Liu Jing, Liu Ge, Chu Teng, Wu Yue, Yang Lele Zixin, Fang Weirong
State Key Laboratory of Natural Medicines, School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, P.R. China.
Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania, PA 19107, USA.
Curr Pharm Des. 2025;31(31):2465-2480. doi: 10.2174/0113816128369016250306050522.
Gout, based on hyperuricemia, is an immune disease characterized by redness and pain caused by monosodium urate (MSU) deposition in the joints. Inflammation is the fundamental cause of gout symptoms, and many immune cells, such as monocytes/macrophages, neutrophils, and T lymphocytes, have been shown to be involved in various processes of pathological progress. This study reviews the changes and functions of different immune cells during the occurrence and development of gout, focusing on the mechanisms and signaling pathways by which macrophages activate nod-like receptor pyrin-containing 3 (NLRP3) inflammasome to initiate gout inflammation in order to further elucidate the pathogenesis of gout and provide new targets for the research of anti-gout drugs.
痛风基于高尿酸血症,是一种免疫性疾病,其特征是尿酸钠(MSU)在关节中沉积导致红肿和疼痛。炎症是痛风症状的根本原因,许多免疫细胞,如单核细胞/巨噬细胞、中性粒细胞和T淋巴细胞,已被证明参与了病理进展的各种过程。本研究综述了痛风发生发展过程中不同免疫细胞的变化和功能,重点关注巨噬细胞激活含吡啉结构域的NOD样受体3(NLRP3)炎性小体引发痛风炎症的机制和信号通路,以进一步阐明痛风的发病机制,并为抗痛风药物的研究提供新靶点。