Decoding the Spontaneous Resolution Nature of Gout: Molecular Crosstalk Between Immune Cells, Neutrophil Extracellular Traps, Non-Coding RNAs, and Inflammatory Factors

Abstract

Gout, a prevalent rheumatic disorder, arises from purine metabolic dysfunction characterized by elevated uric acid levels, which culminates in hyperuricemia, crystallization of sodium urate, and subsequent deposition of these crystals in joints, synovium, and other tissues or organs. Spontaneous resolution of gout is defined as the self-resolution of acute gouty arthritis observed in some patients within 7–10 days without pharmacological intervention, with no residual sequelae. The mechanistic basis underlying this spontaneous resolution remains incompletely understood, involving a spectrum of biological entities including immune cells, RNA, neutrophil extracellular traps, inflammatory mediators, and pattern recognition receptors. This review synthesizes current research progress on the spontaneous resolution of gout, with the objective of delineating directions for future investigations.