in COPD. The gene discussed is PTGIS; the disease is chronic obstructive pulmonary disease.