Abstract
Gout is a metabolic disease caused by the deposition of monosodium urate (MSU) crystals inside joints, which leads to inflammation and tissue damage. Increased concentration of serum urate is an essential step in the development of gout. Serum urate is regulated by urate transporters in the kidney and intestine, especially GLUT9 (SLC2A9), URAT1 (SLC22A12) and ABCG. Activation of NLRP3 inflammasome bodies and subsequent release of IL-1β by monosodium urate crystals induce the crescendo of acute gouty arthritis, while neutrophil extracellular traps (NETs) are considered to drive the self-resolving of gout within a few days. If untreated, acute gout may eventually develop into chronic tophaceous gout characterized by tophi, chronic gouty synovitis, and structural joint damage, leading the crushing burden of treatment. Although the research on the pathological mechanism of gout has been gradually deepened in recent years, many clinical manifestations of gout are still unable to be fully elucidated. Here, we reviewed the molecular pathological mechanism behind various clinical manifestations of gout, with a view to making contributions to further understanding and treatment.
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