• 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

JAK/STAT 信号通路在骨关节炎进展中的潜在作用。

The potential roles of JAK/STAT signaling in the progression of osteoarthritis.

机构信息

Department of Orthopedics, First Affiliated Hospital of Gannan Medical University, Ganzhou, China.

College of Pharmacy, Gannan Medical University, Ganzhou, China.

出版信息

Front Endocrinol (Lausanne). 2022 Nov 24;13:1069057. doi: 10.3389/fendo.2022.1069057. eCollection 2022.

DOI:10.3389/fendo.2022.1069057
PMID:36506076
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9729341/
Abstract

Osteoarthritis (OA) is an age-related chronic progressive degenerative disease that induces persistent pain and disabilities. The development of OA is a complex process, and the risk factors are various, including aging, genetics, trauma and altered biomechanics. Inflammation and immunity play an important role in the pathogenesis of OA. JAK/STAT pathway is one of the most prominent intracellular signaling pathways, regulating cell proliferation, differentiation, and apoptosis. Inflammatory factors can act as the initiators of JAK/STAT pathway, which is implicated in the pathophysiological activity of chondrocyte. In this article, we provide a review on the importance of JAK/STAT pathway in the pathological development of OA. Potentially, JAK/STAT pathway becomes a therapeutic target for managing OA.

摘要

骨关节炎（OA）是一种与年龄相关的慢性进行性退行性疾病，会引起持续的疼痛和残疾。OA 的发展是一个复杂的过程，其危险因素多种多样，包括衰老、遗传、创伤和生物力学改变。炎症和免疫在 OA 的发病机制中起着重要作用。JAK/STAT 通路是最突出的细胞内信号通路之一，调节细胞增殖、分化和凋亡。炎症因子可以作为 JAK/STAT 通路的启动子，参与软骨细胞的病理生理活动。本文综述了 JAK/STAT 通路在 OA 病理发展中的重要性。JAK/STAT 通路可能成为治疗 OA 的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f707/9729341/3291936273c5/fendo-13-1069057-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f707/9729341/298115b01f00/fendo-13-1069057-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f707/9729341/736228ba54ad/fendo-13-1069057-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f707/9729341/3291936273c5/fendo-13-1069057-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f707/9729341/298115b01f00/fendo-13-1069057-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f707/9729341/736228ba54ad/fendo-13-1069057-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f707/9729341/3291936273c5/fendo-13-1069057-g003.jpg

相似文献

1
The potential roles of JAK/STAT signaling in the progression of osteoarthritis.JAK/STAT 信号通路在骨关节炎进展中的潜在作用。
Front Endocrinol (Lausanne). 2022 Nov 24;13:1069057. doi: 10.3389/fendo.2022.1069057. eCollection 2022.
2
Negative Regulators of JAK/STAT Signaling in Rheumatoid Arthritis and Osteoarthritis.类风湿关节炎和骨关节炎中JAK/STAT信号通路的负调控因子
Int J Mol Sci. 2017 Feb 24;18(3):484. doi: 10.3390/ijms18030484.
3
Silence of TANK-binding kinase 1 (TBK1) regulates extracellular matrix degradation of chondrocyte in osteoarthritis by janus kinase (JAK)-signal transducer of activators of transcription (STAT) signaling.TANK 结合激酶 1（TBK1）的沉默通过 Janus 激酶（JAK）-信号转导和转录激活因子（STAT）信号调节骨关节炎软骨细胞细胞外基质的降解。
Bioengineered. 2022 Jan;13(1):1872-1879. doi: 10.1080/21655979.2021.2018976.
4
Roles for the interleukin-4 receptor and associated JAK/STAT proteins in human articular chondrocyte mechanotransduction.白细胞介素-4受体及相关JAK/STAT蛋白在人关节软骨细胞机械转导中的作用。
Osteoarthritis Cartilage. 2006 Oct;14(10):991-1001. doi: 10.1016/j.joca.2006.03.013. Epub 2006 May 6.
5
Interleukin-7 stimulates secretion of S100A4 by activating the JAK/STAT signaling pathway in human articular chondrocytes.白细胞介素-7通过激活人关节软骨细胞中的JAK/STAT信号通路刺激S100A4的分泌。
Arthritis Rheum. 2009 Mar;60(3):792-800. doi: 10.1002/art.24295.
6
Acteoside inhibits inflammatory response via JAK/STAT signaling pathway in osteoarthritic rats.毛蕊花糖苷通过 JAK/STAT 信号通路抑制骨关节炎大鼠的炎症反应。
BMC Complement Altern Med. 2019 Oct 7;19(1):264. doi: 10.1186/s12906-019-2673-7.
7
SOCS modulates JAK-STAT pathway as a novel target to mediate the occurrence of neuroinflammation: Molecular details and treatment options.SOCS 调节 JAK-STAT 通路作为介导神经炎症发生的新靶点：分子细节和治疗选择。
Brain Res Bull. 2024 Jul;213:110988. doi: 10.1016/j.brainresbull.2024.110988. Epub 2024 May 27.
8
Downregulation of long noncoding RNA LOC101928134 inhibits the synovial hyperplasia and cartilage destruction of osteoarthritis rats through the activation of the Janus kinase/signal transducers and activators of transcription signaling pathway by upregulating IFNA1.长链非编码 RNA LOC101928134 的下调通过上调 IFNA1 激活 Janus 激酶/信号转导和转录激活因子信号通路，抑制骨关节炎大鼠的滑膜增生和软骨破坏。
J Cell Physiol. 2019 Jul;234(7):10523-10534. doi: 10.1002/jcp.27730. Epub 2018 Nov 19.
9
Age-related remodeling of the JAK/STAT/SOCS signaling pathway and associated myocardial changes: From histological to molecular level.JAK/STAT/SOCS信号通路的年龄相关性重塑及相关心肌变化：从组织学水平到分子水平
Ann Anat. 2017 Nov;214:21-30. doi: 10.1016/j.aanat.2017.07.003. Epub 2017 Aug 4.
10
JAK/STAT as a Potential Therapeutic Target for Osteolytic Diseases.JAK/STAT 作为溶骨性疾病的潜在治疗靶点。
Int J Mol Sci. 2023 Jun 17;24(12):10290. doi: 10.3390/ijms241210290.

引用本文的文献

1
Breaking Down Osteoarthritis: Exploring Inflammatory and Mechanical Signaling Pathways.剖析骨关节炎：探索炎症和机械信号通路
Life (Basel). 2025 Aug 4;15(8):1238. doi: 10.3390/life15081238.
2
Research progress on mesenchymal stem cell‑derived exosomes in the treatment of osteoporosis induced by knee osteoarthritis (Review).间充质干细胞来源的外泌体治疗膝骨关节炎所致骨质疏松的研究进展（综述）
Int J Mol Med. 2025 Oct;56(4). doi: 10.3892/ijmm.2025.5601. Epub 2025 Aug 1.
3
Serotonergic neurons regulate the Drosophila vascular niche to control immune stress hematopoiesis.

本文引用的文献

1
Nrf2-mediated anti-inflammatory polarization of macrophages as therapeutic targets for osteoarthritis.Nrf2 介导的巨噬细胞抗炎极化作为骨关节炎的治疗靶点。
Front Immunol. 2022 Aug 12;13:967193. doi: 10.3389/fimmu.2022.967193. eCollection 2022.
2
Targeting inflammation and redox perturbations by lisinopril mitigates Freund's adjuvant-induced arthritis in rats: role of JAK-2/STAT-3/RANKL axis, MMPs, and VEGF.赖诺普利通过靶向炎症和氧化还原失调减轻弗氏佐剂诱导的大鼠关节炎：JAK-2/STAT-3/RANKL 轴、MMPs 和 VEGF 的作用。
Inflammopharmacology. 2022 Oct;30(5):1909-1926. doi: 10.1007/s10787-022-00998-w. Epub 2022 Jun 28.
3
血清素能神经元调节果蝇的血管微环境以控制免疫应激造血作用。
Nat Commun. 2025 Jun 3;16(1):5152. doi: 10.1038/s41467-025-60493-y.
4
Mechanistic insights into Sanbi Decoction for osteoarthritis treatment based on network pharmacology and experimental validation.基于网络药理学和实验验证对三痹汤治疗骨关节炎的作用机制洞察
Sci Rep. 2025 May 28;15(1):18707. doi: 10.1038/s41598-025-99055-z.
5
Primary cilia and inflammatory response: unveiling new mechanisms in osteoarthritis progression.原发性纤毛与炎症反应：揭示骨关节炎进展中的新机制
Exp Biol Med (Maywood). 2025 Apr 28;250:10490. doi: 10.3389/ebm.2025.10490. eCollection 2025.
6
S-propargyl-cysteine attenuates temporomandibular joint osteoarthritis by regulating macrophage polarization via Inhibition of JAK/STAT signaling.S-炔丙基半胱氨酸通过抑制JAK/STAT信号通路调节巨噬细胞极化来减轻颞下颌关节骨关节炎。
Mol Med. 2025 Apr 7;31(1):128. doi: 10.1186/s10020-025-01186-6.
7
STAT3 Signaling Pathway in Health and Disease.健康与疾病中的信号转导和转录激活因子3（STAT3）信号通路
MedComm (2020). 2025 Mar 30;6(4):e70152. doi: 10.1002/mco2.70152. eCollection 2025 Apr.
8
[High expression of hexokinase 2 promotes proliferation, migration and invasion of colorectal cancer cells by activating the JAK/STAT pathway and regulating tumor immune microenvironment].己糖激酶2高表达通过激活JAK/STAT通路和调节肿瘤免疫微环境促进结肠癌细胞的增殖、迁移和侵袭
Nan Fang Yi Ke Da Xue Xue Bao. 2025 Mar 20;45(3):542-553. doi: 10.12122/j.issn.1673-4254.2025.03.12.
9
Transcriptional Analysis Reveals That the FHL1/JAK-STAT Pathway is Involved in Acute Cartilage Injury in Mice.转录分析表明FHL1/JAK-STAT通路参与小鼠急性软骨损伤。
Cartilage. 2025 Mar 21:19476035251323601. doi: 10.1177/19476035251323601.
10
7-Geranyloxycoumarin modulated metastatic potential of osteosarcoma cells via interaction with MMPs and JAK1/2.7-香叶氧基香豆素通过与基质金属蛋白酶和JAK1/2相互作用调节骨肉瘤细胞的转移潜能。
Naunyn Schmiedebergs Arch Pharmacol. 2025 Feb 15. doi: 10.1007/s00210-025-03847-z.
Identification of Transcription Factors Responsible for a Transforming Growth Factor-β-Driven Hypertrophy-like Phenotype in Human Osteoarthritic Chondrocytes.
鉴定转录因子在人骨关节炎软骨细胞转化生长因子-β驱动的肥大样表型中的作用。
Cells. 2022 Apr 5;11(7):1232. doi: 10.3390/cells11071232.
4
Hypoxia-Preconditioned Extracellular Vesicles from Mesenchymal Stem Cells Improve Cartilage Repair in Osteoarthritis.间充质干细胞来源的缺氧预处理细胞外囊泡改善骨关节炎中的软骨修复
Membranes (Basel). 2022 Feb 16;12(2):225. doi: 10.3390/membranes12020225.
5
Silence of TANK-binding kinase 1 (TBK1) regulates extracellular matrix degradation of chondrocyte in osteoarthritis by janus kinase (JAK)-signal transducer of activators of transcription (STAT) signaling.TANK 结合激酶 1（TBK1）的沉默通过 Janus 激酶（JAK）-信号转导和转录激活因子（STAT）信号调节骨关节炎软骨细胞细胞外基质的降解。
Bioengineered. 2022 Jan;13(1):1872-1879. doi: 10.1080/21655979.2021.2018976.
6
The Identified Hub Gene GlcN in Osteoarthritis Progression and Treatment.GlcN 在骨关节炎进展和治疗中的关键作用研究。
Comput Math Methods Med. 2021 Oct 31;2021:5499450. doi: 10.1155/2021/5499450. eCollection 2021.
7
Astragaloside IV protects cardiomyocytes against hypoxia injury via and the pathway.黄芪甲苷IV通过 和 途径保护心肌细胞免受缺氧损伤。
Ann Transl Med. 2021 Sep;9(18):1435. doi: 10.21037/atm-21-4080.
8
Tanshinone IIA and Astragaloside IV Inhibit miR-223/JAK2/STAT1 Signalling Pathway to Alleviate Lipopolysaccharide-Induced Damage in Nucleus Pulposus Cells.丹参酮 IIA 和黄芪甲苷 IV 通过抑制 miR-223/JAK2/STAT1 信号通路缓解脂多糖诱导的髓核细胞损伤。
Dis Markers. 2021 Oct 12;2021:6554480. doi: 10.1155/2021/6554480. eCollection 2021.
9
LncRNA ZNF667-AS1 alleviates rheumatoid arthritis by sponging miR-523-3p and inactivating the JAK/STAT signalling pathway.长链非编码 RNA ZNF667-AS1 通过海绵吸附 miR-523-3p 并使 JAK/STAT 信号通路失活来缓解类风湿性关节炎。
Autoimmunity. 2021 Nov;54(7):406-414. doi: 10.1080/08916934.2021.1966770. Epub 2021 Aug 23.
10
The JAK inhibitor Tofacitinib inhibits structural damage in osteoarthritis by modulating JAK1/TNF-alpha/IL-6 signaling through Mir-149-5p.JAK 抑制剂托法替尼通过调节 JAK1/TNF-α/IL-6 信号通路来抑制骨关节炎的结构损伤，其作用机制与 Mir-149-5p 有关。
Bone. 2021 Oct;151:116024. doi: 10.1016/j.bone.2021.116024. Epub 2021 May 28.