FIGURE 7.

Schematic representation illustrates the involvements of BP‐mediated NLRP3 inflammasomes in cardiac fibrosis in postinfarcted rats. Activation of NLRP3 inflammasome, composed of NLRP3, ASC and pro‐caspase‐1, is tightly regulated by two‐step signals. The first “priming” signal, such as MI‐mediated DAMP, enhances the expression of inflammasome components and target proteins via activation of transcription factor NF‐κB. The second “activation” signal activates NLRP3 which recruits the ASC scaffolding protein and procaspase‐1 allowing for homodimerization and autocatalytic activation of caspase‐1. Active caspase‐1 cleaves pro–IL‐1β into the active isoform. BP inhibits ROS production, which in turn suppresses two‐step signals of NLRP3 inflammasome activation. Inhibition of these signalling pathways by their respective inhibitors is indicated by the vertical lines. TLR, Toll‐like receptor; DAMPs, danger‐associated molecular patterns