The classical pyroptosis pathway was activated upon recognition of exogenous and endogenous PAMPs or DAMPs. Two steps mediate the NLRP3 inflammasome activation. In the first step, PAMPs or DAMPs bind to TLRs and activate the MyD88/NF-κB signaling pathway, which results in the production of pro-IL-1β/18. The second step is centered on caspase-1 activation and inflammasome assembly. This step transcriptionally promotes the expression of the NLRP3 gene by activating NF-κB and promotes diverse post-transcriptional alterations of the NLRP3 protein. The NLRP3 oligomerization and ASC recruitment cleavage of the pro-caspase-1 resulted in caspase-1 autocatalytic activation. Importantly, activated caspase-1 cleaves GSDMD to produce GSDMD-NT, which forms plasma membrane pores to induce IL-1β/18 secretions. In more detail, three specific mechanisms are involved in NLRP3 inflammasome assembly. Firstly, extracellular ATP binds to the P2X7 receptor and forms a pore in the cell membrane, resulting in K+ efflux and NLRP3 activation. Secondly, particulate or crystalline agonists lead to lysosomal rupture, resulting in the leakage of lysosomal cathepsins B and L that aid in NLRP3 inflammasome assembly. Under the third model, mtDNA and TXNIP stimulate the generation of ROS, which in turn activates the NLRP3 inflammasome.