自噬在类风湿关节炎发病机制中的研究进展

doi:10.12114/j.issn.1007-9572.2023.0149

摘要/Abstract

摘要： 类风湿关节炎（RA）是一种难治的自身免疫性疾病，具有慢性、系统性的特点，但是该病的发病机制至今尚未完全明确。自噬是一种存在于真核生物细胞，维持细胞正常生理活动及细胞稳态的代谢过程，自噬失调与RA等多种疾病的发生、发展有关。本文检索中国知网、万方数据知识服务平台、维普网、PubMed、Web of Science、Elsevier等数据库，查阅RA发病与自噬相关的文献，从维持滑膜炎症（提高滑膜细胞的抗凋亡率、调控滑膜细胞表型转化）、促进骨破坏（参与破骨细胞生成、调控软骨细胞凋亡）、破坏免疫系统稳态（调节免疫细胞活化及成熟、参与瓜氨酸化蛋白呈递、诱导蛋白质氨基甲酰化）三方面归纳、总结自噬在RA发病机制中的作用，为RA的发病机制研究和治疗提供参考。

关键词: 关节炎，类风湿, 自噬, 发病机制, 滑膜, 骨破坏, 免疫稳态, 综述

Abstract:

Rheumatoid arthritis (RA) is a refractory autoimmune disease with chronic and systemic characteristics, however, the pathogenesis of this disease has not been fully defined. Autophagy is a metabolic process that exists in eukaryotic cells and maintains normal physiological activities and cell homeostasis. Dysregulation of autophagy is related to the occurrence and development of various diseases such as RA. The databases of CNKI, Wanfang Data, VIP, PubMed, Web of Science, Elsevier, etc. were searched for the literature related to autophagy in RA pathogenesis. The role of autophagy in the pathogenesis of RA was summarized in terms of maintaining synovial inflammation (improving anti-apoptosis rate of synovial cells and regulating the phenotype transformation of synovial cells), promoting bone destruction (participating in osteoclastogenesis and regulating chondrocyte apoptosis) and disrupting immune system homeostasis (regulating the activation and maturation of immune cells, participating in the presentation of citrullinated proteins, and inducing carbamoylation of proteins), in order to provide basis and reference for the pathogenesis research and treatment of RA.

Key words: Arthritis, rheumatoid, Autophagy, Pathogenesis, Synovial membrane, Bone destruction, Immune homeostasis, Review

刘煜,岳婷,杨东宇,等. 自噬在类风湿关节炎发病机制中的研究进展[J]. 中国全科医学, 2023, 26(29): 3710-3714. DOI: 10.12114/j.issn.1007-9572.2023.0149.
LIU Yu,YUE Ting,YANG Dongyu, et al. Research Progress on Mechanism of Autophagy in the Pathogenesis of Rheumatoid Arthritis[J]. Chinese General Practice, 2023, 26(29): 3710-3714. DOI: 10.12114/j.issn.1007-9572.2023.0149.

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