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类风湿关节炎中的DNA和RNA甲基化——一篇综述

DNA and RNA Methylation in Rheumatoid Arthritis-A Narrative Review.

作者信息

Kiełbowski Kajetan, Bakinowska Estera, Gorący-Rosik Anna, Figiel Karolina, Judek Roksana, Rosik Jakub, Dec Paweł, Modrzejewski Andrzej, Pawlik Andrzej

机构信息

Department of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland.

Department of Clinical and Molecular Biochemistry, Pomeranian Medical University, 70-111 Szczecin, Poland.

出版信息

Epigenomes. 2025 Jan 8;9(1):2. doi: 10.3390/epigenomes9010002.


DOI:10.3390/epigenomes9010002
PMID:39846569
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11755448/
Abstract

Rheumatoid arthritis (RA) is a progressive autoimmune disease leading to structural and functional joint damage and, eventually, to physical disability. The pathogenesis of the disease is highly complex and involves interactions between fibroblast-like synoviocytes (FLSs) and immune cells, which stimulate the secretion of pro-inflammatory factors, leading to chronic inflammation. In recent years, studies have demonstrated the importance of epigenetics in RA. Specifically, epigenetic alterations have been suggested to serve as diagnostic and treatment biomarkers, while epigenetic mechanisms are thought to be involved in the pathogenesis of RA. Epigenetic regulators coordinate gene expression, and in the case of inflammatory diseases, they regulate the expression of a broad range of inflammatory molecules. In this review, we discuss current evidence on the involvement of DNA and RNA methylation in RA.

摘要

类风湿性关节炎(RA)是一种进行性自身免疫性疾病,会导致关节结构和功能受损,并最终导致身体残疾。该疾病的发病机制高度复杂,涉及成纤维样滑膜细胞(FLS)与免疫细胞之间的相互作用,这些相互作用会刺激促炎因子的分泌,从而导致慢性炎症。近年来,研究表明表观遗传学在类风湿性关节炎中具有重要作用。具体而言,表观遗传改变已被认为可作为诊断和治疗的生物标志物,而表观遗传机制被认为参与了类风湿性关节炎的发病过程。表观遗传调节因子协调基因表达,在炎症性疾病中,它们调节多种炎症分子的表达。在这篇综述中,我们讨论了关于DNA和RNA甲基化参与类风湿性关节炎的现有证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c13f/11755448/d4eb9d9539fa/epigenomes-09-00002-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c13f/11755448/f8996be9187e/epigenomes-09-00002-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c13f/11755448/d4eb9d9539fa/epigenomes-09-00002-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c13f/11755448/f8996be9187e/epigenomes-09-00002-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c13f/11755448/d4eb9d9539fa/epigenomes-09-00002-g002.jpg

相似文献

[1]
DNA and RNA Methylation in Rheumatoid Arthritis-A Narrative Review.

Epigenomes. 2025-1-8

[2]
Epigenetics in rheumatoid arthritis; fibroblast-like synoviocytes as an emerging paradigm in the pathogenesis of the disease.

Immunol Cell Biol. 2020-1-26

[3]
MeCP2 Regulates PTCH1 Expression Through DNA Methylation in Rheumatoid Arthritis.

Inflammation. 2017-10

[4]
Increased m6A RNA methylation and METTL3 expression may contribute to the synovitis progression of rheumatoid arthritis.

Exp Cell Res. 2024-10-1

[5]
MALAT1-Driven Inhibition of Wnt Signal Impedes Proliferation and Inflammation in Fibroblast-Like Synoviocytes Through CTNNB1 Promoter Methylation in Rheumatoid Arthritis.

Hum Gene Ther. 2019-6-26

[6]
Syndecan-4 involves in the pathogenesis of rheumatoid arthritis by regulating the inflammatory response and apoptosis of fibroblast-like synoviocytes.

J Cell Physiol. 2019-7-15

[7]
DNA Methylation as a Future Therapeutic and Diagnostic Target in Rheumatoid Arthritis.

Cells. 2019-8-22

[8]
CYLD suppression enhances the pro-inflammatory effects and hyperproliferation of rheumatoid arthritis fibroblast-like synoviocytes by enhancing NF-κB activation.

Arthritis Res Ther. 2018-10-3

[9]
The role of non-coding RNAs in fibroblast-like synoviocytes in rheumatoid arthritis.

Int J Rheum Dis. 2024-10

[10]
The p53 status in rheumatoid arthritis with focus on fibroblast-like synoviocytes.

Immunol Res. 2021-6

本文引用的文献

[1]
Emerging influence of RNA post-transcriptional modifications in the synovial homeostasis of rheumatoid arthritis.

Front Immunol. 2024-12-9

[2]
Autoimmune disease: a view of epigenetics and therapeutic targeting.

Front Immunol. 2024

[3]
DNA methylation inhibitors adverse reaction characteristic analysis: a descriptive analysis from WHO-VigiAccess.

Front Pharmacol. 2024-10-2

[4]
Genetics, epigenetics and autoimmunity constitute a Bermuda triangle for the pathogenesis of rheumatoid arthritis.

Life Sci. 2024-11-15

[5]
Increased m6A RNA methylation and METTL3 expression may contribute to the synovitis progression of rheumatoid arthritis.

Exp Cell Res. 2024-10-1

[6]
Sequential ChIP-Seq.

Methods Mol Biol. 2024

[7]
Revisiting Epigenetics Fundamentals and Its Biomedical Implications.

Int J Mol Sci. 2024-7-19

[8]
Givinostat: First Approval.

Drugs. 2024-7

[9]
The miR-29-3p family suppresses inflammatory osteolysis.

J Cell Physiol. 2024-8

[10]
Epi-revolution in rheumatology: the potential of histone deacetylase inhibitors for targeted rheumatoid arthritis intervention.

Inflammopharmacology. 2024-8

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