文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期,新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2025

椎间盘退变过程中N6-甲基腺苷(m6A)修饰潜在靶点的鉴定与表征

Identification and Characterisation of Potential Targets for N6-methyladenosine (m6A) Modification during Intervertebral Disc Degeneration.

作者信息

Shen Jianlin, Zhang Qiang, Lan Yujian, Peng Qingping, Ji Ziyu, Wu Yanjiao, Liu Huan

机构信息

Department of Orthopaedics, Affiliated Hospital of Putian University, 351100 Putian, Fujian, China.

Central Laboratory, Affiliated Hospital of Putian University, 351100 Putian, Fujian, China.

出版信息

Front Biosci (Landmark Ed). 2024 Nov 28;29(12):405. doi: 10.31083/j.fbl2912405.


DOI:10.31083/j.fbl2912405
PMID:39735982
Abstract

BACKGROUND: The mechanism for RNA methylation during disc degeneration is unclear. The aim of this study was to identify N6-methyladenosine (m6A) markers and therapeutic targets for the prevention and treatment of intervertebral disc degeneration (IDD). METHODS: Methylated RNA immunoprecipitation sequencing (MeRIP-seq) and quantitative reverse transcription PCR (RT-qPCR) were employed to analyze m6A modifications of IDD-related gene expression. Bioinformatics was used to identify enriched gene pathways in IDD. m6A-RIP-qPCR was used to validate potential targets and markers. RESULTS AND CONCLUSION: Human IDD samples exhibited a distinct m6A modification pattern that allowed associated genes and pathways to be identified. These genes had functions such as "nuclear factor kappa-B (NF-κB) binding" and "extracellular matrix components", which are crucial for IDD pathogenesis. showed increased m6A modification in IDD, while and showed decreased m6A methylation. The results of this study offer novel insights for the prevention and treatment of IDD.

摘要

背景:椎间盘退变过程中RNA甲基化的机制尚不清楚。本研究旨在鉴定N6-甲基腺苷(m6A)标记物及预防和治疗椎间盘退变(IDD)的治疗靶点。 方法:采用甲基化RNA免疫沉淀测序(MeRIP-seq)和定量逆转录PCR(RT-qPCR)分析IDD相关基因表达的m6A修饰。利用生物信息学鉴定IDD中富集的基因通路。m6A-RIP-qPCR用于验证潜在靶点和标记物。 结果与结论:人类IDD样本呈现出独特的m6A修饰模式,据此可鉴定相关基因和通路。这些基因具有“核因子κB(NF-κB)结合”和“细胞外基质成分”等功能,对IDD发病机制至关重要。[具体基因名称]在IDD中m6A修饰增加,而[具体基因名称]和[具体基因名称]的m6A甲基化减少。本研究结果为IDD的预防和治疗提供了新的见解。

相似文献

[1]
Identification and Characterisation of Potential Targets for N6-methyladenosine (m6A) Modification during Intervertebral Disc Degeneration.

Front Biosci (Landmark Ed). 2024-11-28

[2]
METTL3 Promotes Nucleus Pulposus Cell Senescence in Intervertebral Disc Degeneration by Regulating TLR2 m6A Methylation and Gut Microbiota.

J Gerontol A Biol Sci Med Sci. 2024-8-1

[3]
Comprehensive analysis of N6-methyladenosine (mA) modification during the degeneration of lumbar intervertebral disc in mice.

J Orthop Translat. 2021-12-15

[4]
Dynamics of N6-methyladenosine modification during aging and their potential roles in the degeneration of intervertebral disc.

JOR Spine. 2024-1-25

[5]
Novel insights into the interaction between N6-methyladenosine methylation and noncoding RNAs in musculoskeletal disorders.

Cell Prolif. 2022-10

[6]
Abnormal stress promotes intervertebral disc degeneration through WTAP/YTHDF2-dependent TIMP3 m6A modification.

J Cell Physiol. 2024-5

[7]
SIAH1 promotes senescence and apoptosis of nucleus pulposus cells to exacerbate disc degeneration through ubiquitinating XIAP.

Tissue Cell. 2022-6

[8]
m6A hypomethylation of DNMT3B regulated by ALKBH5 promotes intervertebral disc degeneration via E4F1 deficiency.

Clin Transl Med. 2022-3

[9]
Upregulated Plant Homeodomain Finger Protein 6 Promotes Extracellular Matrix Degradation in Intervertebral Disc Degeneration Based on Microarray Analysis.

Spine (Phila Pa 1976). 2020-10-1

[10]
ZNF667 alleviates the inflammatory damage in intervertebral disc degeneration via inhibiting NF-κB signaling pathway.

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2024-10-28

引用本文的文献

[1]
N-methyladenosine and intervertebral disc degeneration: Advances in detection and pathological insights.

J Orthop Translat. 2025-6-5

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

推荐工具

医学文档翻译智能文献检索