Cell death resulting from myocardial infarction releases a large amount of DAMPs, such as high-mobility group box 1 (HMGB1), extracellular ATP, and uric acid crystals, which activate pattern recognition receptors (PRRs) on macrophage surfaces, such as Toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE), initiating macrophage inflammation (34). Here, TLR4 is linked to myocardial infarction.