Table 2.

Redox-signalling pathways-induced inflammasome activation in AKI.

AKI model	Redox-Signalling-Induced Inflammasome Activation	Effects	Reference
PQ-induced nephrotoxicity	ROS/NF-κB/DAPK/NLRP3	PQ produces ROS, activating to NF-κB and DAPK that in turn activates NLRP3	[98]
Methotrexate-induced nephrotoxicity	decreasedNrf2/ARE/HO-1 signalling and PPARγ	Methotrexate induces the decreasing of Nrf2 and PPARγ by promoting ROS, leading to antioxidant system decrease and lipid peroxidation	[99]
Ceftriaxone-induced urolithiasis	decreasedNrf2/HO-1	Ceftriaxone promotes inflammation and oxidative stress by activating NLRP3 and inducing ROS production and decreasing the antioxidant system.	[100]

NF-κB: nuclear factor κB; NLRP3: Nod-like receptor (NLR) family pyrin domain containing 3; Nrf2: nuclear factor erythroid 2-related factor 2; ROS: reactive oxygen species; PQ: paraquat; DAPK: death-associated; antioxidant response element (ARE); heme oxygenase 1 (HO-1); PPARγ: peroxisome proliferator-activated receptor-gamma; mitogen-activated protein kinases (MAPK).