Hyperuricemia (HUA) is a metabolic disorder that contributes to the pathogenesis of gout arthritis (GA), chronic kidney disease (CKD), and cardiovascular disease (CVD). While current urate-lowering therapies effectively reduce serum uric acid levels, they fail to address the underlying metabolic dysregulation driving HUA progression and associated tissue damage. Emerging evidence highlights that dysregulated amino acid (AA) metabolism in bone, kidney, and vascular tissues plays a pivotal role in HUA-related complications. This review synthesizes recent advances in understanding AA metabolic pathways involved in HUA complications and elucidates the therapeutic potential of targeting tissue-specific AA metabolism. We propose precision modulation of AA metabolism as a promising strategy for both preventing and treating HUA-associated complications.
Zhang et al. (2026) studied this question.