ReviewFrontiers in immunology2026
Trained immunity in gout: epigenetic and metabolic reprogramming of innate immune memory.
Review in Frontiers in immunology, 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
Gout is a chronic inflammatory arthritis driven by monosodium urate (MSU) crystal deposition. Its global prevalence is rising steadily. Only a minority of hyperuricemic individuals develop gout, and flares often recur despite controlled serum urate, pointing to mechanisms beyond simple crystal-induced inflammation. This review synthesizes evidence that trained immunity-the persistent epigenetic and metabolic reprogramming of innate immune cells-underpins these paradoxes. MSU crystals and soluble urate act as dual inducers: crystals trigger acute flares via NOD-, LRR- and pyrin domain-containing protein 3(NLRP3) and also establish long-lived myeloid memory through c-Jun N-terminal kinase (JNK)-c-Jun proto-oncogene (JUN) and mechanistic target of rapamycin (mTOR)-hypoxia-inducible factor 1-alpha (HIF-1α) axes, while soluble urate primes cells via DNA hypomethylation and histone modifications. We detail the molecular architecture of trained immunity in gout, including central [hematopoietic stem and progenitor cells (HSPC)] and peripheral training, metabolic rewiring (glycolysis, succinate), epigenetic marks (H3K4me3, H3K27ac, DNA methylation), and non-coding RNA regulation. We discuss how trained macrophages and Th17 cells form a self-amplifying loop, and how systemic trained immunity links gout to cardiovascular disease, chronic kidney disease, and metabolic syndrome, with clonal haematopoiesis of indeterminate potential (CHIP) as an age-related amplifier. Finally, we evaluate therapeutic strategies targeting epigenetic enzymes, metabolic nodes, and interleukin-1 beta (IL-1β), and highlight biomarkers and trial design needed to translate trained immunity modulation into clinical practice.
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