In the early stages of MI/R, neutrophil-derived cathelicidin aggravates MI/R injury by over-activating TLR4 signaling and the P2X7R/NLRP3 inflammasome in heart-infiltrating neutrophils, which leads to the excessive secretion of IL-1β and subsequent inflammatory injury (27). Here, TLR4 is linked to myocardial infarction.