NLRP3 knockout (KO) improved renal function, attenuated glomerular hypertrophy, glomerulosclerosis, mesangial expansion, interstitial fibrosis, inflammation and expression of TGF-β1 and connective tissue growth factor (CTGF), as well as the activation of Smad3 in kidneys of STZ-induced diabetic mice.
Finally, we observed a striking induction of NLRP3 in glomeruli and renal tubules in line with an enhanced urinary IL-18 output in nephrotic syndrome patients with minimal change disease or focal segmental glomerular sclerosis.
It is concluded that inhibition of NLRP3 inflammasome activation is one of the important mechanisms mediating the beneficial action of RvD1 and 17S-HDHA on Hcys-induced podocyte injury and glomerular sclerosis.