HSP60 Regulates Monosodium Urate Crystal-Induced Inflammation by Activating the TLR4-NF-κB-MyD88 Signaling Pathway and Disrupting Mitochondrial Function

Figure 7

Schema of the signaling pathway involved in HSP60-mediated NLRP3 inflammasome activation and subsequent IL-1β production. After MSU crystal stimulation, the secretion of HSP60 to the extracellular level is greatly increased, which activates the signaling pathway and promotes the transcription of IL-1β and NLRP3. MSU crystal treatment also leads to a large amount of HSP60 aggregation in mitochondria, causing mitochondrial dysfunction, thereby activating NLRP3 inflammasome and promoting IL-1β precursor processing and ultimately leading to IL-1β release and inflammatory response.