Table 1.

Roles of inflammasomes in inflammatory kidney diseases.

Disease	Inflammasomes involved	Roles and potential mechanism	Reference
Acute kidney injury	NLRP3	Nlrp3 gene deletion protected mice from AKI.	[143, 144]
		ATP-sensitive P2X7 receptor activates the NLRP3 inflammasomes.	[145]
		Cell debris (histones, HGBM1, etc.) mediated NLRP3 inflammasome activation.	[70, 72, 74]
IgA nephropathy	NLRP3	Nlrp3 deficiency improved renal function and renal injury in a mouse IgAN model.	[85]
		NLRP3 gene expression was correlated with clinical outcome in IgAN patients.	[82]
		IgA-immune complexes activated NLRP3 inflammasomes involving ROS production in macrophages, dendritic cells, and renal intrinsic cells.	[85]
		Generation of ROS and activation of NF-κB lead to NLRP3 activation, which is a key event in IgAN.	[84]
Diabetic nephropathy	NLRP3	Nlrp3-deficient mice are protected against diabetic nephropathy.	[88, 89]
		Mitochondrial ROS, TLR4 signaling, and NLRP3 inflammasome activation aggravate diabetic nephropathy.	[89, 91]
		TXNIP activated NLRP3 inflammasomes in podocytes of diabetic nephropathy.	[95, 146]
		High glucose and LPS activate ROS/TXNIP/NLRP3/IL-1β inflammasome signaling in glomerular mesangial cells.	[96]
		ATP-P2X4 signaling mediated high glucose-induced activation of NLRP3 inflammasomes.	[90]
	NLRC4	Nlrc4 deficiency resulted in diminished disease progression in diabetic mice. Activation of NF-κB and MAPK pathways was blocked by Nlrc4 deficiency.	[98]
Lupus nephritis	NLRP1	Polymorphism of NLRP1 was related to the pathogenesis of lupus.	[119]
	NLRP3	NLRP3 inflammasomes were activated in podocytes from NZM2328 mice and patients of LN; P2X7/NLRP3 is a key signaling pathway.	[110, 111]
		Immune complex containing dsDNA induced IL-1β production through NLRP3 inflammasomes.	[104, 105]
		Lack of NLRP3 enhanced lupus symptom in B6lpr mice by inhibiting TGF target genes.	[114]
	AIM2	AIM2 expression was increased in lupus patients and closely correlated with the severity of disease in SLE patients. AIM2 facilitates the apoptotic DNA-induced lupus damage via arbitrating macrophage functional maturation.	[100, 131]
	IFI16	IFI16 expression was increased in leukocytes but not in kidney biopsies of lupus patients.	[129, 131]
		Anti-IFI16 antibody titers were higher in lupus patients and inversely correlated with proteinuria.	[110]