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Although current literature provides limited detail on pathways such as A20, SIRT1, and Nrf2, available evidence suggests that any endogenous mechanism capable of suppressing NLRP3 activation, reducing NETosis, or mitigating fibrosis has the potential to delay the transition from acute gouty inflammation to chronic tophaceous lesions (181183)

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[DOI] [PubMed] [Google Scholar] 246.Ariza ME, Cox B, Martinez B, Mena-Palomo I, Zarate GJ, Williams MV

H., van der Poel, A

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