蛋白翻译后修饰在类风湿关节炎中的作用及机制

IF 4.2 2区 医学 Q2 IMMUNOLOGY
Journal of Inflammation Research Pub Date : 2025-07-11 eCollection Date: 2025-01-01 DOI:10.2147/JIR.S528487
Jianting Wen, Jian Liu, Lei Wan, Fanfan Wang
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引用次数: 0

摘要

类风湿性关节炎(RA)是一种慢性自身免疫性疾病,由于其高患病率和致残风险,严重影响患者的生活质量。虽然其病因尚不完全清楚,但越来越多的证据强调了表观遗传机制,特别是翻译后修饰(PTMs)在RA发病机制中的关键作用。蛋白质组学的进展已经确定了各种ptms -包括磷酸化、甲基化、乙酰化、泛素化、糖基化、乳酸化、瓜氨酸化和氨甲酰化-作为RA炎症、免疫反应和组织重塑的关键调节因子。重要的是,失调的ptm可能改变蛋白质结构和功能,从而促进疾病进展。本文系统总结了目前对主要PTMs在RA中的作用和机制的研究,重点介绍了PTMs之间的串扰、它们与非编码rna的相互作用,以及中药靶向PTMs的新兴治疗潜力。这些见解可能为类风湿关节炎的诊断和治疗提供新的视角。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Role and Mechanism of Protein Post‑Translational Modification in Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is a chronic autoimmune disease that significantly compromises patient quality of life due to its high prevalence and risk of disability. While its etiology remains incompletely understood, increasing evidence highlights the critical involvement of epigenetic mechanisms, particularly post-translational modifications (PTMs), in RA pathogenesis. Advances in proteomics have identified various PTMs-including phosphorylation, methylation, acetylation, ubiquitination, glycosylation, lactylation, as well as citrullination and carbamylation-as key regulators of inflammation, immune response, and tissue remodeling in RA. Importantly, dysregulated PTMs may alter protein structure and function, thereby contributing to disease progression. This review systematically summarizes current knowledge on the roles and mechanisms of major PTMs in RA, with a special focus on the cross-talk between PTMs, their interaction with non-coding RNAs, and the emerging therapeutic potential of traditional Chinese medicine (TCM) targeting PTMs. These insights may provide novel perspectives for the diagnosis and treatment of RA.

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来源期刊
Journal of Inflammation Research
Journal of Inflammation Research Immunology and Microbiology-Immunology
CiteScore
6.10
自引率
2.20%
发文量
658
审稿时长
16 weeks
期刊介绍: An international, peer-reviewed, open access, online journal that welcomes laboratory and clinical findings on the molecular basis, cell biology and pharmacology of inflammation.
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