As shown in Figure 12, in the state of heart failure and stress-stimulated cardiomyocyte injury after TAC, NLRP3 can be activated and further affect mitochondrial homeostasis and inhibition of mitophagy, increase mitochondrial oxidative stress, and reduce mitochondrial energy metabolism; it is accompanied by the disorder of intestinal flora and finally leads to myocardial fibrosis/cardiomyocyte hypertrophy and aggravation of cardiomyocyte injury. This evidence concerns the gene NLRP3 and Myocardial fibrosis.