IL1B and diabetic kidney disease: Hyperglycemia activates NOX in podocytes, thereby inducing the production of ROS, activating the specific NLRP3 inflammasome NLRP3A350V in podocytes, significantly promoting the secretion of inflammatory exosomes (MVB) in podocytes, releasing inflammatory cytokines such as IL-1β, and death in the GBM, thereby destroying the glomerular filtration barrier, aggravating kidney damage, and further developing DKD (46, 54, 55).