vtRNA1-1/p62 regulates macrophages autophagy in ankylosing spondylitis

IF 3 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular immunology Pub Date : 2026-05-01 Epub Date: 2026-03-06 DOI:10.1016/j.molimm.2026.02.014

Minxin Jiang , Jianping Ni , Xueying Yu , Hui Zhao , Xiaofeng Lu , Lerong Cheng , Ziqi Li , Hanqing Wu , Zelong Pan , Lianchi Qu , Mengyao Gao , Guoqi Cai , Mengmeng Wang , Faming Pan

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引用次数: 0

Abstract

This research aims to investigate the role and mechanisms of the vtRNA1–1/p62 molecular axis in the regulation of autophagy in AS, with the goal of identifying novel diagnostic and therapeutic targets for AS. Clinical sample analysis revealed that the transcription levels of vtRNA1–1 and p62 decreased in the peripheral blood mononuclear cells (PBMCs) of the AS group; conversely, the levels of canonical autophagy-related genes (ATG3, ATG5) and inflammatory factors (TNF-α) significantly increased. Correlation analysis revealed that vtRNA1–1 levels were positively associated with p62 but were inversely associated with ATG3, ATG5, and TNF-α. In vitro cell experiments demonstrated that vtRNA1–1 depletion reduced p62 expression while increasing ATG3, ATG5, and LC3B levels. Computational modeling further confirmed significant interactions between vtRNA1–1 and p62. Notably, vtRNA1–1 and p62 demonstrated unique diagnostic value for AS, with their combination showing even greater diagnostic significance. This study innovatively links noncoding RNA regulatory networks with autophagy homeostasis imbalance, revealing that vtRNA1–1 may regulate macrophage autophagy through p62, thereby participating in the molecular pathogenesis of AS.

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vtrna -1/p62调控强直性脊柱炎巨噬细胞自噬。

本研究旨在探讨vtRNA1-1/p62分子轴在AS自噬调控中的作用及机制，以期发现新的AS诊断和治疗靶点。临床样本分析显示，AS组外周血单个核细胞（PBMCs）中vtrna -1和p62的转录水平下降；相反，典型自噬相关基因（ATG3、ATG5）和炎症因子（TNF-α）水平显著升高。相关分析显示，vtrna -1水平与p62呈正相关，与ATG3、ATG5、TNF-α呈负相关。体外细胞实验表明，vtrna -1缺失降低了p62的表达，同时增加了ATG3、ATG5和LC3B的水平。计算模型进一步证实了vtrna -1与p62之间的显著相互作用。值得注意的是，vtRNA1-1和p62对AS的诊断具有独特的价值，它们的联合诊断意义更大。本研究创新性地将非编码RNA调控网络与自噬稳态失衡联系起来，揭示了vtrna -1可能通过p62调控巨噬细胞自噬，从而参与AS的分子发病机制。

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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来源期刊

Molecular immunology 医学-免疫学

CiteScore

6.90

自引率

2.80%

发文量

324

审稿时长

50 days

期刊介绍： Molecular Immunology publishes original articles, reviews and commentaries on all areas of immunology, with a particular focus on description of cellular, biochemical or genetic mechanisms underlying immunological phenomena. Studies on all model organisms, from invertebrates to humans, are suitable. Examples include, but are not restricted to: Infection, autoimmunity, transplantation, immunodeficiencies, inflammation and tumor immunology Mechanisms of induction, regulation and termination of innate and adaptive immunity Intercellular communication, cooperation and regulation Intracellular mechanisms of immunity (endocytosis, protein trafficking, pathogen recognition, antigen presentation, etc) Mechanisms of action of the cells and molecules of the immune system Structural analysis Development of the immune system Comparative immunology and evolution of the immune system "Omics" studies and bioinformatics Vaccines, biotechnology and therapeutic manipulation of the immune system (therapeutic antibodies, cytokines, cellular therapies, etc) Technical developments.