Abstract
Gouty arthritis (GA) is an immune disease caused by the deposition of monosodium urate (MSU) crystals. As living standards improve and lifestyles change, GA exhibits a high incidence rate, low cure rate, and multiple complications. However, the pathophysiological mechanism of GA remains incompletely understood, underscoring the importance of identifying effective therapeutic targets. Neutrophil extracellular traps (NETs) are complex network structures composed of DNA, histones, and various granule proteins, possessing antimicrobial and pathogen clearance functions. Their formation process, termed NETosis, is a programmed cell death mode unique to neutrophils. In GA, MSU crystals can activate NETosis through multiple mechanisms. The resulting NETs can either form aggregates to degrade and package MSU crystals and inflammatory factors, alleviating GA, or promote GA inflammation and tissue damage by activating macrophages to release inflammatory factors. In recent years, NETs have garnered significant attention as potential therapeutic targets for GA. This article reviews the functions and structures of NETs and summarizes several key mechanisms involved in regulating MSU crystal-induced NETosis, while elucidating the specific roles of these NETs in GA. In addition, beyond neutrophils, other myeloid cells such as eosinophils, basophils, and macrophages can also release extracellular traps, and this review explores their potential roles and mechanisms in GA. Finally, this review summarizes some drugs with the potential to target NETs for GA treatment and outlines their limitations. These findings enhance the understanding of interactions between NETs and GA, aiming to propose innovative therapeutic strategies and new approaches for GA prevention and treatment.