NLRP3 and myocardial infarction: The results of our study suggested that M-CSF could inhibit the inflammatory response, cardiomyocyte hypertrophy, apoptosis, fibrosis, etc. and myocardial injury after MI by increasing the polarization and maturation of M2 macrophages and inhibiting the inflammatory effect of M1 macrophages, P2X7R/NLRP3/IL-1β signaling pathway played an essential role in this process.