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Journal of Central South University Medical Sciences logoLink to Journal of Central South University Medical Sciences
. 2023 May 28;48(5):750–759. [Article in Chinese] doi: 10.11817/j.issn.1672-7347.2023.220621

CeRNA网络在类风湿关节炎的炎症细胞中的作用

Role of ceRNA network in inflammatory cells of rheumatoid arthritis

HE Xiaoyu 1,1, HE Haohua 1, ZHANG Yan 2, WU Tianyu 3, CHEN Yongjie 3, TANG Chengzhi 3, XIA Tian 2, ZHANG Xiaonan 4,✉, XIE Changhao 1,5,✉
Editor: 田 朴
PMCID: PMC10930406  PMID: 37539578

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease caused by inflammatory cells. Various inflammatory cells involved in RA include fibroblast-like synoviocytes, macrophages, CD4+T-lymphocytes, B lymphocytes, osteoclasts and chondrocytes. The close interaction between various inflammatory cells leads to imbalance of immune response and disorder of the expression of mRNA in inflammatory cells. It helps to drive production of pro-inflammatory cytokines and stimulate specific antigen-specific T- and B-lymphocytes to produce autoantibodies which is an important pathogenic factor for RA. Competing endogenous RNA (ceRNA) can regulate the expression of mRNA by competitively binding to miRNA. The related ceRNA network is a new regulatory mechanism for RNA interaction. It has been found to be involved in the regulation of abnormal biological processes such as proliferation, apoptosis, invasion and release of inflammatory factors of RA inflammatory cells. Understanding the ceRNA network in 6 kinds of RA common inflammatory cells provides a new idea for further elucidating the pathogenesis of RA, and provides a theoretical basis for the discovery of new biomarkers and effective therapeutic targets.

Keywords: competing endogenous RNA network, long non-coding RNA, circular RNA, microRNA, rheumatoid arthritis, inflammatory cells

类风湿关节炎(rheumatoid arthritis，RA)是一种发病机制复杂、病程迁延的慢性全身性炎症疾病，以滑膜组织持续增生、关节软骨和骨的进行性破坏为主要特征，患病率和病死率较高[1-3]。临床上将RA的发病过程主要分为3个阶段：首先是机体自身抗原的自我耐受性丧失，其标志是抗瓜氨酸化和氨基甲酰化抗原的自身抗体出现异常增高，并逐渐出现由自身抗体介导的自体反应和多反应B细胞的异常积累[4-5]；然后进入无症状自身免疫阶段，以先天性和获得性免疫细胞进入滑膜腔内导致早期滑膜炎的产生为主要病理特点，其中由产生抗瓜氨酸化蛋白抗体(anti-citrullinated protein antibody，ACPA)的自我耐受阶段进展到滑膜炎阶段，初始CD4+T细胞频率的降低是有效预测因子[5]；最后，随着炎症因子的蓄积和滑膜细胞的异常增殖分化，疾病过渡至慢性滑膜炎阶段，导致血管翳形成，造成肌腱、软骨和骨的不可逆转的组织损伤[4]。传统药物在预防和缓解RA患者临床症状中仍有较大的局限性，这将有待于发现新的靶向药物和创新的治疗方法。而RA中竞争性内源RNA(competing endogenous RNA，ceRNA)在炎症和免疫疾病中的作用越来越受到重视，在ceRNA网络的基础上寻找有效靶点有助于RA的诊断和治疗[6]。

1. CeRNA网络概述

不同物种之间存在着RNA复杂的相互作用，非编码RNA(non-coding RNA，ncRNA)参与的表观遗传调控在RA发病机制中发挥重要作用[7]。MiRNA可以通过与mRNA结合而导致基因沉默，ceRNA包含miRNA的互补结合位点，可以隔离目标miRNAs，从而抑制它们的功能[7]。与ncRNA等概念不同，ceRNA并不代表某种特定类型的RNA，而是为竞争miRNA提供了一个框架。包含miRNA结合位点的RNA都可以相互通信和调节，从而起到ceRNA的作用[8]，如长链非编码RNA(long non-coding RNA，lncRNA)、环状RNAs(circular RNA，circRNA)和伪基因等[8-9]。本文总结由miRNA介导的2种常见的ceRNA网络，并围绕其在RA炎症细胞中的调节机制进行详细的阐述。

1.1. MiRNA

MiRNA是一种21∼22 nt RNA，通过转录后调控基因表达参与发育和应激反应的各个方面，作为一种小的非编码单链RNA，具有良好的非侵袭性生物标志物的潜力[10-11]。MiRNA被负载到蛋白上，形成转录后基因沉默效应复合体(miRNA-induced silencing complexes，miRISCs)，miRISC由miRNA引导，通过序列互补与靶RNAs结合，从而促进靶向mRNA的翻译抑制和降解[12-13]，是ceRNA网络的中心角色(图1)。Wu等[14]发现miRNA可参与肿瘤免疫逃逸机制，进一步说明miRNA与机体免疫系统存在某种密切联系。

图 1.

图 1

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CeRNA调控网络的机制

Figure 1 Mechanisms of ceRNA regulatory

MiRNA gene is transcribed as pri-miRNA, which are then processed by Drosha-DGCR8 into pre-miRNA. Following export through exportin-5, the pre-miRNAs are cleaved by Dicer and TRBP form a miRNA/miRNA duplex. Then the miRNA duplex associates with AGO family proteins to form the RISC and finally a single stranded mature miRNA is formed. A mature miRNA binds to mRNAs with complementary sites results in degradation of target mRNAs. Different ceRNAs (including lncRNAs, circRNAs and pseudogenes) have the same miRNA recognition elements could compete for the same miRNAs and further impact gene expression. miRNA: MicroRNA; pri-miRNAs: Primary miRNAs; DGCR8: DiGeorge syndrome critical region 8; pre-miRNAs: Precursor miRNAs; TRBP: TAR RNA-binding protein; AGO: Argonaute; RISC: RNA-induced silencing complex; mRNA：Messenger RNA；lncRNA: Long non-coding RNA; circRNA: Circular RNA.

1.2. LncRNA

LncRNA是一种长度超过200个核苷酸、缺乏完整的开放阅读框架，是几乎没有蛋白质编码能力的RNA，但可以被剪接、封端和/或多腺苷化[15-16]。它们可以折叠成复杂的二级和三级结构，与蛋白质、DNA和其他RNA相互作用，从而调节多蛋白质复合体的活性、定位或相互作用[17]。但对于lncRNA来说，决定功能及其相互作用的结构域尚不清楚[17]。并且，在不同物种发育和分化的基因表达调控中lncRNA都起着至关重要的作用[17]。有意思的是，lncRNA被发现通过调节Triadin基因的选择性剪接来维持心脏功能，揭示选择性剪接的调节是lncRNA控制心脏功能的一种新机制[18]。

1.3. CircRNA

CircRNA是哺乳动物细胞中的一大类RNA，在各种生物学过程中发挥重要作用[19]。在真核生物中发现了大量内含子、外显子或基因间隔区被反向剪接产生的circRNA，并受内含子互补序列(intronic complementary sequences，ICSS)和RNA结合蛋白(RNA binding proteins，RBPs)调控[20-21]。CircRNA还被证明与植物寄主基因的基因组DNA能发生直接的相互作用，从而导致亲本基因表达的改变，即circRNA通过与宿主基因相互作用抑制DNA损伤修复[20]，并且可以编码蛋白质[22]，在新型冠状病毒疫情肆虐的情况下，circRNA编码蛋白的功能被运用于新型冠状病毒疫苗的研制，并被证实circRNARBD-Delta疫苗对病毒Delta和Omicron的感染者都有保护作用[23]。

1.4. CeRNA网络在疾病中的相互作用

所有类别的RNA转录本之间都有通信网络，通过竞争miRNA中的共享序列来调节彼此的表达，即编码RNA和ncRNA之间真正通信的ceRNA[24]。

在RA中，lncRNA能够竞争性地与miRNA结合，降低miRNA的表达，从而参与炎症的发生，炎症细胞的增殖、凋亡和自噬等生物学过程[25]。circRNA以不同的方式发挥其功能，通过形成circRNA-miRNA-mRNA网络调节基因转录，与蛋白质相互作用，从而参与基因调控[20, 22]。CeRNA网络参与调节RA内炎症细胞活性、增殖、迁移和凋亡等生物学特性以介导炎症反应。通过调节如mTOR通路、多巴胺能系统和Wnt等信号通路，参与RA的发生、发展[26]。而信号通路上游调控因子如miRNA、lncRNA、cicrRNA可能被用作治疗RA的新靶点(图1)。

2. CeRNA网络在RA各种炎症细胞中的调控作用

参与RA炎症的细胞包括成纤维样滑膜细胞(fibroblast-like synoviocyte，FLS)、巨噬细胞、CD4+T淋巴细胞、破骨细胞、B淋巴细胞、软骨细胞等，这些细胞相互作用最终导致RA的慢性炎症，促使RA的进展[27-29]。

2.1. CeRNA网络在成纤维样滑膜细胞中的调控

RA的发病过程涉及FLS的激活[30]。FLS通过侵袭细胞外基质、分泌炎症介质，以及通过抗原提呈激活淋巴细胞、巨噬细胞等滑膜浸润性免疫细胞来相互发挥作用，还可产生软骨降解基质金属蛋白(matrix metalloproteases，MMPs)，是RA的滑膜侵袭和关节破坏的主要原因[31-32]。上调miR-3150a-3p的表达来抑制FLS的TNF-α和IL-1β的产生，可改善RA[33]。抑制miR-30-5p可以通过抑制PI3K/AKT信号通路来促进FLS的凋亡[34]。

LncRNA MIR31HG、lncRNA OIP5-AS1、lncRNA CASC2、lncRNA OSER1-AS1、lncRNA NEAT1_1通过调节miR-214/PTEN/AKT、miR-410-3p/Wnt7b、miR-18a-5p/BTG3、miR-1298-5p/E2F1、miR-221-3p/uPAR信号通路抑制FLS的肿瘤样生物学行为，缓解RA[35-39]；而lncRNA NR-133666通过调节miR-133c/MAPK1轴促进FLS的增殖和迁移[40](图2)。

图2.

图2

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RA-FLS中ceRNA网络的复杂串扰

Figure 2 Complex crosstalk of ceRNA network in RA-FLS

RA-FLS: Rheumatoid arthritis fibroblast-like synoviocytes; PTEN: Phosphatase and tensin homolog deleted on chromosome ten; AKT: Protein kinase B; Wnt7b: Wnt family member 7B; BTG3: B-cell translocation gene 3; E2F1: E2F transcription factor 1; uPAR: Urokinase-type plasminogen activator receptor; TLR4: Toll-like receptor 4; MDM4: Murine double minute 4; HDAC4: Histone deacetylase 4; SIRT 1: Silent information regulator 1; STAT3: Signal transducer and activator of transcription 3; HIPK2: Homeodomain-interacting protein kinase 2; PPM1A: Phosphatase magnesium-dependent 1A; CNP: 2',3'-cyclic nucleotide 3'- phosphodiesterase; TAB2: TAK1-binding 2; MMP2: Matrix metalloproteinase 2; MAPK1: Mitogen-activated protein kinase 1.

有报道[41-48]发现circ0088036、circ_0001947、ciRS-7、circASH2L、circMAPK9、circ_0088194、circ-AFF2通过调节miR-140-3p/SIRT 1、miR-671-5p/STAT3、miR-7、miR-129-5p/HIPK2、miR-140-3p/PPM1A、miR-766-3p/MMP2、miR-650/CNP、miR-375/TAB2促进FLS的细胞增殖、侵袭、迁移和炎症，并抑制细胞凋亡和维持肿瘤样生物学特性。而circ-FAM120A、circ-PTTG1IP、circFBXW7、circ-Sirt1通过靶向miR-671-5p/MDM4、miR-671-5p/TLR4、miR-216a-3p/HDAC4和miR-132/Sirt1抑制FLS的增殖、迁移，改善炎症[49-52](图2)。Circ-AFF2可调节2种miRNA，而miR-671-5p受到3种circRNA调节[42, 47-50]，说明单个circRNA可能调控多个miRNA，而单个miRNA可能受到多个circRNA的调控，ceRNA之间的串扰非常复杂，仍需进一步探索。

2.2. CeRNA网络在巨噬细胞中的调控

RA患者的滑膜组织被巨噬细胞渗透后，在病理生理反应中起着关键作用[53]。巨噬细胞通常分成M1和M2这2个亚群[54]。其中，被激活的巨噬细胞，称为M1型巨噬细胞，产生一系列炎症细胞因子(如TNF-α等)加重关节炎症[53, 55]。因此，促进M1型巨噬细胞到M2型巨噬细胞的复极化被认为是缓解RA症状的有效策略[53]。研究[27]发现ACPA是RA自身免疫的特异性标志，而ACPA复合体激活释放TNF-α，说明RA患者体内的ACPA复合物通过激活M1型巨噬细胞释放TNF-α，从而促进RA的疾病进展。

MiRNA是巨噬细胞基因表达的修饰物[55]，可诱导M1型巨噬细胞到M2型巨噬细胞的极化而高效地减轻炎症[56]。在RA患者中，M1巨噬细胞中上调最多的是miR-155，这与包括TNF-α在内的促炎介质的产生有关[55]，说明miRNA可促使RA患者的M1巨噬细胞产生TNF-α而加重RA的炎症反应。Wan等[57]发现lncRNA H19通过与miR-21和PDCD4 mRNA形成ceRNA网络来调节NLRP3/6炎症小体平衡、凋亡和无菌炎症，故lncRNA通过调控miRNA抑制ACPA复合物来抑制M1巨噬细胞产生TNF-α，从而减弱RA的炎症反应。

LncRNA HIX003209、lncRNA SNHG14、lncRNA CDKN2B-AS1通过调节miR-6089/TLR4/NF-κB和miR-17-5p/MINK1-JNK、miR-497/TXNIP通路调节巨噬细胞介导的炎症来促进RA的进展[6, 58-59]。CircRNA_09505在巨噬细胞中可作为miR-6089的分子海绵，通过ceRNA机制促进TNF-α、IL-6和IL-12的产生，并通过miR-6089/AKT1/NF-κB轴加重炎症[60]。

2.3. CeRNA网络在CD4+ T淋巴细胞中的调控

遗传相关性和体内外的功能研究确定CD4+ T淋巴细胞是RA病理的关键促进者[61]。CD4+ T淋巴细胞包括Th1、Th2、调节性T细胞(regulatory T cell，Treg)、Th17等亚群[62]；其中，Treg可预防自身免疫和控制炎症[63]。

研究[64-66]发现：miR-155、miR-27作为关键的炎症调节因子，在激活的免疫细胞中过度表达，对许多炎症刺激作出反应，如控制Th1、Th2和Th17的分化及上调Treg。LINC01140、lncRNA XIST直接抑制miR-377-3p的表达，从而抑制Th17细胞分化[67-68]。说明lncRNA通过调控miRNA来调节CD4+ T细胞(如Treg、Th1、Th2和Th17等)的分化表达，从而促进RA的疾病进展。LncRNA可抑制miRNA的表达、下调Th17的分化表达和上调Treg的数量，故可用来治疗RA。在RA患者中，circNUP214可作为miR-125a-3p的ceRNA，且circNUP214水平的升高有助于RA患者的Th17细胞反应[69]。

2.4. CeRNA网络在破骨细胞中的调控

RA作为炎症性骨病，其特征是滑膜炎症失控，导致随后的骨和软骨破坏[70]。其中，破骨细胞的形成，参与RA的发生和发展[71]。而且RA患者破骨细胞的形成和功能增强，导致更多的骨糜烂[70]。

在RA中，药物靶向关节中的破骨细胞，可以有效地诱导这些细胞的凋亡，从而减轻滑膜炎症，逆转晚期RA的骨侵蚀[72]。MiR-92a-1-5p可促进破骨细胞分化[73]。而在骨重建过程中，破骨细胞的骨吸收之后是成骨细胞的骨形成，这个过程是通过耦合来平衡的[74]。LncRNA MIAT通过海绵结合miR-150-5p来调节其与靶基因的结合，抑制成骨分化[75]。MiRNA可直接调节或被lncRNA间接调节和控制破骨细胞的分化以减轻滑膜炎症，逆转晚期RA的骨侵蚀。CircRNA_28313通过发挥ceRNA的作用而调节破骨细胞的分化[76]。

2.5. CeRNA网络在B淋巴细胞中的调控

在RA患者滑膜组织中发现的浆母细胞和能产生自身抗体的长寿命浆细胞，是ACPA的主要来源[77]。RA患者滑膜中双阴性(CD27-IgD-)和类别转换的记忆性(CD27+IgD-)B细胞群在RA的发病机制中可能起关键作用[78]。通过高通量测序来评估外周血CD19+B细胞的miRNA谱系，发现氨甲蝶呤治疗的RA患者中，miR-223-3p在CD19+B细胞中表达显著增加，let-7 miRNA家族的部分RNA的表达水平显著降低，促进激活的B细胞中抗体的产生[79]。

B细胞激活因子受体siRNA及与多肽结合，达到抑制促炎细胞因子的产生和耗竭产生ACPA的特异性B细胞的百分比和数量的作用[80-82]。一项高通量测序技术研究[83]发现：在早期B细胞中具有已知作用的转录因子的反义转录产物的lncRNA。其中，lncRNA淋巴增强子结合因子1反义RNA1(lymphoenhancer binding factor 1 antisense RNA1，LEF1-AS1)有多个外显子，并编码转录本变体[83]，推测LEF1-AS1在RA患者B细胞中发挥重要作用。LEF1-AS1通过miR-5100/DEK/AMPK-mTOR轴、miR-4893p/HIGD1A轴、miR-30-5p/SOX9轴调控胃癌细胞的凋亡和自噬，胶质瘤细胞的增殖，结肠癌细胞的迁移、侵袭和转移[84-86]，说明lncRNA LEF1-AS1可以通过靶向miRNA调控的信号通路调节细胞的增殖、迁移等能力。推测血清ACPA阳性的RA患者可通过lncRNA海绵miRNA抑制与ACPA复合物相关的B淋巴细胞(如浆细胞、浆母细胞)的形成，从而减少自身抗体的产生来治疗RA。

CircRNA在从祖B细胞到前B细胞的发育过程中发挥着持续而稳定的调节作用[87]。通过对B细胞发育中的全转录组谱分析构建了circRNA-miRNA-mRNA调控网络。并且，在B细胞分化和发育过程中，circRNA可作为潜在的ceRNA来调节miRNA靶向mRNA的表达。

2.6. CeRNA网络在软骨细胞中的调控

在疾病潜伏期，软骨细胞能够通过细胞增殖等行为修复被侵蚀的软骨基质和关节软骨。但随着疾病的进展，在炎症因子和滑膜内其他炎症细胞的持续刺激下，软骨细胞的自我修复能力逐渐降低，最终导致关节软骨的不可逆性损伤。在RA患者中，对软骨造成破坏的因素有很多，而软骨细胞在RA的发病机制中可能起着重要作用[88]。

相关研究[89-90]报道：在RA中，miR-26a、miR-27b-3p刺激软骨细胞增殖，抑制软骨细胞的凋亡。而miR-106b通过下调丙酮酸脱氢酶激酶4(pyruvate dehydrogenase kinase 4，PDK4)抑制软骨细胞的增殖和迁移刺激RA的启动[91]。Zhuo等[92]发现lncRNA 的过表达通过海绵状miR-523-3p抑制内毒素刺激的软骨细胞中的信号通路，在RA的发展中起到保护作用。circFADS2调节miR-498/mTOR信号通路，对脂多糖诱导的软骨细胞有保护作用[93]。

3. 结 语

通过分析ceRNA网络与RA炎症细胞的相关性，发现lncRNA和circRNA可以作为ceRNA海绵调控miRNA，从而调控RA相关的炎症细胞。MiRNA不仅特异性地沉默疾病基因的表达，还具有复杂的调控网络，其作为ceRNA网络的核心，在不同表型条件下存在多种模式的调控机制。同种miRNA受到不同ceRNA网络的调控，并且在不同细胞中特异性靶向多个基因，能更好地了解在RA中各种RNA的病理特征及作用机制。现今，快速发展的高通量转录组分析技术已证实许多 miRNA和ceRNA作为生物标志物稳定存在于诸多体液中，包括血浆、血清、外泌体和尿液等。而生物标志物作为新的、有效的RA诊断指标，与不同免疫细胞浸润物之间存在相关性[94]。分析ceRNA网络在RA炎症细胞中的相互作用，可为RA的精准治疗提供潜在意义。

基金资助

安徽省自然科学基金(2108085MH258)；国家级大学生创新训练项目(202210367059)；安徽省大学生创新训练项目(S202110367076)；蚌埠医学院研究生创新计划(Byycx22024，Byycx22028)。

This work was supported by the Natural Science Foundation of Anhui Province (2108085MH258), the National College Student Innovation Training Program (202210367059), the Innovative Training Program for College Students of Anhui Province (S202110367076), and the Graduate Research and Innovation Project in Bengbu Medical College (Byycx22024, Byycx22028), China.

利益冲突声明

作者声称无任何利益冲突

作者贡献

何晓宇 论文构思和撰写；何豪华、吴天宇 论文审阅和修改；张妍 图片制作；陈永杰、唐承志、夏天 文献查阅和整理；张小楠、谢长好 写作指导和校正。所有作者阅读并同意最终的文本。

原文网址

http://xbyxb.csu.edu.cn/xbwk/fileup/PDF/202305750.pdf

参考文献

  • 1. Bi X, Guo XH, Mo BY, et al. LncRNA PICSAR promotes cell proliferation, migration and invasion of fibroblast-like synoviocytes by sponging miRNA-4701-5p in rheumatoid arthritis[J]. EBio Medicine, 2019, 50: 408-420. 10.1016/j.ebiom.2019.11.024. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2. Hao F, Lee RJ, Zhong LH, et al. Hybrid micelles containing methotrexate-conjugated polymer and co-loaded with microRNA-124 for rheumatoid arthritis therapy[J]. Theranostics, 2019, 9(18): 5282-5297. 10.7150/thno.32268. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3. Humby F, Durez P, Buch MH, et al. Rituximab versus tocilizumab in anti-TNF inadequate responder patients with rheumatoid arthritis (R4RA): 16-week outcomes of a stratified, biopsy-driven, multicentre, open-label, phase 4 randomised controlled trial[J]. Lancet, 2021, 397(10271): 305-317. 10.1016/S0140-6736(20)32341-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4. Weyand CM, Goronzy JJ. The immunology of rheumatoid arthritis[J]. Nat Immunol, 2021, 22(1): 10-18. 10.1038/s41590-020-00816-x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5. Ponchel F, Burska AN, Hunt L, et al. T-cell subset abnormalities predict progression along the Inflammatory Arthritis disease continuum: implications for management[J]. Sci Rep, 2020, 10(1): 3669. 10.1038/s41598-020-60314-w. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6. Yan SS, Wang PP, Wang JH, et al. Long non-coding RNA HIX003209 promotes inflammation by sponging miR-6089 via TLR4/NF-κB signaling pathway in rheumatoid arthritis[J]. Front Immunol, 2019, 10: 2218. 10.3389/fimmu.2019.02218. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7. Karreth FA, Pandolfi PP. ceRNA cross-talk in cancer: when ce-bling rivalries go awry[J]. Cancer Discov, 2013, 3(10): 1113-1121. 10.1158/2159-8290.CD-13-0202. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8. Tay Y, Rinn J, Pandolfi PP. The multilayered complexity of ceRNA crosstalk and competition[J]. Nature, 2014, 505(7483): 344-352. 10.1038/nature12986. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9. Salmena L, Poliseno L, Tay Y, et al. A ceRNA hypothesis: the Rosetta stone of a hidden RNA language?[J]. Cell, 2011, 146(3): 353-358. 10.1016/j.cell.2011.07.014. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10. Wang AL, Li J, Kho AT, et al. Enhancing the prediction of childhood asthma remission: integrating clinical factors with microRNAs[J]. J Allergy Clin Immunol, 2021, 147(3): 1093-1095. 10.1016/j.jaci.2020.08.019. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11. Mahnke AH, Sideridis GD, Salem NA, et al. Infant circulating microRNAs as biomarkers of effect in fetal alcohol spectrum disorders[J]. Sci Rep, 2021, 11(1): 1429. 10.1038/s41598-020-80734-y. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12. Wang SD, Talukder A, Cha MY, et al. Computational annotation of miRNA transcription start sites[J]. Brief Bioinform, 2021, 22(1): 380-392. 10.1093/bib/bbz178. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13. Gebert LFR, MacRae IJ. Regulation of microRNA function in animals[J]. Nat Rev Mol Cell Biol, 2019, 20(1): 21-37. 10.1038/s41580-018-0045-7. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14. Wu MZ, Cheng WC, Chen SF, et al. miR-25/93 mediates hypoxia-induced immunosuppression by repressing cGAS[J]. Nat Cell Biol, 2017, 19(10): 1286-1296. 10.1038/ncb3615. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15. Wang QC, Wang ZY, Xu Q, et al. lncRNA expression profiles and associated ceRNA network analyses in epicardial adipose tissue of patients with coronary artery disease[J]. Sci Rep, 2021, 11(1): 1567. 10.1038/s41598-021-81038-5. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16. Du ML, Wang WZ, Jin H, et al. The association analysis of lncRNA HOTAIR genetic variants and gastric cancer risk in a Chinese population[J]. Oncotarget, 2015, 6(31): 31255-31262. 10.18632/oncotarget.5158. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17. Graf J, Kretz M. From structure to function: route to understanding lncRNA mechanism[J/OL]. Bioessays, 2020, 42(12): e2000027[2022-12-01]. 10.1002/bies.202000027. [DOI] [PubMed] [Google Scholar]
  • 18. Zhao YB, Riching AS, Knight WE, et al. Cardiomyocyte-specific long noncoding RNA regulates alternative splicing of the triadin gene in the heart[J]. Circulation, 2022, 146(9): 699-714. 10.1161/CIRCULATIONAHA.121.058017. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 19. Chen CK, Cheng R, Demeter J, et al. Structured elements drive extensive circular RNA translation[J]. Mol Cell, 2021, 81(20): 4300-4318. 10.1016/j.molcel.2021.07.042. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20. Liu CX, Li X, Nan F, et al. Structure and degradation of circular RNAs regulate PKR activation in innate immunity[J]. Cell, 2019, 177(4): 865-880. 10.1016/j.cell.2019.03.046. [DOI] [PubMed] [Google Scholar]
  • 21. Xu XL, Zhang JW, Tian YH, et al. CircRNA inhibits DNA damage repair by interacting with host gene[J]. Mol Cancer, 2020, 19(1): 128. 10.1186/s12943-020-01246-x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22. Meng XW, Chen Q, Zhang PJ, et al. CircPro: an integrated tool for the identification of circRNAs with protein-coding potential[J]. Bioinformatics, 2017, 33(20): 3314-3316. 10.1093/bioinformatics/btx446. [DOI] [PubMed] [Google Scholar]
  • 23. Qu L, Yi ZY, Shen Y, et al. Circular RNA vaccines against SARS-CoV-2 and emerging variants[J]. Cell, 2022, 185(10): 1728-1744. 10.1016/j.cell.2022.03.044. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 24. Abdollahzadeh R, Daraei A, Mansoori Y, et al. Competing endogenous RNA (ceRNA) cross talk and language in ceRNA regulatory networks: a new look at hallmarks of breast cancer[J]. J Cell Physiol, 2019, 234(7): 10080-10100. 10.1002/jcp.27941. [DOI] [PubMed] [Google Scholar]
  • 25. Zheng YL, Song G, Guo JB, et al. Interactions among lncRNA/circRNA, miRNA, and mRNA in musculoskeletal degenerative diseases[J]. Front Cell Dev Biol, 2021, 9: 753931. 10.3389/fcell.2021.753931. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 26. Huang ZY, Kuang NZ. Construction of a ceRNA network related to rheumatoid arthritis[J]. Genes, 2022, 13(4): 647. 10.3390/genes13040647. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27. Winkler A, Sun WY, De S, et al. The interleukin-1 receptor-associated kinase 4 inhibitor PF-06650833 blocks inflammation in preclinical models of rheumatic disease and in humans enrolled in a randomized clinical trial[J]. Arthritis Rheumatol, 2021, 73(12): 2206-2218. 10.1002/art.41953. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 28. Tsai CY, Hsieh SC, Liu CW, et al. The expression of non-coding RNAs and their target molecules in rheumatoid arthritis: a molecular basis for rheumatoid pathogenesis and its potential clinical applications[J]. Int J Mol Sci, 2021, 22(11): 5689. 10.3390/ijms22115689. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 29. Liu H, Zhu YL, Gao YT, et al. NR1D1 modulates synovial inflammation and bone destruction in rheumatoid arthritis[J]. Cell Death Dis, 2020, 11(2): 129. 10.1038/s41419-020-2314-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30. Takeuchi T, Tanaka Y, Erdman J, et al. ASP5094, a humanized monoclonal antibody against integrin alpha-9, did not show efficacy in patients with rheumatoid arthritis refractory to methotrexate: results from a phase 2a, randomized, double-blind, placebo-controlled trial[J]. Arthritis Res Ther, 2020, 22(1): 252. 10.1186/s13075-020-02336-3. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 31. Wynn TA. Two types of fibroblast drive arthritis[J]. Nature, 2019, 570(7760): 169-170. 10.1038/d41586-019-01594-9. [DOI] [PubMed] [Google Scholar]
  • 32. Croft AP, Campos J, Jansen K, et al. Distinct fibroblast subsets drive inflammation and damage in arthritis[J]. Nature, 2019, 570(7760): 246-251. 10.1038/s41586-019-1263-7. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 33. Huang CC, Chiou CH, Liu SC, et al. Melatonin attenuates TNF-α and IL-1β expression in synovial fibroblasts and diminishes cartilage degradation: implications for the treatment of rheumatoid arthritis[J/OL]. J Pineal Res, 2019, 66(3): e12560[2022-12-01]. 10.1111/jpi.12560. [DOI] [PubMed] [Google Scholar]
  • 34. Zhang XN, Zhang X, Wang XP, et al. Efficient delivery of triptolide plus a miR-30-5p inhibitor through the use of near infrared laser responsive or CADY modified MSNs for efficacy in rheumatoid arthritis therapeutics[J]. Front Bioeng Biotechnol, 2020, 8: 170. 10.3389/fbioe.2020.00170. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 35. Cao L, Jiang HF, Yang J, et al. LncRNA MIR31HG is induced by tocilizumab and ameliorates rheumatoid arthritis fibroblast-like synoviocyte-mediated inflammation via miR-214-PTEN-AKT signaling pathway[J]. Aging, 2021, 13(21): 24071-24085. 10.18632/aging.203644. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 36. Pan LY, Sun Y, Jiang H, et al. Total saponins of Radix Clematis regulate fibroblast-like synoviocyte proliferation in rheumatoid arthritis via the lncRNA OIP5-AS1/MiR-410-3p/Wnt7b signaling pathway[J]. Evid Based Complement Alternat Med, 2022, 2022: 8393949. 10.1155/2022/8393949. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 37. Ye ZQ, Wei L, Yin XT, et al. Long non-coding RNA cancer susceptibility candidate 2 regulates the function of human fibroblast-like synoviocytes via the microRNA-18a-5p/B-cell translocation gene 3 signaling axis in rheumatoid arthritis[J]. Bioengineered, 2022, 13(2): 3240-3250. 10.1080/21655979.2021.2022075. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 38. Fu QA, Song MJ, Fang J. LncRNA OSER1-AS1 regulates the inflammation and apoptosis of rheumatoid arthritis fibroblast like synoviocytes via regulating miR-1298-5p/E2F1 axis[J]. Bioengineered, 2022, 13(3): 4951-4963. 10.1080/21655979.2022.2037854. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 39. Wang ML, Chen YX, Bi X, et al. LncRNA NEAT1_1 suppresses tumor-like biologic behaviors of fibroblast-like synoviocytes by targeting the miR-221-3p/uPAR axis in rheumatoid arthritis[J]. J Leukoc Biol, 2022, 111(3): 641-653. 10.1002/JLB.3A0121-067RRR. [DOI] [PubMed] [Google Scholar]
  • 40. Zhang NW, Zheng NN, Luo DX, et al. Long non-coding RNA NR-133666 promotes the proliferation and migration of fibroblast-like synoviocytes through regulating the miR-133c/MAPK1 axis[J]. Front Pharmacol, 2022, 13: 887330. 10.3389/fphar.2022.887330. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 41. Zhong SP, Ouyang QQ, Zhu DJ, et al. Hsa_circ_0088036 promotes the proliferation and migration of fibroblast-like synoviocytes by sponging miR-140-3p and upregulating SIRT 1 expression in rheumatoid arthritis[J]. Mol Immunol, 2020, 125: 131-139. 10.1016/j.molimm.2020.07.004. [DOI] [PubMed] [Google Scholar]
  • 42. Yang Y, Lin SD, Yang Z, et al. Circ_0001947 promotes cell proliferation, invasion, migration and inflammation and inhibits apoptosis in human rheumatoid arthritis fibroblast-like synoviocytes through miR-671-5p/STAT3 axis[J]. J Orthop Surg Res, 2022, 17(1): 54. 10.1186/s13018-022-02939-3. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 43. Hu ZY, Chen JR, Wang ML, et al. Rheumatoid arthritis fibroblast-like synoviocytes maintain tumor-like biological characteristics through ciRS-7-dependent regulation of miR-7[J]. Mol Biol Rep, 2022, 49(9): 8473-8483. 10.1007/s11033-022-07666-w. [DOI] [PubMed] [Google Scholar]
  • 44. Li X, Qu MT, Zhang J, et al. CircASH2L facilitates tumor-like biologic behaviours and inflammation of fibroblast-like synoviocytes via miR-129-5p/HIPK2 axis in rheumatoid arthritis[J]. J Orthop Surg Res, 2021, 16(1): 302. 10.1186/s13018-021-02432-3. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 45. Luo Z, Chen S, Chen X. CircMAPK9 promotes the progression of fibroblast-like synoviocytes in rheumatoid arthritis via the miR-140-3p/PPM1A axis[J]. J Orthop Surg Res, 2021, 16(1): 395. 10.1186/s13018-021-02550-y. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 46. Cai YJ, Liang RG, Xiao SB, et al. Circ_0088194 promotes the invasion and migration of rheumatoid arthritis fibroblast-like synoviocytes via the miR-766-3p/MMP2 axis[J]. Front Immunol, 2021, 12: 628654. 10.3389/fimmu.2021.628654. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 47. Qu W, Jiang L, Hou GH. Circ-AFF2/miR-650/CNP axis promotes proliferation, inflammatory response, migration, and invasion of rheumatoid arthritis synovial fibroblasts[J]. J Orthop Surg Res, 2021, 16(1): 165. 10.1186/s13018-021-02306-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 48. Zhi LQ, Liang JQ, Huang W, et al. Circ_AFF2 facilitates proliferation and inflammatory response of fibroblast-like synoviocytes in rheumatoid arthritis via the miR-375/TAB2 axis[J]. Exp Mol Pathol, 2021, 119: 104617. 10.1016/j.yexmp.2021.104617. [DOI] [PubMed] [Google Scholar]
  • 49. Ma JF, Meng QL, Zhan JP, et al. Paeoniflorin suppresses rheumatoid arthritis development via modulating the circ-FAM120A/miR-671-5p/MDM4 axis[J]. Inflammation, 2021, 44(6): 2309-2322. 10.1007/s10753-021-01504-0. [DOI] [PubMed] [Google Scholar]
  • 50. Chen LF, Huang HS, Chen L, et al. Circ-PTTG1IP/miR-671-5p/TLR4 axis regulates proliferation, migration, invasion and inflammatory response of fibroblast-like synoviocytes in rheumatoid arthritis[J]. Gen Physiol Biophys, 2021, 40(3): 207-219. 10.4149/gpb_2021014. [DOI] [PubMed] [Google Scholar]
  • 51. Chang LH, Kan LA. Mesenchymal stem cell-originated exosomal circular RNA circFBXW7 attenuates cell proliferation, migration and inflammation of fibroblast-like synoviocytes by targeting miR-216a-3p/HDAC4 in rheumatoid arthritis[J]. J Inflamm Res, 2021, 14: 6157-6171. 10.2147/jir.s336099. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 52. Zhang SH, Zhao J, Ma WQ. Circ-Sirt1 inhibits proliferation, induces apoptosis, and ameliorates inflammation in human rheumatoid arthritis fibroblast-like synoviocytes[J]. Autoimmunity, 2021, 54(8): 514-525. 10.1080/08916934.2021.1969550. [DOI] [PubMed] [Google Scholar]
  • 53. Yang YH, Guo LN, Wang Z, et al. Targeted silver nanoparticles for rheumatoid arthritis therapy via macrophage apoptosis and re-polarization[J]. Biomaterials, 2021, 264: 120390. 10.1016/j.biomaterials.2020.120390. [DOI] [PubMed] [Google Scholar]
  • 54. Spiller KL, Nassiri S, Witherel CE, et al. Sequential delivery of immunomodulatory cytokines to facilitate the M1-to-M2 transition of macrophages and enhance vascularization of bone scaffolds[J]. Biomaterials, 2015, 37: 194-207. 10.1016/j.biomaterials.2014.10.017. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 55. Paoletti A, Rohmer J, Ly B, et al. Monocyte/macrophage abnormalities specific to rheumatoid arthritis are linked to miR-155 and are differentially modulated by different TNF inhibitors[J]. J Immunol, 2019, 203(7): 1766-1775. 10.4049/jimmunol.1900386. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 56. Quero L, Tiaden AN, Hanser E, et al. miR-221-3p drives the shift of M2-macrophages to a pro-inflammatory function by suppressing JAK3/STAT3 activation[J]. Front Immunol, 2019, 10: 3087. 10.3389/fimmu.2019.03087. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 57. Wan PX, Su WR, Zhang YY, et al. LncRNA H19 initiates microglial pyroptosis and neuronal death in retinal ischemia/reperfusion injury[J]. Cell Death Differ, 2020, 27(1): 176-191. 10.1038/s41418-019-0351-4. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 58. Zhang JH, Lei HW, Li X. LncRNA SNHG14 contributes to proinflammatory cytokine production in rheumatoid arthritis via the regulation of the miR-17-5p/MINK1-JNK pathway[J]. Environ Toxicol, 2021, 36(12): 2484-2492. 10.1002/tox.23361. [DOI] [PubMed] [Google Scholar]
  • 59. Li Y, Gu CX, Liu GL, et al. Polarization of rheumatoid macrophages is regulated by the CDKN2B-AS1/MIR497/TXNIP axis[J]. Immunol Lett, 2021, 239: 23-31. 10.1016/j.imlet.2021.08.001. [DOI] [PubMed] [Google Scholar]
  • 60. Yang JH, Cheng M, Gu BJ, et al. CircRNA_09505 aggravates inflammation and joint damage in collagen-induced arthritis mice via miR-6089/AKT1/NF-κB axis[J]. Cell Death Dis, 2020, 11(10): 833. 10.1038/s41419-020-03038-z. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 61. Aldridge J, Andersson K, Gjertsson I, et al. Blood PD-1+TFh and CTLA-4+CD4+ T cells predict remission after CTLA-4Ig treatment in early rheumatoid arthritis[J]. Rheumatology, 2022, 61(3): 1233-1242. 10.1093/rheumatology/keab454. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 62. Saravia J, Chapman NM, Chi HB. Helper T cell differentiation[J]. Cell Mol Immunol, 2019, 16(7): 634-643. 10.1038/s41423-019-0220-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 63. Rosenzwajg M, Lorenzon R, Cacoub P, et al. Immunological and clinical effects of low-dose interleukin-2 across 11 autoimmune diseases in a single, open clinical trial[J]. Ann Rheum Dis, 2019, 78(2): 209-217. 10.1136/annrheumdis-2018-214229. [DOI] [PubMed] [Google Scholar]
  • 64. Cho S, Wu CJ, Yasuda T, et al. miR-23∼27∼24 clusters control effector T cell differentiation and function[J]. J Exp Med, 2016, 213(2): 235-249. 10.1084/jem.20150990. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 65. Ahmadi M, Hajialilo M, Dolati S, et al. The effects of nanocurcumin on Treg cell responses and treatment of ankylosing spondylitis patients: a randomized, double-blind, placebo-controlled clinical trial[J]. J Cell Biochem, 2020, 121(1): 103-110. 10.1002/jcb.28901. [DOI] [PubMed] [Google Scholar]
  • 66. Amerikanou C, Papada E, Gioxari A, et al. Mastiha has efficacy in immune-mediated inflammatory diseases through a microRNA-155 Th17 dependent action[J]. Pharmacol Res, 2021, 171: 105753. 10.1016/j.phrs.2021.105753. [DOI] [PubMed] [Google Scholar]
  • 67. Xia RM, Geng GJ, Yu XY, et al. LINC01140 promotes the progression and tumor immune escape in lung cancer by sponging multiple microRNAs[J/OL]. J Immunother Cancer, 2021, 9(8): e002746[2022-12-02]. 10.1136/jitc-2021-002746. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 68. Yao C, Li C, Liu ZJ, et al. LNCRNA XIST inhibits miR-377-3p to hinder Th17 cell differentiation through upregulating ETS1[J]. Comput Intell Neurosci, 2022, 2022: 6545834. 10.1155/2022/6545834. [DOI] [PMC free article] [PubMed] [Google Scholar] [Retracted]
  • 69. Peng HY, Xing J, Wang XH, et al. Circular RNA circNUP214 modulates the T helper 17 cell response in patients with rheumatoid arthritis[J]. Front Immunol, 2022, 13: 885896. 10.3389/fimmu.2022.885896. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 70. Kar S, Gupta R, Malhotra R, et al. Interleukin-9 facilitates osteoclastogenesis in rheumatoid arthritis[J]. Int J Mol Sci, 2021, 22(19): 10397. 10.3390/ijms221910397. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 71. 赵志平, 王向宇, 贾斌, 等. BRD4对钛颗粒诱导破骨细胞形成和骨吸收功能作用[J]. 青岛大学学报(医学版), 2022, 58(4): 489-493. 10.11712/jms.2096-5532.2022.58.108. [DOI] [Google Scholar]; ZHAO Zhiping, WANG Xiangyu, JIA Bin, et al. Effect of BRD4 on osteoclast formation and bone resorption induced by titanium particle[J]. Journal of Qingdao University. Medical Sciences, 2022, 58(4): 489-493. 10.11712/jms.2096-5532.2022.58.108. [DOI] [Google Scholar]
  • 72. Deng CF, Zhang Q, He PH, et al. Targeted apoptosis of macrophages and osteoclasts in arthritic joints is effective against advanced inflammatory arthritis[J]. Nat Commun, 2021, 12(1): 2174. 10.1038/s41467-021-22454-z. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 73. Yu LJ, Sui BD, Fan WX, et al. Exosomes derived from osteogenic tumor activate osteoclast differentiation and concurrently inhibit osteogenesis by transferring COL1A1-targeting miRNA-92a-1-5p[J/OL]. J Extracell Vesicles, 2021, 10(3): e12056[2022-12-02]. 10.1002/jev2.12056. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 74. Weivoda MM, Chew CK, Monroe DG, et al. Identification of osteoclast-osteoblast coupling factors in humans reveals links between bone and energy metabolism[J]. Nat Commun, 2020, 11(1): 87. 10.1038/s41467-019-14003-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 75. Wang F, Deng HM, Chen JM, et al. LncRNA MIAT can regulate the proliferation, apoptosis, and osteogenic differentiation of bone marrow-derived mesenchymal stem cells by targeting miR-150-5p[J]. Bioengineered, 2022, 13(3): 6343-6352. 10.1080/21655979.2021.2011632. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 76. Chen XA, Ouyang ZX, Shen Y, et al. CircRNA_28313/miR-195a/CSF1 axis modulates osteoclast differentiation to affect OVX-induced bone absorption in mice[J]. RNA Biol, 2019, 16(9): 1249-1262. 10.1080/15476286.2019.1624470. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 77. Baert L, Manfroi B, Casez O, et al. The role of APRIL - A proliferation inducing ligand-in autoimmune diseases and expectations from its targeting[J]. J Autoimmun, 2018, 95: 179-190. 10.1016/j.jaut.2018.10.016. [DOI] [PubMed] [Google Scholar]
  • 78. Floudas A, Canavan M, McGarry T, et al. ACPA status correlates with differential immune profile in patients with rheumatoid arthritis[J]. Cells, 2021, 10(3): 647. 10.3390/cells10030647. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 79. Heinicke F, Zhong XF, Flåm ST, et al. microRNA expression differences in blood-derived CD19+ B cells of methotrexate treated rheumatoid arthritis patients[J]. Front Immunol, 2021, 12: 663736. 10.3389/fimmu.2021.663736. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 80. Wu HH, Su SS, Wu YF, et al. Nanoparticle-facilitated delivery of BAFF-R siRNA for B cell intervention and rheumatoid arthritis therapy[J]. Int Immunopharmacol, 2020, 88: 106933. 10.1016/j.intimp.2020.106933. [DOI] [PubMed] [Google Scholar]
  • 81. Szarka E, Aradi P, Huber K, et al. Affinity purification and comparative biosensor analysis of citrulline-peptide-specific antibodies in rheumatoid arthritis[J]. Int J Mol Sci, 2018, 19(1): 326. 10.3390/ijms19010326. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 82. Pozsgay J, Babos F, Uray K, et al. In vitro eradication of citrullinated protein specific B-lymphocytes of rheumatoid arthritis patients by targeted bifunctional nanoparticles[J]. Arthritis Res Ther, 2016, 18: 15. 10.1186/s13075-016-0918-0. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 83. Petri A, Dybkær K, Bøgsted M, et al. Long noncoding RNA expression during human B-cell development[J/OL]. PLoS One, 2015, 10(9): e0138236[2022-12-02]]. 10.1371/journal.pone.0138236. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 84. Zhang HM, Wang J, Wang YD, et al. Long non-coding LEF1-AS1 sponge miR-5100 regulates apoptosis and autophagy in gastric cancer cells via the miR-5100/DEK/AMPK-mTOR axis[J]. Int J Mol Sci, 2022, 23(9): 4787. 10.3390/ijms23094787. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 85. Cheng ZH, Wang GY, Zhu WY, et al. LEF1-AS1 accelerates tumorigenesis in glioma by sponging miR-489-3p to enhance HIGD1A[J]. Cell Death Dis, 2020, 11(8): 690. 10.1038/s41419-020-02823-0. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 86. Sun T, Liu ZX, Zhang R, et al. Long non-coding RNA LEF1-AS1 promotes migration, invasion and metastasis of colon cancer cells through miR-30-5p/SOX9 axis[J]. Onco Targets Ther, 2020, 13: 2957-2972. 10.2147/OTT.S232839. [DOI] [PMC free article] [PubMed] [Google Scholar] [Retracted]
  • 87. Pan J, Hu SN, Ren XY, et al. Whole-transcriptome profiling and circRNA-miRNA-mRNA regulatory networks in B-cell development[J]. Front Immunol, 2022, 13: 812924. 10.3389/fimmu.2022.812924. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 88. Zhang HJ, Wei QF, Wang SJ, et al. Retraction notice to “LncRNA HOTAIR alleviates rheumatoid arthritis by targeting miR-138 and inactivating NF-κB pathway”[J]. Int Immunopharmacol, 2021, 95: 107500. 10.1016/j.intimp.2021.107500. [DOI] [PubMed] [Google Scholar]
  • 89. Jiang LD, Cao S. Role of microRNA-26a in cartilage injury and chondrocyte proliferation and apoptosis in rheumatoid arthritis rats by regulating expression of CTGF[J]. J Cell Physiol, 2020, 235(2): 979-992. 10.1002/jcp.29013. [DOI] [PubMed] [Google Scholar]
  • 90. Zhou YZ, Li SH, Chen P, et al. microRNA-27b-3p inhibits apoptosis of chondrocyte in rheumatoid arthritis by targeting HIPK2 [J]. Artif Cells Nanomed Biotechnol, 2019, 47(1): 1766-1771. 10.1080/21691401.2019.1607362. [DOI] [PubMed] [Google Scholar]
  • 91. Liu D, Fang YX, Rao YJ, et al. Synovial fibroblast-derived exosomal microRNA-106b suppresses chondrocyte proliferation and migration in rheumatoid arthritis via down-regulation of PDK4[J]. J Mol Med, 2020, 98(3): 409-423. 10.1007/s00109-020-01882-2. [DOI] [PubMed] [Google Scholar]
  • 92. Zhuo Q, Wei L, Yin XT, et al. LncRNA ZNF667-AS1 alleviates rheumatoid arthritis by sponging miR-523-3p and inactivating the JAK/STAT signalling pathway[J]. Autoimmunity, 2021, 54(7): 406-414. 10.1080/08916934.2021.1966770. [DOI] [PubMed] [Google Scholar]
  • 93. Li GQ, Tan W, Fang YX, et al. circFADS2 protects LPS-treated chondrocytes from apoptosis acting as an interceptor of miR-498/mTOR cross-talking[J]. Aging, 2019, 11(10): 3348-3361. 10.18632/aging.101986. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 94. Zhou S, Lu HC, Xiong M. Identifying immune cell infiltration and effective diagnostic biomarkers in rheumatoid arthritis by bioinformatics analysis[J]. Front Immunol, 2021, 12: 726747. 10.3389/fimmu.2021.726747. [DOI] [PMC free article] [PubMed] [Google Scholar]

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