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After myocardial infarction, neutrophils can also release S100A8/A9 in the infarction area through NETosis, interact with Toll-like receptor (TLR) 4 on nave neutrophils, activate the NLRP3 inflammasome of the NOD-like receptor (NLR) family pyrin domain-containing 3, and amplify granule production through IL-1 and IL-18 dependent signaling pathways (132), eventually promoting the development of myocardial fibrosis (133)
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