MYD88 and Sepsis: Luo et al. (2020) found that the protective effect of TBMS I on sepsis mice was achieved by repressing the TLR4-MyD88-NF-κB-iNOS pathway; while similar pharmacological studies have shown that it may alleviate the pathological factors of sepsis-induced cardiac dysfunction and endothelial dysfunction (such as inflammation, oxidative stress, and apoptosis, etc.), which was raised by SIRT3 (Cheng et al., 2021; Yang et al., 2021).