• 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

关于肥大软骨细胞表型变化在骨关节炎发生和发展中作用的最新见解

Recent Insights into the Contribution of the Changing Hypertrophic Chondrocyte Phenotype in the Development and Progression of Osteoarthritis.

作者信息

Ripmeester Ellen G J, Timur Ufuk Tan, Caron Marjolein M J, Welting Tim J M

机构信息

Laboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University Medical Center, Maastricht, Netherlands.

出版信息

Front Bioeng Biotechnol. 2018 Mar 19;6:18. doi: 10.3389/fbioe.2018.00018. eCollection 2018.

DOI:10.3389/fbioe.2018.00018
PMID:29616218
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5867295/
Abstract

Osteoarthritis (OA) is an extremely prevalent age-related condition. The economic and societal burden due to the cost of symptomatic treatment, inability to work, joint replacement, and rehabilitation is huge and increasing. Currently, there are no effective medical therapies that delay or reverse the pathological manifestations of OA. Current treatment options are, without exception, focused on slowing down progression of the disease to postpone total joint replacement surgery for as long as possible and keeping the associated pain and joint immobility manageable. Alterations in the articular cartilage chondrocyte phenotype might be fundamental in the pathological mechanisms of OA development. In many ways, the changing chondrocyte phenotype in osteoarthritic cartilage resembles the process of endochondral ossification as seen, for instance, in developing growth plates. However, the relative contribution of endochondral ossification to the changing chondrocyte phenotype in the development and progression of OA remains poorly described. In this review, we will discuss the current knowledge regarding the cartilage endochondral phenotypic changes occurring during OA development and progression, as well as the molecular and environmental effectors driving these changes. Understanding how these molecular mechanisms determine the chondrocyte cell fate in OA will be essential in enabling cartilage regenerative approaches in future treatments of OA.

摘要

骨关节炎(OA)是一种极为常见的与年龄相关的病症。由于对症治疗成本、无法工作、关节置换及康复等造成的经济和社会负担巨大且不断增加。目前,尚无有效的医学疗法能够延缓或逆转OA的病理表现。当前所有的治疗选择无一例外都聚焦于减缓疾病进展,以尽可能推迟全关节置换手术,并使相关疼痛和关节活动障碍处于可控状态。关节软骨软骨细胞表型的改变可能是OA发病病理机制的根本所在。在许多方面,骨关节炎软骨中不断变化的软骨细胞表型类似于例如发育中的生长板中所见的软骨内成骨过程。然而,软骨内成骨在OA发生发展过程中对软骨细胞表型变化的相对贡献仍描述甚少。在本综述中,我们将讨论有关OA发生发展过程中软骨内表型变化的现有知识,以及驱动这些变化的分子和环境效应物。了解这些分子机制如何决定OA中软骨细胞的细胞命运对于在未来OA治疗中实现软骨再生方法至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5867295/d0c976c30505/fbioe-06-00018-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5867295/b6c6bb6ca61b/fbioe-06-00018-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5867295/3d6c0f83ba7a/fbioe-06-00018-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5867295/78d84022d097/fbioe-06-00018-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5867295/809dfd9bcab5/fbioe-06-00018-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5867295/a86def05873c/fbioe-06-00018-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5867295/d0c976c30505/fbioe-06-00018-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5867295/b6c6bb6ca61b/fbioe-06-00018-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5867295/3d6c0f83ba7a/fbioe-06-00018-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5867295/78d84022d097/fbioe-06-00018-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5867295/809dfd9bcab5/fbioe-06-00018-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5867295/a86def05873c/fbioe-06-00018-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5867295/d0c976c30505/fbioe-06-00018-g006.jpg

相似文献

1
Recent Insights into the Contribution of the Changing Hypertrophic Chondrocyte Phenotype in the Development and Progression of Osteoarthritis.关于肥大软骨细胞表型变化在骨关节炎发生和发展中作用的最新见解
Front Bioeng Biotechnol. 2018 Mar 19;6:18. doi: 10.3389/fbioe.2018.00018. eCollection 2018.
2
Identification of TGFβ-related genes regulated in murine osteoarthritis and chondrocyte hypertrophy by comparison of multiple microarray datasets.通过比较多个微阵列数据集鉴定与小鼠骨关节炎和软骨细胞肥大相关的 TGFβ 调控基因。
Bone. 2018 Nov;116:67-77. doi: 10.1016/j.bone.2018.07.008. Epub 2018 Jul 21.
3
Functional Duality of Chondrocyte Hypertrophy and Biomedical Application Trends in Osteoarthritis.软骨细胞肥大的功能二元性与骨关节炎的生物医学应用趋势
Pharmaceutics. 2021 Jul 26;13(8):1139. doi: 10.3390/pharmaceutics13081139.
4
Cartilage degradation in osteoarthritis: A process of osteochondral remodeling resembles the endochondral ossification in growth plate?骨关节炎中的软骨降解:类似于生长板的软骨内骨化过程的骨软骨重塑?
Med Hypotheses. 2018 Dec;121:183-187. doi: 10.1016/j.mehy.2018.08.023. Epub 2018 Aug 27.
5
Col10a1-Runx2 transgenic mice with delayed chondrocyte maturation are less susceptible to developing osteoarthritis.软骨细胞成熟延迟的Col10a1-Runx2转基因小鼠患骨关节炎的易感性较低。
Am J Transl Res. 2014 Nov 22;6(6):736-45. eCollection 2014.
6
Promoting Endochondral Bone Repair Using Human Osteoarthritic Articular Chondrocytes.利用人骨关节炎关节软骨细胞促进软骨内骨修复
Tissue Eng Part A. 2016 Mar;22(5-6):427-35. doi: 10.1089/ten.TEA.2014.0705. Epub 2016 Mar 14.
7
[RESEARCH PROGRESS OF PATHOLOGY OF ENDOCHONDRAL OSSIFICATION IN OSTEOARTHRITIS].[骨关节炎中软骨内成骨的病理学研究进展]
Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2016 Dec 8;30(12):1556-1561. doi: 10.7507/1002-1892.20160320.
8
Molecular regulation of articular chondrocyte function and its significance in osteoarthritis.关节软骨细胞功能的分子调控及其在骨关节炎中的意义。
Histol Histopathol. 2011 Mar;26(3):377-94. doi: 10.14670/HH-26.377.
9
Chondrocyte and mesenchymal stem cell-based therapies for cartilage repair in osteoarthritis and related orthopaedic conditions.基于软骨细胞和间充质干细胞的疗法用于骨关节炎及相关骨科疾病的软骨修复
Maturitas. 2014 Jul;78(3):188-98. doi: 10.1016/j.maturitas.2014.04.017. Epub 2014 May 2.
10
Chondrocyte Hypertrophy in Osteoarthritis: Mechanistic Studies and Models for the Identification of New Therapeutic Strategies.骨关节炎中的软骨细胞肥大:机制研究和新治疗策略的鉴定模型。
Cells. 2022 Dec 13;11(24):4034. doi: 10.3390/cells11244034.

引用本文的文献

1
Translational genomics of osteoarthritis in 1,962,069 individuals.1962069例个体骨关节炎的转化基因组学研究
Nature. 2025 Apr 9. doi: 10.1038/s41586-025-08771-z.
2
Pararamosis, a Neglected Tropical Disease Induced by Caterpillar Toxins: Investigating Their Effects on Synovial Cell Inflammation.副拉雷莫斯病,一种由毛虫毒素引起的被忽视的热带病:探究其对滑膜细胞炎症的影响。
Int J Mol Sci. 2024 Dec 6;25(23):13149. doi: 10.3390/ijms252313149.
3
Differential Expression of Neurodegeneration-Related Genes in SH-SY5Y Neuroblastoma Cells Under the Influence of Cyclophilin A: Could the Enzyme be a Likely Trigger and Therapeutic Target for Alzheimer's Disease?

本文引用的文献

1
Classification of patients with knee osteoarthritis in clinical phenotypes: Data from the osteoarthritis initiative.膝关节骨关节炎患者临床表型分类:骨关节炎倡议组织的数据。
PLoS One. 2018 Jan 12;13(1):e0191045. doi: 10.1371/journal.pone.0191045. eCollection 2018.
2
Toward classification criteria for early osteoarthritis of the knee.膝关节早期骨关节炎的分类标准研究。
Semin Arthritis Rheum. 2018 Feb;47(4):457-463. doi: 10.1016/j.semarthrit.2017.08.006. Epub 2017 Aug 9.
3
Knee osteoarthritis phenotypes and their relevance for outcomes: a systematic review.
亲环蛋白A影响下SH-SY5Y神经母细胞瘤细胞中神经退行性变相关基因的差异表达:该酶可能是阿尔茨海默病的触发因素和治疗靶点吗?
Neurochem Res. 2024 Dec 5;50(1):47. doi: 10.1007/s11064-024-04253-2.
4
New role of calcium-binding fluorescent dye alizarin complexone in detecting permeability from articular cartilage to subchondral bone.钙结合荧光染料茜素氨羧络合剂在检测关节软骨至软骨下骨通透性中的新作用。
FASEB Bioadv. 2024 Oct 7;6(11):539-554. doi: 10.1096/fba.2024-00103. eCollection 2024 Nov.
5
Effects of the oral administration of glycosaminoglycans with or without native type II collagen on the articular cartilage transcriptome in an osteoarthritic-induced rabbit model.在骨关节炎诱导的兔模型中,口服含或不含天然II型胶原蛋白的糖胺聚糖对关节软骨转录组的影响。
Genes Nutr. 2024 Sep 4;19(1):19. doi: 10.1186/s12263-024-00749-2.
6
Ossification of the posterior longitudinal ligament is linked to heterotopic ossification of the ankle/foot tendons.后纵韧带骨化与踝/足部肌腱异位骨化有关。
J Bone Miner Metab. 2024 Sep;42(5):538-550. doi: 10.1007/s00774-024-01518-2. Epub 2024 Jun 8.
7
Klf10 is involved in extracellular matrix calcification of chondrocytes alleviating chondrocyte senescence.Klf10 参与软骨细胞细胞外基质钙化,从而缓解软骨细胞衰老。
J Transl Med. 2024 Jan 13;22(1):52. doi: 10.1186/s12967-023-04666-7.
8
Small RNA signatures of the anterior cruciate ligament from patients with knee joint osteoarthritis.膝关节骨关节炎患者前交叉韧带的小RNA特征
Front Mol Biosci. 2023 Dec 21;10:1266088. doi: 10.3389/fmolb.2023.1266088. eCollection 2023.
9
The CREB1 inhibitor 666-15 maintains cartilage homeostasis and mitigates osteoarthritis progression.CREB1抑制剂666-15维持软骨稳态并减轻骨关节炎进展。
Bone Joint Res. 2024 Jan 2;13(1):4-18. doi: 10.1302/2046-3758.131.BJR-2023-0016.R2.
10
A New Bioactive Fibrin Formulation Provided Superior Cartilage Regeneration in a Caprine Model.新型生物活性纤维蛋白配方在山羊模型中提供了更优的软骨再生效果。
Int J Mol Sci. 2023 Nov 29;24(23):16945. doi: 10.3390/ijms242316945.
膝关节骨关节炎表型及其与结局的相关性:系统评价。
Osteoarthritis Cartilage. 2017 Dec;25(12):1926-1941. doi: 10.1016/j.joca.2017.08.009. Epub 2017 Aug 25.
4
The changing role of TGFβ in healthy, ageing and osteoarthritic joints.TGFβ 在健康、衰老和骨关节炎关节中的作用变化。
Nat Rev Rheumatol. 2017 Mar;13(3):155-163. doi: 10.1038/nrrheum.2016.219. Epub 2017 Feb 2.
5
mTORC1 activation downregulates FGFR3 and PTH/PTHrP receptor in articular chondrocytes to initiate osteoarthritis.mTORC1激活下调关节软骨细胞中的FGFR3和PTH/PTHrP受体,从而引发骨关节炎。
Osteoarthritis Cartilage. 2017 Jun;25(6):952-963. doi: 10.1016/j.joca.2016.12.024. Epub 2016 Dec 31.
6
The inhibition of EZH2 ameliorates osteoarthritis development through the Wnt/β-catenin pathway.EZH2 的抑制通过 Wnt/β-catenin 通路改善骨关节炎的发展。
Sci Rep. 2016 Aug 19;6:29176. doi: 10.1038/srep29176.
7
Notch signalling in context.Notch 信号通路在语境中的作用。
Nat Rev Mol Cell Biol. 2016 Nov;17(11):722-735. doi: 10.1038/nrm.2016.94. Epub 2016 Aug 10.
8
Corrigendum: Pterosin B prevents chondrocyte hypertrophy and osteoarthritis in mice by inhibiting Sik3.勘误:蝶黄素B通过抑制Sik3预防小鼠软骨细胞肥大和骨关节炎。
Nat Commun. 2016 Jun 27;7:12117. doi: 10.1038/ncomms12117.
9
Chondromodulin-1 ameliorates osteoarthritis progression by inhibiting HIF-2α activity.软骨调节素-1 通过抑制 HIF-2α 活性来改善骨关节炎的进展。
Osteoarthritis Cartilage. 2016 Nov;24(11):1970-1980. doi: 10.1016/j.joca.2016.06.005. Epub 2016 Jun 16.
10
Fibroblast Growth Factor 23 drives MMP13 expression in human osteoarthritic chondrocytes in a Klotho-independent manner.成纤维细胞生长因子 23 以 Klotho 非依赖的方式驱动人骨性关节炎软骨细胞中 MMP13 的表达。
Osteoarthritis Cartilage. 2016 Nov;24(11):1961-1969. doi: 10.1016/j.joca.2016.06.003. Epub 2016 Jun 13.