单细胞水平上超载诱导TMJ髁突软骨终末分化的机制研究。

IF 11.6
Smart medicine Pub Date : 2025-07-30 eCollection Date: 2025-09-01 DOI:10.1002/smmd.70011
Dian Zhou, Yiling Jiang, Yingcui Li, Huanyu Zeng, Xinchun Li, Yufang He, Xin Wang, Yiteng Liang, Vojtech Parizek, Ousheng Liu, Zhangui Tang, Yueying Zhou
{"title":"单细胞水平上超载诱导TMJ髁突软骨终末分化的机制研究。","authors":"Dian Zhou, Yiling Jiang, Yingcui Li, Huanyu Zeng, Xinchun Li, Yufang He, Xin Wang, Yiteng Liang, Vojtech Parizek, Ousheng Liu, Zhangui Tang, Yueying Zhou","doi":"10.1002/smmd.70011","DOIUrl":null,"url":null,"abstract":"<p><p>The incidence of temporomandibular joint (TMJ) degeneration has been steadily increasing, with overloading identified as a major risk factor. This condition often leads to condylar cartilage degeneration, significantly affecting patients' quality of life; however, the molecular mechanisms underlying this process remain poorly understood, and effective treatments are still lacking. We utilized single-nucleus RNA sequencing to analyze the condylar cartilage in an overloading mouse model. This approach enabled the identification of 11 distinct cell types within the condylar chondrocytes. Through the application of pseudotime trajectory Analysis and cellchat analyses, we identified the key gene Acvr1b and its associated signaling pathway, which are crucial for regulating the terminal differentiation of condylar chondrocytes. This study utilized single-nucleus RNA sequencing and in vitro validation to investigate the role of Acvr1b in TMJ cartilage degeneration under overloading stress. Our findings reveal key pathways involved in chondrocyte differentiation, providing a theoretical basis for the development of targeted therapeutic interventions.</p>","PeriodicalId":74816,"journal":{"name":"Smart medicine","volume":"4 3","pages":"e70011"},"PeriodicalIF":11.6000,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12362756/pdf/","citationCount":"0","resultStr":"{\"title\":\"Mechanistic Insights Into Overloading-Induced Terminal Differentiation of TMJ Condylar Cartilage at the Single Cell Level.\",\"authors\":\"Dian Zhou, Yiling Jiang, Yingcui Li, Huanyu Zeng, Xinchun Li, Yufang He, Xin Wang, Yiteng Liang, Vojtech Parizek, Ousheng Liu, Zhangui Tang, Yueying Zhou\",\"doi\":\"10.1002/smmd.70011\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The incidence of temporomandibular joint (TMJ) degeneration has been steadily increasing, with overloading identified as a major risk factor. This condition often leads to condylar cartilage degeneration, significantly affecting patients' quality of life; however, the molecular mechanisms underlying this process remain poorly understood, and effective treatments are still lacking. We utilized single-nucleus RNA sequencing to analyze the condylar cartilage in an overloading mouse model. This approach enabled the identification of 11 distinct cell types within the condylar chondrocytes. Through the application of pseudotime trajectory Analysis and cellchat analyses, we identified the key gene Acvr1b and its associated signaling pathway, which are crucial for regulating the terminal differentiation of condylar chondrocytes. This study utilized single-nucleus RNA sequencing and in vitro validation to investigate the role of Acvr1b in TMJ cartilage degeneration under overloading stress. Our findings reveal key pathways involved in chondrocyte differentiation, providing a theoretical basis for the development of targeted therapeutic interventions.</p>\",\"PeriodicalId\":74816,\"journal\":{\"name\":\"Smart medicine\",\"volume\":\"4 3\",\"pages\":\"e70011\"},\"PeriodicalIF\":11.6000,\"publicationDate\":\"2025-07-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12362756/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Smart medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1002/smmd.70011\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/9/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Smart medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/smmd.70011","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/9/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

颞下颌关节(TMJ)退变的发病率一直在稳步上升,超载被认为是一个主要的危险因素。这种情况常导致髁突软骨退变,明显影响患者的生活质量;然而,这一过程背后的分子机制仍然知之甚少,并且仍然缺乏有效的治疗方法。我们利用单核RNA测序来分析超载小鼠模型中的髁软骨。这种方法能够鉴定出髁突软骨细胞内11种不同的细胞类型。通过伪时间轨迹分析和细胞chat分析,我们确定了调控髁突软骨细胞终末分化的关键基因Acvr1b及其相关信号通路。本研究利用单核RNA测序和体外验证研究Acvr1b在超载应激下TMJ软骨退变中的作用。我们的发现揭示了参与软骨细胞分化的关键途径,为靶向治疗干预的发展提供了理论基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanistic Insights Into Overloading-Induced Terminal Differentiation of TMJ Condylar Cartilage at the Single Cell Level.

The incidence of temporomandibular joint (TMJ) degeneration has been steadily increasing, with overloading identified as a major risk factor. This condition often leads to condylar cartilage degeneration, significantly affecting patients' quality of life; however, the molecular mechanisms underlying this process remain poorly understood, and effective treatments are still lacking. We utilized single-nucleus RNA sequencing to analyze the condylar cartilage in an overloading mouse model. This approach enabled the identification of 11 distinct cell types within the condylar chondrocytes. Through the application of pseudotime trajectory Analysis and cellchat analyses, we identified the key gene Acvr1b and its associated signaling pathway, which are crucial for regulating the terminal differentiation of condylar chondrocytes. This study utilized single-nucleus RNA sequencing and in vitro validation to investigate the role of Acvr1b in TMJ cartilage degeneration under overloading stress. Our findings reveal key pathways involved in chondrocyte differentiation, providing a theoretical basis for the development of targeted therapeutic interventions.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信