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REVIEW article

Front. Immunol.

Sec. Inflammation

Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1671548

Fatty Acid Metabolism in Gouty Arthritis: Mechanisms to Therapeutic Targeting

Provisionally accepted
Xueping ZhaoXueping Zhao1,2,3,4Ye SunYe Sun1,2Le YangLe Yang1,2Hui SunHui Sun3,4,5Xinya ZhangXinya Zhang1,2,3,4Hui SunHui Sun1,2Guangli YanGuangli Yan3,4Xijun WangXijun Wang1,2,3,4*
  • 1State Key Laboratory of Dampness Syndrome of Chinese Medicine, Guangzhou, China
  • 2The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China
  • 3State Key laboratory of Integration and Innovation for Classic formula and Modern Chinese Medicine, Harbin, China
  • 4Heilongjiang University of Chinese Medicine, Harbin, China
  • 5National Chinmedomics Research Center, Harbin, China

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Gouty arthritis (GA), a condition characterized by monosodium urate (MSU) crystal deposition and NLRP3 inflammasome-driven inflammation, is a result of a complex interplay between hyperuricemia and immune dysregulation, which leads to systemic complications and joint damage. Current therapies for GA exhibit certain limitations, including cardiovascular risks, hepatotoxicity, low efficacy in special populations, and difficulty in dissolving tophi. Emerging evidence implicates fatty acid metabolism disorders as key pathogenic factors in GA. Elevated fatty acids (FAs) activate Toll-like receptors (TLRs) in macrophages, which act in synergy with MSU crystals to trigger NLRP3 inflammasome activation and pro-inflammatory cytokine release (e.g., IL-1β), thereby initiating the inflammatory cascade. Dysregulated FA metabolism promotes neutrophil recruitment through aberrant arachidonic acid (AA) metabolism and exacerbates hyperuricemia by increasing purine synthesis while inhibiting uric acid excretion. Consequently, future clinical practice may leverage the detection of FA signatures in GA patients to enable tailored therapeutic and dietary management, thereby maximizing treatment efficacy while minimizing adverse effects. The combined application of FA-modulating agents and anti-GA therapeutics synergistically enhances therapeutic efficacy, enabling comprehensive disease-modifyi ng control over GA progression. This review systematically elucidates the mechanisms through which FA metabolism disorders drive the progression of GA, providing a scientific basis for the subsequent research on GA.

Keywords: Macrophages, Neutrophil, fatty acid, Gouty arthritis, Monosodium urate, fatty acid metabolis

Received: 23 Jul 2025; Accepted: 29 Sep 2025.

Copyright: © 2025 Zhao, Sun, Yang, Sun, Zhang, Sun, Yan and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Xijun Wang, xijunw@sina.com

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

Supplementary Material