• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
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
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
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 @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

骨关节炎中的JNK信号通路:病理及治疗方面

JNK pathway in osteoarthritis: pathological and therapeutic aspects.

作者信息

Ge Hong-Xing, Zou Fu-Man, Li Yan, Liu An-Min, Tu Min

机构信息

a Department of Orthopaedics , Second People's Hospital of Jingmen , Jingmen , China.

b Department of General Medicine , Second People's Hospital of Jingmen , Jingmen , China.

出版信息

J Recept Signal Transduct Res. 2017 Oct;37(5):431-436. doi: 10.1080/10799893.2017.1360353.

DOI:10.1080/10799893.2017.1360353
PMID:28812968
Abstract

CONTEXT

Osteoarthritis (OA) is a common chronic degenerative joint disease resulting in physical disability and reduced quality of life. Different biochemical signaling pathways are involved in the progression of OA, including the c-Jun NH2-terminal kinase (JNK) signal transduction pathway.

OBJECTIVE

In this study, we have reviewed the recent updates on the association of JNK pathway with OA.

METHODS

In this review, we have explored the databases like PubMed, Google Scholar, Medline, Scopus, etc., and collected the most relevant papers of JNK signaling pathway involved in the pathogenesis and therapeutics of OA Results: JNK has been shown by scientific studies to be activated (phosphorylated) in OA that can play a key role in the cartilage destruction. Activation of JNK causes the phosphorylation of c-Jun that causes decreased proteoglycan synthesis and enhanced production of matrix metalloproteinase 13 (MMP-13). Overproduction of MMP-13 by chondrocytes plays a central role in cartilage degeneration in OA. Thus, targeting JNK pathway might be a promising therapeutic application for the prevention and treatment of OA. A number of JNK-inhibitors have been used in vitro and in vivo studies; however, not yet been translated into human use.

CONCLUSIONS

This review study indicates that JNK pathway plays an important role in development and progression of OA, and targeting the JNK pathway might be a potential approach for the treatment of OA in future.

摘要

背景

骨关节炎(OA)是一种常见的慢性退行性关节疾病,会导致身体残疾并降低生活质量。不同的生化信号通路参与了OA的进展,包括c-Jun氨基末端激酶(JNK)信号转导通路。

目的

在本研究中,我们回顾了JNK通路与OA关联的最新进展。

方法

在本综述中,我们检索了PubMed、谷歌学术、Medline、Scopus等数据库,并收集了与JNK信号通路参与OA发病机制和治疗相关的最具相关性的论文。结果:科学研究表明,JNK在OA中被激活(磷酸化),这在软骨破坏中可能起关键作用。JNK的激活导致c-Jun磷酸化,进而导致蛋白聚糖合成减少和基质金属蛋白酶13(MMP-13)产生增加。软骨细胞过度产生MMP-13在OA的软骨退变中起核心作用。因此,靶向JNK通路可能是预防和治疗OA的一种有前景的治疗方法。许多JNK抑制剂已用于体外和体内研究;然而,尚未转化为人体应用。

结论

本综述研究表明,JNK通路在OA的发生和发展中起重要作用,靶向JNK通路可能是未来治疗OA的一种潜在方法。

相似文献

1
JNK pathway in osteoarthritis: pathological and therapeutic aspects.骨关节炎中的JNK信号通路:病理及治疗方面
J Recept Signal Transduct Res. 2017 Oct;37(5):431-436. doi: 10.1080/10799893.2017.1360353.
2
JNK pathway in osteosarcoma: pathogenesis and therapeutics.骨肉瘤中的JNK信号通路:发病机制与治疗方法
J Recept Signal Transduct Res. 2016 Oct;36(5):465-70. doi: 10.3109/10799893.2015.1122045. Epub 2015 Dec 16.
3
Casein kinase 1 epsilon facilitates cartilage destruction in osteoarthritis through JNK pathway.酪蛋白激酶 1 epsilon 通过 JNK 通路促进骨关节炎软骨破坏。
FASEB J. 2020 May;34(5):6466-6478. doi: 10.1096/fj.201902672R. Epub 2020 Mar 16.
4
Hepatocyte growth factor induction of collagenase 3 production in human osteoarthritic cartilage: involvement of the stress-activated protein kinase/c-Jun N-terminal kinase pathway and a sensitive p38 mitogen-activated protein kinase inhibitor cascade.肝细胞生长因子诱导人骨关节炎软骨中胶原酶3的产生:应激激活蛋白激酶/c-Jun氨基末端激酶途径及敏感的p38丝裂原活化蛋白激酶抑制剂级联反应的参与
Arthritis Rheum. 2001 Jan;44(1):73-84. doi: 10.1002/1529-0131(200101)44:1<73::AID-ANR11>3.0.CO;2-E.
5
Phenyl N-tert-butylnitrone down-regulates interleukin-1 beta-stimulated matrix metalloproteinase-13 gene expression in human chondrocytes: suppression of c-Jun NH2-terminal kinase, p38-mitogen-activated protein kinase and activating protein-1.苯基 N-叔丁基亚硝基酮下调白细胞介素-1β刺激的人软骨细胞中基质金属蛋白酶-13基因表达:对c-Jun氨基末端激酶、p38丝裂原活化蛋白激酶和活化蛋白-1的抑制作用
J Pharmacol Exp Ther. 2003 Jun;305(3):981-8. doi: 10.1124/jpet.102.048611. Epub 2003 Mar 6.
6
PGE2 inhibits MMP expression by suppressing MKK4-JNK MAP kinase-c-JUN pathway via EP4 in human articular chondrocytes.PGE2 通过 EP4 抑制人关节软骨细胞中的 MKK4-JNK MAP 激酶-c-JUN 通路抑制 MMP 的表达。
J Cell Biochem. 2010 Feb 1;109(2):425-33. doi: 10.1002/jcb.22421.
7
Explore the variation of MMP3, JNK, p38 MAPKs, and autophagy at the early stage of osteoarthritis.探索骨关节炎早期基质金属蛋白酶3(MMP3)、应激活化蛋白激酶(JNK)、p38丝裂原活化蛋白激酶(p38 MAPKs)及自噬的变化情况。
IUBMB Life. 2016 Apr;68(4):293-302. doi: 10.1002/iub.1482. Epub 2016 Feb 13.
8
Effects of sodium selenite on c-Jun N-terminal kinase signalling pathway induced by oxidative stress in human chondrocytes and c-Jun N-terminal kinase expression in patients with Kashin-Beck disease, an endemic osteoarthritis.亚硒酸钠对氧化应激诱导的人软骨细胞中c-Jun氨基末端激酶信号通路及大骨节病(一种地方性骨关节炎)患者c-Jun氨基末端激酶表达的影响
Br J Nutr. 2016 May;115(9):1547-55. doi: 10.1017/S0007114516000362. Epub 2016 Mar 7.
9
c-Jun N-terminal kinase - c-Jun pathway transactivates Bim to promote osteoarthritis.c-Jun N-末端激酶 - c-Jun 通路反式激活 Bim 促进骨关节炎。
Can J Physiol Pharmacol. 2014 Feb;92(2):132-9. doi: 10.1139/cjpp-2013-0228. Epub 2013 Nov 15.
10
c-Jun transactivates Puma gene expression to promote osteoarthritis.c-Jun激活Puma基因表达以促进骨关节炎。
Mol Med Rep. 2014 May;9(5):1606-12. doi: 10.3892/mmr.2014.1981. Epub 2014 Feb 24.

引用本文的文献

1
Non-coding RNA in cartilage regeneration: regulatory mechanism and therapeutic strategies.软骨再生中的非编码RNA:调控机制与治疗策略
Front Bioeng Biotechnol. 2025 Mar 26;13:1522303. doi: 10.3389/fbioe.2025.1522303. eCollection 2025.
2
Mechanisms Underlying the Stimulation of DUSP10/MKP5 Expression in Chondrocytes by High Molecular Weight Hyaluronic Acid.高分子量透明质酸刺激软骨细胞中DUSP10/MKP5表达的潜在机制
Biomedicines. 2025 Feb 5;13(2):376. doi: 10.3390/biomedicines13020376.
3
The Interplay of Aging and PANoptosis in Osteoarthritis Pathogenesis: Implications for Novel Therapeutic Strategies.
衰老与PAN细胞焦亡在骨关节炎发病机制中的相互作用:对新型治疗策略的启示
J Inflamm Res. 2025 Feb 10;18:1951-1967. doi: 10.2147/JIR.S489613. eCollection 2025.
4
LncRNA RMRP promotes chondrocyte injury by regulating the FOXC1/RBP4 axis.长链非编码RNA RMRP通过调控FOXC1/RBP4轴促进软骨细胞损伤。
Cent Eur J Immunol. 2024;49(4):366-382. doi: 10.5114/ceji.2024.145312. Epub 2024 Dec 6.
5
Enhancing Industrial Hemp () Leaf By-Products: Bioactive Compounds, Anti-Inflammatory Properties, and Potential Health Applications.提升工业大麻()叶副产品:生物活性化合物、抗炎特性及潜在健康应用。 (注:原文括号处内容缺失)
Int J Mol Sci. 2025 Jan 10;26(2):548. doi: 10.3390/ijms26020548.
6
Potential role of gut-related factors in the pathology of cartilage in osteoarthritis.肠道相关因素在骨关节炎软骨病理中的潜在作用。
Front Nutr. 2025 Jan 8;11:1515806. doi: 10.3389/fnut.2024.1515806. eCollection 2024.
7
Tamarixetin Protects Chondrocytes against IL-1β-Induced Osteoarthritis Phenotype by Inhibiting NF-κB and Activating Nrf2 Signaling.柽柳素通过抑制NF-κB和激活Nrf2信号通路保护软骨细胞免受IL-1β诱导的骨关节炎表型影响。
Antioxidants (Basel). 2024 Sep 25;13(10):1166. doi: 10.3390/antiox13101166.
8
Application of kartogenin for the treatment of cartilage defects: current practice and future directions.软骨生成素在软骨缺损治疗中的应用:当前实践与未来方向。
RSC Adv. 2024 Oct 21;14(45):33206-33222. doi: 10.1039/d4ra06558a. eCollection 2024 Oct 17.
9
Osteoarthritis as a Systemic Disease Promoted Prostate Cancer In Vivo and In Vitro.骨关节炎作为一种系统性疾病促进前列腺癌在体内和体外的发生。
Int J Mol Sci. 2024 May 30;25(11):6014. doi: 10.3390/ijms25116014.
10
Integrated Network Pharmacology and Experimental Validation Approach to Investigate the Mechanisms of Radix Rehmanniae Praeparata - Angelica Sinensis - Radix Achyranthis Bidentatae in Treating Knee Osteoarthritis.基于整合网络药理学与实验验证探究地黄-当归-牛膝治疗膝骨关节炎作用机制的方法。
Drug Des Devel Ther. 2024 May 15;18:1583-1602. doi: 10.2147/DDDT.S455006. eCollection 2024.