王影, 卜妍红, 庞静, 吴虹. 类风湿关节炎中糖脂代谢交互机制与干预策略的研究进展J. 药学学报, 2025, 60(12): 3655-3664. DOI: 10.16438/j.0513-4870.2025-0601
引用本文: 王影, 卜妍红, 庞静, 吴虹. 类风湿关节炎中糖脂代谢交互机制与干预策略的研究进展J. 药学学报, 2025, 60(12): 3655-3664. DOI: 10.16438/j.0513-4870.2025-0601
WANG Ying, BU Yan-hong, PANG Jing, WU Hong. Research progress on the interaction mechanism of glucose and lipid metabolism and intervention strategies in rheumatoid arthritisJ. Acta Pharmaceutica Sinica, 2025, 60(12): 3655-3664. DOI: 10.16438/j.0513-4870.2025-0601
Citation: WANG Ying, BU Yan-hong, PANG Jing, WU Hong. Research progress on the interaction mechanism of glucose and lipid metabolism and intervention strategies in rheumatoid arthritisJ. Acta Pharmaceutica Sinica, 2025, 60(12): 3655-3664. DOI: 10.16438/j.0513-4870.2025-0601

类风湿关节炎中糖脂代谢交互机制与干预策略的研究进展

Research progress on the interaction mechanism of glucose and lipid metabolism and intervention strategies in rheumatoid arthritis

  • 摘要: 类风湿关节炎(rheumatoid arthritis, RA) 作为一种慢性自身免疫性疾病, 其病理进程与糖脂代谢存在复杂的相互影响。糖代谢重编程通过破坏微环境代谢稳态, 激活有氧糖酵解驱动滑膜细胞增殖与炎症; 脂代谢紊乱通过脂源性介质重塑炎症调控网络。糖脂代谢交互影响共同驱动“代谢-炎症”恶性循环, 其中乙酰辅酶A的代谢枢纽作用、代谢物乳酸的双向调控、代谢信号的协同调控以及线粒体-脂滴的细胞器互作加重RA病理进程。本文聚焦RA糖代谢、脂代谢两大核心途径的异常特征及其交互机制, 并基于代谢靶点提出靶向代谢稳态的干预策略及研究方向, 为深入解析RA病理机制及开发靶向代谢干预疗法提供重要科学参考。

     

    Abstract: Rheumatoid arthritis (RA), a chronic autoimmune disease, has a complex interaction with glucose and lipid metabolism in pathological process. Glucose metabolism reprogramming disrupts the metabolic homeostasis of the microenvironment and activates aerobic glycolysis to drive synovial proliferation and inflammation; lipid metabolism dysfunction reshapes the inflammatory regulatory network through lipid-derived mediators. The interplay between glucose and lipid metabolism jointly drives the "metabolism-inflammation" vicious cycle, in which the metabolic hub role of acetyl coenzyme A, the bidirectional regulatory role of lactate, the synergistic regulation of metabolic signals, and the organelle interaction between mitochondria and lipid droplets collectively exacerbate the pathological progression of RA. This review systematically focuses on the abnormal characteristics and interaction mechanisms of the two core pathways of glucose and lipid metabolism in RA, proposes intervention strategies and research directions targeting metabolic homeostasis based on metabolic targets, and provides important scientific references for the in-depth analysis of the pathological mechanism of RA and the development of targeted metabolic intervention therapies.

     

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