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Updated: Nov 23, 2025

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
The roles of NLRP3 inflammasome-mediated signaling pathways in hyperuricemic nephropathy
Li Wen1, Hongliu Yang1, Liang Ma2,3
1Division of Nephrology and National Clinical Research Center for Geriatrics, Kidney Research Institute, West China Hospital of Sichuan University, Chengdu, 610041, China.
Abstract:
Hyperuricemic nephropathy (HN) is a common clinical complication of hyperuricemia. High-serum uric acid can trigger renal inflammation. The inflammasome family has several members and shows a significant effect on inflammatory responses. NLRP3 (NOD-, LRR-, and pyrin domain-containing 3) senses the stimuli signal of excessive uric acid and then it recruits apoptosis-related specular protein (ASC) as well as aspartic acid-specific cysteine protease (caspase)-1 precursor to form NLRP3 inflammasome. NLRP3 inflammasome is activated in acute kidney injury (AKI), chronic kidney diseases (CKD), diabetic nephropathy (DN), and HN. This review focuses on important role for the involvement of NLRP3 inflammasome and associated signaling pathways in the pathogenesis of hyperuricemia-induced renal injury and the potential therapeutic implications. Additionally, several inhibitors targeting NLRP3 inflammasome are under development, most of them for experiment. Therefore, researches into NLRP3 inflammasome modulators may provide novel therapies for HN.
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