It has been found that TLR4 mediates the activation of the NF-κB pathway and contributes to the development of heart failure by inducing oxidative stress and inflammation, impairing endothelial cells, increasing cardiac fibrosis, and promoting cardiomyocyte hypertrophy, apoptosis, pyroptosis, and autophagy, thereby causing damage to cardiomyocytes [39]. Here, NFKB1 is linked to fibrosis.