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类风湿关节炎中非编码RNA与细胞凋亡相互作用的新见解:诊断功能与治疗应用

Novel insights into the crosstalk between non-coding RNA and apoptosis in rheumatoid arthritis: diagnostic functions and therapeutic applications.

作者信息

Wen Jianting, Liu Jian, Wan Lei, Wang Fanfan

机构信息

Department of Rheumatology and Immunology, First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui, China.

Institute of Rheumatology, Anhui Academy of Chinese Medicine, Hefei, Anhui, China.

出版信息

Front Immunol. 2025 May 16;16:1550839. doi: 10.3389/fimmu.2025.1550839. eCollection 2025.


DOI:10.3389/fimmu.2025.1550839
PMID:40453089
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12122316/
Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disorder and a leading cause of disability worldwide, significantly impairing patients' quality of life. As current therapeutic options remain limited, there is an urgent need for novel strategies, including the use of medicinal plants, to delay the development and progression of RA. Acute inflammation in RA is often accompanied by impaired apoptosis, which contributes to disease pathogenesis. With advances in high-throughput sequencing technologies, an increasing number of non-coding RNAs (ncRNAs) have been identified and extensively studied for their roles in both physiological and pathological processes. Dysregulation of these ncRNAs-particularly long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs)-has been implicated in various disorders, including RA. Given the well-established association between apoptosis and ncRNA expression in RA, a comprehensive understanding of their intricate interplay is essential. In this study, we systematically explore the complex interactions between lncRNAs and circRNAs in regulating apoptosis during the pathogenesis of RA. Additionally, we highlight emerging evidence, suggesting that ncRNA-mediated modulation of apoptosis can be achieved through herbal medicines, offering promising therapeutic avenues for RA treatment.

摘要

类风湿性关节炎(RA)是一种慢性自身免疫性炎症性疾病,是全球致残的主要原因,严重损害患者的生活质量。由于目前的治疗选择仍然有限,迫切需要新的策略,包括使用药用植物,以延缓RA的发展和进程。RA中的急性炎症常伴有细胞凋亡受损,这有助于疾病的发病机制。随着高通量测序技术的进步,越来越多的非编码RNA(ncRNAs)被鉴定出来,并对其在生理和病理过程中的作用进行了广泛研究。这些ncRNAs的失调,特别是长链非编码RNA(lncRNAs)和环状RNA(circRNAs),与包括RA在内的各种疾病有关。鉴于RA中细胞凋亡与ncRNA表达之间已确立的关联,全面了解它们之间复杂的相互作用至关重要。在本研究中,我们系统地探讨了lncRNAs和circRNAs在RA发病机制中调节细胞凋亡的复杂相互作用。此外,我们强调了新出现的证据,表明ncRNA介导的细胞凋亡调节可以通过草药实现,为RA治疗提供了有前景的治疗途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33e3/12122316/f9f138889078/fimmu-16-1550839-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33e3/12122316/e90eb35af7fc/fimmu-16-1550839-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33e3/12122316/67dbbe0f16eb/fimmu-16-1550839-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33e3/12122316/1ae009e35690/fimmu-16-1550839-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33e3/12122316/54b6ec05c932/fimmu-16-1550839-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33e3/12122316/f9f138889078/fimmu-16-1550839-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33e3/12122316/e90eb35af7fc/fimmu-16-1550839-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33e3/12122316/67dbbe0f16eb/fimmu-16-1550839-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33e3/12122316/1ae009e35690/fimmu-16-1550839-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33e3/12122316/54b6ec05c932/fimmu-16-1550839-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33e3/12122316/f9f138889078/fimmu-16-1550839-g005.jpg

相似文献

[1]
Novel insights into the crosstalk between non-coding RNA and apoptosis in rheumatoid arthritis: diagnostic functions and therapeutic applications.

Front Immunol. 2025-5-16

[2]
The role of non-coding RNAs (miRNA and lncRNA) in the clinical management of rheumatoid arthritis.

Pharmacol Res. 2022-12

[3]
Non-Coding RNAs in Neurological and Neuropsychiatric Disorders: Unraveling the Hidden Players in Disease Pathogenesis.

Cells. 2024-6-19

[4]
Functional Interactions Between lncRNAs/circRNAs and miRNAs: Insights Into Rheumatoid Arthritis.

Front Immunol. 2022

[5]
Long noncoding RNA/circular RNA regulates competitive endogenous RNA networks in rheumatoid arthritis: molecular mechanisms and traditional Chinese medicine therapeutic significances.

Ann Med. 2023-12

[6]
Noncoding RNAs in rheumatoid arthritis: modulators of the NF-κB signaling pathway and therapeutic implications.

Front Immunol. 2024

[7]
Non-coding RNAs involved in fibroblast-like synoviocyte functioning in arthritis rheumatoid: From pathogenesis to therapy.

Cytokine. 2024-1

[8]
The Role of Long Non-Coding RNA in Rheumatoid Arthritis.

Int J Mol Sci. 2025-1-10

[9]
Inhibitory role of long non-coding RNA OIP5-AS1 in rheumatoid arthritis progression through the microRNA-448-paraoxonase 1-toll-like receptor 3-nuclear factor κB axis.

Exp Physiol. 2020-10

[10]
Dysregulation of non-coding RNAs in Rheumatoid arthritis.

Biomed Pharmacother. 2020-10

本文引用的文献

[1]
NF-κB Signaling Pathway in Rheumatoid Arthritis: Mechanisms and Therapeutic Potential.

Mol Neurobiol. 2025-6

[2]
Noncoding RNAs in rheumatoid arthritis: modulators of the NF-κB signaling pathway and therapeutic implications.

Front Immunol. 2024

[3]
[Serum from Xinfeng Capsule-treated rats affect the proliferation and apoptosis of fibroblast-like synoviocytes in rheumatoid arthritis by regulating circular RNA Cbl proto-oncogene B (circ-CBLB)].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2024-9

[4]
Regulating the lncRNA DSCR9/RPLP2/PI3K/AKT axis: an important mechanism of Xinfeng capsules in improving rheumatoid arthritis.

Front Immunol. 2024

[5]
Exploration of the molecular mechanism guiding Xinfeng capsule regulatory mechanism for rheumatoid arthritis inflammation.

Am J Transl Res. 2024-3-15

[6]
Brucine alleviates fibroblast-like synoviocytes dysfunction and inflammation by regulating YY1 during rheumatoid arthritis.

Chem Biol Drug Des. 2024-3

[7]
LncRNA HOTTIP regulates TLR4 promoter methylation by recruiting H3K4 methyltransferase MLL1 to affect apoptosis and inflammatory response of fibroblast-like synoviocyte in rheumatoid arthritis.

Kaohsiung J Med Sci. 2024-4

[8]
mA-mediated lncRNA MAPKAPK5-AS1 induces apoptosis and suppresses inflammation via regulating miR-146a-3p/SIRT1/NF-κB axis in rheumatoid arthritis.

Cell Cycle. 2023

[9]
Mechanistic role of quercetin as inhibitor for adenosine deaminase enzyme in rheumatoid arthritis: systematic review.

Cell Mol Biol Lett. 2024-1-16

[10]
Long Non-Coding RNA AL928768.3 Promotes Rheumatoid Arthritis Fibroblast-Like Synoviocytes Proliferation, Invasion and Inflammation, While Inhibits Apoptosis Via Activating Lymphotoxin Beta Mediated NF-κB Signaling Pathway.

Inflammation. 2024-4

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