类风湿关节炎的生物钟视角

IF 4.5 2区 医学 Q2 CELL BIOLOGY Inflammation Pub Date : 2024-08-10 DOI:10.1007/s10753-024-02120-4
Qingxue Liu, Yihao Zhang
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引用次数: 0

摘要

类风湿性关节炎(RA)是一种以全身多关节疼痛为特征的慢性自身免疫性疾病,其主要病理特征包括炎性细胞浸润、滑膜成纤维细胞增生和软骨侵蚀。免疫细胞、滑膜细胞和神经内分泌因子在类风湿关节炎的病理生理机制中起着关键作用。生物钟基因调控免疫细胞功能,这与关节炎病理的节律性变化有关。此外,生物钟基因与神经内分泌因子之间的相互作用也参与了类风湿关节炎的节律性变化。本综述概述了昼夜节律基因对类风湿性关节炎病理的贡献,包括它们与免疫系统的相互作用以及参与调节神经内分泌因子的分泌和功能。从分子角度了解昼夜节律在 RA 中的作用可为有效的疾病管理提供启示。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Biological Clock Perspective in Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by systemic polyarticular pain, and its main pathological features include inflammatory cell infiltration, synovial fibroblast proliferation, and cartilage erosion. Immune cells, synovial cells and neuroendocrine factors play pivotal roles in the pathophysiological mechanism underlying rheumatoid arthritis. Biological clock genes regulate immune cell functions, which is linked to rhythmic changes in arthritis pathology. Additionally, the interaction between biological clock genes and neuroendocrine factors is also involved in rhythmic changes in rheumatoid arthritis. This review provides an overview of the contributions of circadian rhythm genes to RA pathology, including their interaction with the immune system and their involvement in regulating the secretion and function of neuroendocrine factors. A molecular understanding of the role of the circadian rhythm in RA may offer insights for effective disease management.

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来源期刊
Inflammation
Inflammation 医学-免疫学
CiteScore
9.70
自引率
0.00%
发文量
168
审稿时长
3.0 months
期刊介绍: Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.
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