IL-18. They also observed that NLRP3 mediates the release of mtDNA which seems to function as a co-activator of caspase-1. In contrast, Zhou et al. [27] reported that ROS could dissociate the complex between thioredoxin (TRX) and thioredoxin-interacting protein (TXNIP), and consequently TXNIP activated NLRP3. Xiang et al. [58] demonstrated in endothelial cells that ROS produced by NADPH oxidase stimulated the release of TXNIP and its binding to NLRP3 and subsequently induced IL-1β secretion. There is also the possibility that ROS could directly oxidize thiol groups in leucine-rich repeat (LRR) domain of NLRP3 and in that way activate the inflammasomal pathway [17]. Interestingly, there are several studies which demonstrate that ROS can activate autophagy and thus enhance the autophagic cleansing of dysfunctional mitochondria or misfolded proteins [59] and in that way reduce the activation of inflammasomes and the risk for tissue injuries.
