FIGURE 6.

Working model of pyroptosis caused by Clmp knockdown in cardiac fibroblasts after MI Clmp deficiency may induce the self‐assembly of inflammasome triggered by myocardial ischaemia. The activation of inflammasome promoted the maturation of CASP1 protein from pro‐CASP1. On the one hand, matured CASP1 induced the cleavage of pro‐interleukin 1β (pro‐IL‐1β) to IL‐1β. On the other hand, GSDMD was cleaved by CASP1 in the inflammasome and promoted the release of IL‐1β by forming pores in the plasma membrane. Excessive IL‐1β released into the surrounding environment in short period of time and aggravated the recruitment of neutrophils. Excessive IL‐1β could also trigger severe inflammation response and led to a more severe myocardial injury