TWEAK/Fn14 axis may promote vascular smooth muscle cell senescence via p38 signaling pathway: preliminary evidence.

IF 2.4 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Future Science OA Pub Date : 2025-12-01 Epub Date: 2025-01-22 DOI:10.1080/20565623.2025.2455906
Chunyang Wei, Xiaoying Liu, Zhuang Miao, Hua Zhang, Yanfu Wang, Guoxian Qi
{"title":"TWEAK/Fn14 axis may promote vascular smooth muscle cell senescence via p38 signaling pathway: preliminary evidence.","authors":"Chunyang Wei, Xiaoying Liu, Zhuang Miao, Hua Zhang, Yanfu Wang, Guoxian Qi","doi":"10.1080/20565623.2025.2455906","DOIUrl":null,"url":null,"abstract":"<p><strong>Aim: </strong>The primary objective of this study is to investigate the impact of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its functional receptor, fibroblast growth factor-inducible 14 (Fn14), on the process of vascular smooth muscle cell (VSMC) senescence.</p><p><strong>Methods: </strong>Rat arterial VSMCs were cultured with angiotensin II to establish a model of premature senescence. The effects of TWEAK and Fn14 on senescent VSMCs were evaluated. Additionally, the role of p38 phosphorylation pathway in the effect of TWEAK on VSMCs senescence was assessed.</p><p><strong>Results: </strong>Expressions of TWEAK and Fn14 were significantly elevated in senescent VSMCs. TWEAK activated the p38 phosphorylation pathway and promoted the SA-β-gal staining and P53 expression.</p><p><strong>Conclusion: </strong>These preliminary findings suggest that the TWEAK/Fn14 axis may play a crucial role in promoting VSMC senescence.</p>","PeriodicalId":12568,"journal":{"name":"Future Science OA","volume":"11 1","pages":"2455906"},"PeriodicalIF":2.4000,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11756581/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Future Science OA","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/20565623.2025.2455906","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/22 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0

Abstract

Aim: The primary objective of this study is to investigate the impact of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its functional receptor, fibroblast growth factor-inducible 14 (Fn14), on the process of vascular smooth muscle cell (VSMC) senescence.

Methods: Rat arterial VSMCs were cultured with angiotensin II to establish a model of premature senescence. The effects of TWEAK and Fn14 on senescent VSMCs were evaluated. Additionally, the role of p38 phosphorylation pathway in the effect of TWEAK on VSMCs senescence was assessed.

Results: Expressions of TWEAK and Fn14 were significantly elevated in senescent VSMCs. TWEAK activated the p38 phosphorylation pathway and promoted the SA-β-gal staining and P53 expression.

Conclusion: These preliminary findings suggest that the TWEAK/Fn14 axis may play a crucial role in promoting VSMC senescence.

TWEAK/Fn14轴可能通过p38信号通路促进血管平滑肌细胞衰老:初步证据
目的:研究肿瘤坏死因子样细胞凋亡弱诱导剂(TWEAK)及其功能受体成纤维细胞生长因子诱导14 (Fn14)对血管平滑肌细胞(VSMC)衰老过程的影响。方法:采用血管紧张素ⅱ培养大鼠动脉VSMCs,建立早衰模型。观察TWEAK和Fn14对衰老VSMCs的影响。此外,我们还评估了p38磷酸化途径在TWEAK对VSMCs衰老的影响中的作用。结果:在衰老VSMCs中,TWEAK和Fn14的表达显著升高。TWEAK激活p38磷酸化通路,促进SA-β-gal染色和P53表达。结论:上述初步发现提示TWEAK/Fn14轴可能在VSMC衰老过程中起重要作用。
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
Future Science OA
Future Science OA MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
5.00
自引率
4.00%
发文量
48
审稿时长
13 weeks
期刊介绍: Future Science OA is an online, open access, peer-reviewed title from the Future Science Group. The journal covers research and discussion related to advances in biotechnology, medicine and health. The journal embraces the importance of publishing all good-quality research with the potential to further the progress of research in these fields. All original research articles will be considered that are within the journal''s scope, and have been conducted with scientific rigour and research integrity. The journal also features review articles, editorials and perspectives, providing readers with a leading source of commentary and analysis. Submissions of the following article types will be considered: -Research articles -Preliminary communications -Short communications -Methodologies -Trial design articles -Trial results (including early-phase and negative studies) -Reviews -Perspectives -Commentaries
×
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:481959085
Book学术官方微信