Dual role of autophagy in gouty arthritis (GA): molecular mechanisms and therapeutic potential
Abstract
Autophagy is a conserved lysosomal degradation pathway with complex and context-dependent effects in gouty arthritis (GA). Emerging evidence indicates that the autophagic response is determined primarily by the integrity of autophagic flux rather than autophagic activation. Preserved autophagic flux may contribute to inflammatory resolution, whereas impaired autophagic degradation or dysregulated autophagy may promote inflammasome activation, pro-inflammatory cytokine production, and joint tissue damage. These contrasting effects are largely determined by cellular context, as autophagy exhibits varied responses regulated by distinct signaling pathways in neutrophils, monocytes/macrophages, chondrocytes, and osteoblasts. This review summarizes the current evidence on the dual role of autophagy in monosodium urate-induced inflammation, highlights the challenges associated with interpreting autophagic flux, discusses emerging pharmacological and molecular regulators of autophagy in GA, and supports the development of targeted, mechanism-based therapeutic strategies.
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