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Hyperuricemia (HUA) and gout are endocrine disorders resulting from abnormal uric acid (UA) metabolism, with gout typically developing secondary to HUA and being associated with an exacerbated inflammatory response. Epigenetic modifications and post-translational modifications (PTMs) may contribute to the progression from HUA to gout by modulating the function of UA transporters such as ABCG2 and GLUT9 and involving the NLRP3/IL-β inflammatory axis. However, the specific mechanisms underlying these processes remain incompletely understood. Therefore, this review systematically examines recent research on epigenetic modifications, such as methylation, lactylation, and crotonylation, as well as PTMs including succinylation, phosphorylation, glycosylation, ubiquitination, and acetylation in this process, with the aim of identifying potential therapeutic targets for these two diseases.
Fu et al. (Fri,) studied this question.