Gouty arthritis animal models: limitations, challenges, and optimization strategies

Gouty arthritis (GA) is an inflammatory disease primarily triggered by the deposition of monosodium urate (MSU) crystals in and around the joints. With rising living standards and shifts in dietary patterns, the global incidence of GA is increasing, accompanied by a trend toward earlier onset. Consequently, elucidating its pathogenesis and developing effective treatments are major priorities in clinical research. Animal models of GA serve as an indispensable platform for mechanistic investigation and therapeutic development, especially for novel pharmacological agents. Current animal models of GA are broadly categorized into three types: MSU crystal-induced acute inflammation models, hyperuricemia-combined models, and those designed to simulate chronic gout and tophus formation. While existing approaches successfully replicate the acute inflammatory response characteristic of GA, they remain substantially limited in recapitulating the key features of the chronic disease phase, notably spontaneous tophus formation and persistent synovitis. This article critically examines the defining characteristics and optimal applications of prevailing GA models and proposes targeted strategies for their future optimization.