In our current study, we applied the MCT-induced PAH rat model and supplemented the underlying mechanisms: C3a could promote subsequent inflammasome NLRP3 activation and release proinflammatory cytokines (IL-1β and IL-18), which resulted in vascular remodeling and finally pulmonary arteriole obstruction. The gene discussed is NLRP3; the disease is pulmonary arterial hypertension.