Studies in MCT-induced PAH rat models have shown that the glutaminase 1 inhibitor BPTES can suppress M1 macrophage polarization, NLRP3 activation, and the release of pro-inflammatory cytokines, thereby reducing PASMC proliferation and migration induced by inflammatory stimuli, ultimately ameliorating key pathological features of PAH in rats, including elevated pulmonary arterial pressure, impaired RV function, and vascular remodeling. Here, NLRP3 is linked to pulmonary arterial hypertension.