The roles of NLRP3 inflammasome-mediated signaling pathways in hyperuricemic nephropathy

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.

Automated summary

Hyperuricemic nephropathy is a common clinical complication caused by high serum uric acid levels, which triggers renal inflammation through the activation of the NLRP3 inflammasome. Research is currently focused on exploring potential therapeutic approaches targeting the NLRP3 inflammasome.