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. 2022 Dec 26;33:101417. doi: 10.1016/j.bbrep.2022.101417

Table 2.

The role of NLRP3 in chronic kidney disease.

Disease Relevant factors change Animal or cell role references
Hypertensive nephropathy IL-1β↑,IL-18↑,ASC↑,
Caspase-1↑,NLRP3↑
Mice,Glomerular podocyte Sertoli cell apoptosis,Lysosomal membrane rupture,Renal fibrosis 60–64
lupus nephritis NLRP3↑ Glomerular podocyte Proteinuria increase 66
SLE associated nephritis ASC↑,Caspase-1↑, NLRP3↑ Mice,Glomerular podocyte Increase proteinuria 64
Mesangial proliferative kidney disease ASC↑,Caspase-1↑, NLRP3↑ Renal tubular epithelial cell Renal interstitial inflammation,Renal tubular atrophy 67
Diabetic nephropathy IL-1β↓, IL-18↓, ASC↓,Caspase-1↓ NLRP3−/− mice decrease inflammation in the kidney 71–90
Renal ischemia-reperfusion injury NLRP3↑,ASC↑ NLRP3−/− mice,Renal tubular epithelial cell Decrease neutrophilinfiltration 95–98
Albumin induced nephropathy NLRP3↑,Caspase-1↑,IL-1β↑,IL-18↑,Cathepsin B↑ Mice,Renal tubular epithelial cell Renal tubular cell apoptosis,Lysosome damage 105
Unilateral ureteral obstruction nephropathy ASC↑,Caspase-1↑,IL-1β↑,NLRP3↑ Mice Renal tubular damage,renal interstitial fibrosis 69,70
High uric acid nephropathy NLRP3↑,ASC↑ Rat,Renal tubular epithelial cell Renal epithelial-interstitial transformation 101,103
Azithromycin-treated nephropathy NLRP3↑, lymphocyte↑ Rat,Renal tubular epithelial cell Lymphocyte infiltration 102