Caspase-4/11-Mediated Pyroptosis in Pulmonary Artery Endothelial Cells Drives Pulmonary Arterial Hypertension

This research demonstrates that Caspase-4/11-mediated pyroptosis of pulmonary artery endothelial cells is a significant factor in the development of pulmonary arterial hypertension (PAH). The study utilized a mouse model of PAH and analyzed lung tissue. Results showed that excessive activation of Caspase-4/11 led to pyroptosis and inflammation of pulmonary artery endothelial cells, ultimately contributing to the development of PAH. These findings present novel therapeutic strategies targeting Caspase-4/11 for the prevention and treatment of PAH.