NLRP3 and gout: The excessive ROS activated the NLRP3 inflammasome, promoting the release of proinflammatory factors such as IL-1β, which further damages renal tubular epithelial cells, inhibited the function of uric acid transporters such as ABCG2 and URAT1, and caused impaired uric acid excretion, ultimately leading to the onset of gout.