|
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] |
|