痛风
发病机制
医学
免疫学
关节炎
炎症
类风湿性关节炎
细胞因子
炎性关节炎
受体
疾病
病理
内科学
作者
Zeng Zhang,Peng Wang,Qin Xiong,Shanshan Xu,Dong Won Kang,Zhengguang He,Chengjiao Yao,Guilin Jian
出处
期刊:Cytokine
[Elsevier]
日期:2024-07-25
卷期号:182: 156705-156705
被引量:1
标识
DOI:10.1016/j.cyto.2024.156705
摘要
Gout is an autoinflammatory disease characterized by the deposition of monosodium urate crystals in or around the joints, primarily manifesting as inflammatory arthritis that recurs and resolves spontaneously. Interleukin-6 (IL-6) is a versatile cytokine with both anti-inflammatory and pro-inflammatory capabilities, linked to a variety of inflammatory diseases such as gouty arthritis, rheumatoid arthritis, inflammatory bowel disease, vasculitis, and several types of cancer. The rapid production of IL-6 during infections and tissue damage aids in host defense. However, excessive synthesis of IL-6 and dysregulation of its receptor signaling (IL-6R) might contribute to the pathology of diseases. Recent advancements in clinical and basic research, along with developments in animal models, have established the significant role of IL-6 and its receptors in the pathogenesis of gout, although the precise mechanisms remain to be fully elucidated. This review discusses the role of IL-6 and its receptors in gout progression and examines contemporary research on modulating IL-6 and its signaling pathways for treatment. It aims to provide insights into the pathogenesis of gout and to advance the development of targeted therapies for gout-related inflammation.
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