Wang W. Z. et al. (2019b)found that anti-TLR2 antibody inhibits NF-κB activation and reduces cardiac damage in high-fat-feeding rats. Our study also confirmed that TLR2 regulated the activation of NF-κB. Taken together, our study showed that NOX1 inhibition reduced the activity of the TLR2/NF-κB pathway, improving myocardial fibrosis and cardiac dysfunction in DCM rats. In vitro experiments have shown that NOX1 promoted oxidative stress in HG-induced CFs, and promoted fibrosis by activating the TLR2/NF-κB pathway, which may be regulated by the ROS level (Figure 7). This evidence concerns the gene NFKB1 and myalgic encephalomeyelitis/chronic fatigue syndrome.