NLRP3 and Myocardial fibrosis: There is increasing evidence that shows IS contributes to the mechanism underlying cardiovascular events., IS promotes the expression of myocardial hypertrophic protein and stimulates cardiac fibroblast collagen synthesis by activating the NLRP3 inflammasome signaling pathway [28], and p38 mitogen-activated protein kinase, p42/44 mitogen-activate protein kinase, and NF-kB pathways [29], thereby aggravating myocardial fibrosis and hypertrophy with enhanced oxidative stress and reduced antioxidant capacity.