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. Author manuscript; available in PMC: 2017 Jul 1.
Published in final edited form as: J Cardiovasc Pharmacol Ther. 2016 Nov 2;22(3):219–229. doi: 10.1177/1074248416675731

Figure 2.

Figure 2

The model of nucleotide-binding domain nod-like receptor protein 3 (NLRP3) inflammasome activation through reactive oxygen species (ROS) by ischemia/reperfusion (I/R). The I/R-induced ROS dissociate thioredoxin-interacting protein (Txnip) from cytosolic thioredoxin-1 (TRX1). Free Txnip then binds to NLRP3 and activates NLRP3 inflammasome. The NLRP3 oligomerizes and recruits apoptosis-associated speck-like protein containing a CARD (caspase recruitment domain) (ASC) and pro-caspase 1, triggering the activation of caspase 1. This biological process leads to the maturation of proinflammatory cytokine interleukin 1β (IL-1β). Accumulation of these cytokines within the myocardium induces I/R injury and contributes to cardiac dysfunction.