FIGURE 1.

The role of the intrinsic immune system in the pathogenesis of GN. MSU activates the NF-κB signaling pathway by binding CD14 to Toll-like receptors (TLRs) on the cell membrane to recruit bone marrow differentiation response (MyD88), further activation Iκκ, and activated Iκκ cause phosphorylation of IκB to release NF-κB into the nucleus, which regulates the NF-κB signaling pathway, which modulates nuclear transcription and synthesis of interleukin-1β (Pro-IL-1β). Elevated uric acid levels induce oxidative stress and activate the NF-κB signaling pathway, thereby enhancing NF-κB nuclear transcription and activating the NLRP3 inflammasome, leading to the production of caspase-1. This, in turn, promotes the maturation and release of IL-1β, thereby exacerbating the inflammatory response (All figures were created using the BioRender).