Fig. 3

a NLRP3/caspase-1 signaling pathway and its correlated intervention after MI. NLRP3/caspase-1 inflammasome pathway mediated inflammation, pyroptosis, oxidative stress, fibrosis, cardiac remodeling following MI. When NLRP3 is activated by DAMPs and PAMPs, it binds to ASC adaptor molecule and aggregates with pro-caspase-1. Then the NLRP3 inflammasome converts pro-caspase-1 to caspase-1, which catalyzes the conversion of pro-IL-1β and pro-IL-18 to its mature product IL-1β and IL-18. ATP adenosine triphosphate, LPS lipopolysaccharide, PAMPs pathogen-associated molecular patterns, DAMPs Danger-associated molecular patterns, TLR4 toll-like receptor 4, NLRP3 nucleotide-binding domain, leucine-rich-repeat family, pyrin-domain-containing 3, ASC activating signal cointegrator, IL interleukin, NF-κB nuclear factor-κBn, OLT1177 Dapansutrile. b TLR4/MyD88/NF-κB signaling pathway and its correlated intervention after MI. TLR4/MyD88/NF-κB signaling pathway mediated inflammation, pyroptosis, apoptosis, fibrosis, ventricular arrhythmias and lipid metabolism after myocardial infarction. Cardiac injury generates endogenous signals that activate the TLR4/MyD88/NF-κB signaling pathway. The activation of the TLR signaling pathway originates from the cytoplasmic TIR domain that associates with a TIR domain-containing adaptor, MyD88. This signaling pathway activates NF-κB, a transcription factor, and subsequently induce the production of proinflammatory cytokines. TLR4 Toll-like receptor 4, TIRAP TIR (Toll/IL-1 receptor) domain-containing adapter protein, IRAK-4 IL-1 receptor-associated kinase-4, TRAF6 tumor necrosis factor receptor-associated factor 6, IKK IκB kinase, NF-κB Nuclear factor-κB, Lenti shRNA Lentivirus short hairpin RNA, TAK-242 resatorvid, RP-105 radioprotective 105