IL1B and myocardial infarction: Elssner et al. (2004) found that LL37 could promote the secretion of IL-1β in monocytes through the P2 × 7 receptor. As one of the important inflammatory mediators after TBI, IL-1β can participate in sympathetic excitation by regulating levels of excitatory/inhibitory neurotransmitter and neuronal activity (Wang et al., 2019; Yan et al., 2019). The increased level of IL-1β in the PVN is proved to participate in the sympathetic excitation in hypertension, myocardial infarction, and heart failure (Liu et al., 2014; Qi et al., 2016; Wang et al., 2019).