ArticleJournal of molecular cell biology2026
β-alanine alleviates gout by inhibiting NLRP3 inflammasome activation.
Article in Journal of molecular cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The NLRP3 inflammasome plays a pivotal role in mediating pro-inflammatory cytokine release and inducing pyroptosis. Its aberrant activation is implicated in various inflammatory diseases, including gout, a condition characterized by monosodium urate crystal deposition in the ankle joint. Here, we identify β-alanine, an endogenous amino acid, as a novel NLRP3 inflammasome inhibitor with promising therapeutic potential for gout. Mechanistic investigations reveal that β-alanine binds to NLRP3, sequestering it within the trans-Golgi network. This interaction disrupts NLRP3 inflammasome assembly, thereby inhibiting the secretion of interleukin-1β (IL-1β) and IL-18. Moreover, in vivo experiments demonstrate that β-alanine administration significantly alleviates monosodium urate crystal-induced inflammation and joint swelling in mice without evident toxicity. Collectively, our findings not only uncover a novel endogenous regulatory mechanism for NLRP3-driven inflammation but also position β-alanine as a potential therapeutic candidate for gout.
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