SMAD1 and pulmonary arterial hypertension: This process leads to cell membrane perforation, swelling, and rupture, along with the release of pro-inflammatory factors such as IL-1β and IL-18.62,63 Cathepsin L activated Caspase-3/GSDME-induced pyroptosis of PAECs, dependent on BMPR2 degradation and subsequent Smad1 downregulation, contributing to pulmonary vascular remodeling of MCT-PAH and SU5416-hypoxia-induced PAH (Su/Hx-PAH) rats.64