Coactivator Associated Arginine Methyltransferase 1 Modulates Cartilage Degeneration and Chondrocyte Apoptosis in Osteoarthritis by Regulating ERK1/2 Signaling Pathway.

IF 8 1区 医学 Q1 CELL BIOLOGY
Aging Cell Pub Date : 2025-07-03 DOI:10.1111/acel.70122
Jie Yuan, Jingyuan Tian, Ruxing Liu, Xiaoting Qiu, Dongqin He, Guanghui He, Tao Zhang, Pengcui Li, Bin Zhao, Yongfeng Wang
{"title":"Coactivator Associated Arginine Methyltransferase 1 Modulates Cartilage Degeneration and Chondrocyte Apoptosis in Osteoarthritis by Regulating ERK1/2 Signaling Pathway.","authors":"Jie Yuan, Jingyuan Tian, Ruxing Liu, Xiaoting Qiu, Dongqin He, Guanghui He, Tao Zhang, Pengcui Li, Bin Zhao, Yongfeng Wang","doi":"10.1111/acel.70122","DOIUrl":null,"url":null,"abstract":"<p><p>This study investigates the role and mechanism of Coactivator Associated Arginine Methyltransferase 1 (CARM1) in osteoarthritis (OA). OA is a prevalent joint disease characterized by cartilage degradation, subchondral bone remodeling, and inflammation. Our research revealed that CARM1 expression is significantly increased in the cartilage tissues of OA patients and OA model mice. Experimental results showed that inhibiting CARM1 reduces cartilage matrix degradation and chondrocyte apoptosis, while overexpression of CARM1 exacerbates these conditions. Mechanistically, CARM1 regulates OA progression through the phosphorylation of the ERK1/2 signaling pathway. Inhibition of CARM1 suppresses ERK1/2 activation, thereby reducing extracellular matrix degradation and chondrocyte apoptosis. These findings suggest that the CARM1-ERK1/2 axis is crucial in modulating cartilage matrix metabolism and chondrocyte apoptosis in OA, highlighting CARM1 as a potential therapeutic target for OA treatment.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e70122"},"PeriodicalIF":8.0000,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Aging Cell","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1111/acel.70122","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

This study investigates the role and mechanism of Coactivator Associated Arginine Methyltransferase 1 (CARM1) in osteoarthritis (OA). OA is a prevalent joint disease characterized by cartilage degradation, subchondral bone remodeling, and inflammation. Our research revealed that CARM1 expression is significantly increased in the cartilage tissues of OA patients and OA model mice. Experimental results showed that inhibiting CARM1 reduces cartilage matrix degradation and chondrocyte apoptosis, while overexpression of CARM1 exacerbates these conditions. Mechanistically, CARM1 regulates OA progression through the phosphorylation of the ERK1/2 signaling pathway. Inhibition of CARM1 suppresses ERK1/2 activation, thereby reducing extracellular matrix degradation and chondrocyte apoptosis. These findings suggest that the CARM1-ERK1/2 axis is crucial in modulating cartilage matrix metabolism and chondrocyte apoptosis in OA, highlighting CARM1 as a potential therapeutic target for OA treatment.

辅助激活因子相关精氨酸甲基转移酶1通过调节ERK1/2信号通路调节骨关节炎软骨退变和软骨细胞凋亡。
本研究探讨了辅助激活因子相关精氨酸甲基转移酶1 (CARM1)在骨关节炎(OA)中的作用和机制。骨性关节炎是一种常见的关节疾病,以软骨退化、软骨下骨重塑和炎症为特征。我们的研究发现,CARM1在OA患者和OA模型小鼠的软骨组织中表达明显升高。实验结果表明,抑制CARM1可减少软骨基质降解和软骨细胞凋亡,而过表达CARM1则会加剧这些情况。在机制上,CARM1通过磷酸化ERK1/2信号通路调节OA的进展。CARM1的抑制抑制ERK1/2的激活,从而减少细胞外基质降解和软骨细胞凋亡。这些发现表明,CARM1- erk1 /2轴在骨性关节炎中调节软骨基质代谢和软骨细胞凋亡至关重要,强调CARM1是骨性关节炎治疗的潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Aging Cell
Aging Cell Biochemistry, Genetics and Molecular Biology-Cell Biology
自引率
2.60%
发文量
212
期刊介绍: Aging Cell is an Open Access journal that focuses on the core aspects of the biology of aging, encompassing the entire spectrum of geroscience. The journal's content is dedicated to publishing research that uncovers the mechanisms behind the aging process and explores the connections between aging and various age-related diseases. This journal aims to provide a comprehensive understanding of the biological underpinnings of aging and its implications for human health. The journal is widely recognized and its content is abstracted and indexed by numerous databases and services, which facilitates its accessibility and impact in the scientific community. These include: Academic Search (EBSCO Publishing) Academic Search Alumni Edition (EBSCO Publishing) Academic Search Premier (EBSCO Publishing) Biological Science Database (ProQuest) CAS: Chemical Abstracts Service (ACS) Embase (Elsevier) InfoTrac (GALE Cengage) Ingenta Select ISI Alerting Services Journal Citation Reports/Science Edition (Clarivate Analytics) MEDLINE/PubMed (NLM) Natural Science Collection (ProQuest) PubMed Dietary Supplement Subset (NLM) Science Citation Index Expanded (Clarivate Analytics) SciTech Premium Collection (ProQuest) Web of Science (Clarivate Analytics) Being indexed in these databases ensures that the research published in Aging Cell is discoverable by researchers, clinicians, and other professionals interested in the field of aging and its associated health issues. This broad coverage helps to disseminate the journal's findings and contributes to the advancement of knowledge in geroscience.
×
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