Complication | Evidence | PMID |
Nephropathy | 1. Thrombomodulin domain 1 ameliorates diabetic nephropathy in mice via anti-NF- kappa B/NLRP3 inflammasome-mediated inflammation, enhancement of NRF2 antioxidant activity and inhibition of apoptosis. 2. Taken together, these suggest that ATP-P2X4 signaling mediates high glucose-induced activation of the NLRP3 inflammasome, regulates IL-1 family cytokine secretion, and causes the development of tubulointerstitial inflammation in DN. 3. The findings of this study supported the role of NLRP3 inflammasome in the development of DN. Two signals are required for full NLRP3 activation; the first is a TLR-dependent activation of NF-jB, which may be induced by extracellular HSP72, resulting in the upregulation of NLRP3 and pro-IL-1b expression (?priming?), and the second signal is NLRP3 activating signal which has been mechanistically linked with hyperglycemia and oxidative stress | 24317792 |
Cardiovascular | 1. These data imply that the beneficial effects of PSPC on diabetes-induced endothelial dysfunction and senescence are mediated through ROS and NLRP3 signaling pathways, suggesting a potential target for the prevention of endothelial senescence-related cardiovascular diseases. | 26164602 |
Atherosclerosis | 1. The expression of NLRP3 in SAT, which is affected by lifestyle-related diseases, is associated with the severity of coronary atherosclerosis. | 26282945 |
Insulin resistance and Inflammation | 1. NLRP3 inflammasome are implicated in recognizing certain nonmicrobial originated 'danger signals' leading to caspase-1 activation and subsequent interleukin-1? (IL-1? ) and IL-18 secretion. . | 21217695 |