Additionally, via inhibiting NLRP3-induced inflammation and idiopathic pulmonary fibrosis, the clinically used TGF- β blocker, pirfenidone protected against thoracic aortic constriction (TAC)-induced hypertension and left ventricular hypertrophy, collectively contributing to myocardial fibrosis, via blocking NLRP3-mediated inflammation and fibrosis [85]. Here, NLRP3 is linked to left ventricular hypertrophy.