Inflammation is an important, yet poorly understood cause of renal damage in diabetic nephropathy. Nlrp3-inflammasome activation has now been demonstrated in endothelial cells and podocytes from patients with diabetes in vitro, and in mouse models of diabetes. Nlrp3-inflammasome-mediated damage did not arise from circulating immune cells. Nlrp3 or CASP1 knock out and IL-1 receptor antagonism all protected against diabetic nephropathy in mouse models of diabetes. This research identifies several potential targets for diabetic nephropathy treatment.
References
Shahzad, K. et al. Nlrp3-inflammasome activation in non-myeloid-derived cells aggravates diabetic nephropathy. Kidney Int. 10.1038/ki.2014.271
Rights and permissions
About this article
Cite this article
Nlrp3-inflammasome activated in diabetic nephropathy. Nat Rev Nephrol 10, 542 (2014). https://doi.org/10.1038/nrneph.2014.153
Published:
Issue Date:
DOI: https://doi.org/10.1038/nrneph.2014.153