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. GN can lead to improve cardiac function, regulate the distribution and abundance of intestinal flora, maintain mitochondrial homeostasis, improve mitochondrial function, improve mitophagy, inhibit oxidative stress, and improve mitochondrial energy metabolism.