CircRNA circ_0004058通过miR-221-3p和VE1激活途径调节蛛网膜下腔出血早期脑损伤

IF 4.3 2区 医学 Q1 CLINICAL NEUROLOGY
Hua Gu, Yong Cai
{"title":"CircRNA circ_0004058通过miR-221-3p和VE1激活途径调节蛛网膜下腔出血早期脑损伤","authors":"Hua Gu, Yong Cai","doi":"10.1007/s12975-025-01383-9","DOIUrl":null,"url":null,"abstract":"<p><p>Subarachnoid hemorrhage (SAH) frequently results in early brain injury (EBI), which remains a major barrier to favorable neurological recovery. Understanding the molecular underpinnings of EBI is crucial for developing targeted therapeutics. Circular RNAs (circRNAs) have emerged as influential molecular players in various brain injury contexts. This study focuses on one such molecule, circ_0004058, examining its impact on EBI through interaction with miR-221-3p and the VE1 signaling pathway. Utilizing an established SAH rodent model, our team conducted a detailed investigation of the expression patterns and interactions involving circ_0004058. Our analyses revealed a significant post-SAH upregulation of circ_0004058, which affected miR-221-3p activity and VE1 signaling. Furthermore, functional modulation of circ_0004058 expression altered the severity of EBI, presenting evidence that it serves as a critical determinant in the injury process. The results suggest that circ_0004058 holds promise as a therapeutic target, offering new possibilities for the development of strategies to mitigate SAH-induced brain damage. Through this study, circ_0004058 is highlighted not only as a biomarker but also as a possible avenue for therapeutic modulation in SAH management.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":""},"PeriodicalIF":4.3000,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"CircRNA circ_0004058 Modulates Early Brain Injury in Subarachnoid Hemorrhage Through miR-221-3p and VE1 Activation Pathway.\",\"authors\":\"Hua Gu, Yong Cai\",\"doi\":\"10.1007/s12975-025-01383-9\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Subarachnoid hemorrhage (SAH) frequently results in early brain injury (EBI), which remains a major barrier to favorable neurological recovery. Understanding the molecular underpinnings of EBI is crucial for developing targeted therapeutics. Circular RNAs (circRNAs) have emerged as influential molecular players in various brain injury contexts. This study focuses on one such molecule, circ_0004058, examining its impact on EBI through interaction with miR-221-3p and the VE1 signaling pathway. Utilizing an established SAH rodent model, our team conducted a detailed investigation of the expression patterns and interactions involving circ_0004058. Our analyses revealed a significant post-SAH upregulation of circ_0004058, which affected miR-221-3p activity and VE1 signaling. Furthermore, functional modulation of circ_0004058 expression altered the severity of EBI, presenting evidence that it serves as a critical determinant in the injury process. The results suggest that circ_0004058 holds promise as a therapeutic target, offering new possibilities for the development of strategies to mitigate SAH-induced brain damage. Through this study, circ_0004058 is highlighted not only as a biomarker but also as a possible avenue for therapeutic modulation in SAH management.</p>\",\"PeriodicalId\":23237,\"journal\":{\"name\":\"Translational Stroke Research\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":4.3000,\"publicationDate\":\"2025-09-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Translational Stroke Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s12975-025-01383-9\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Translational Stroke Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12975-025-01383-9","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0

摘要

蛛网膜下腔出血(SAH)经常导致早期脑损伤(EBI),这仍然是神经系统良好恢复的主要障碍。了解EBI的分子基础对于开发靶向治疗方法至关重要。环状rna (circRNAs)已成为各种脑损伤背景下有影响的分子参与者。本研究关注其中一个分子circ_0004058,通过与miR-221-3p和VE1信号通路的相互作用,研究其对EBI的影响。利用已建立的SAH啮齿动物模型,我们的团队对circ_0004058的表达模式和相互作用进行了详细的调查。我们的分析揭示了sah后circ_0004058的显著上调,这影响了miR-221-3p活性和VE1信号传导。此外,circ_0004058表达的功能调节改变了EBI的严重程度,这表明它在损伤过程中起着关键的决定作用。结果表明circ_0004058有望成为一种治疗靶点,为开发减轻sah诱导的脑损伤的策略提供了新的可能性。通过这项研究,circ_0004058不仅是一种生物标志物,而且是SAH治疗调节的可能途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
CircRNA circ_0004058 Modulates Early Brain Injury in Subarachnoid Hemorrhage Through miR-221-3p and VE1 Activation Pathway.

Subarachnoid hemorrhage (SAH) frequently results in early brain injury (EBI), which remains a major barrier to favorable neurological recovery. Understanding the molecular underpinnings of EBI is crucial for developing targeted therapeutics. Circular RNAs (circRNAs) have emerged as influential molecular players in various brain injury contexts. This study focuses on one such molecule, circ_0004058, examining its impact on EBI through interaction with miR-221-3p and the VE1 signaling pathway. Utilizing an established SAH rodent model, our team conducted a detailed investigation of the expression patterns and interactions involving circ_0004058. Our analyses revealed a significant post-SAH upregulation of circ_0004058, which affected miR-221-3p activity and VE1 signaling. Furthermore, functional modulation of circ_0004058 expression altered the severity of EBI, presenting evidence that it serves as a critical determinant in the injury process. The results suggest that circ_0004058 holds promise as a therapeutic target, offering new possibilities for the development of strategies to mitigate SAH-induced brain damage. Through this study, circ_0004058 is highlighted not only as a biomarker but also as a possible avenue for therapeutic modulation in SAH management.

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
Translational Stroke Research
Translational Stroke Research CLINICAL NEUROLOGY-NEUROSCIENCES
CiteScore
13.80
自引率
4.30%
发文量
130
审稿时长
6-12 weeks
期刊介绍: Translational Stroke Research covers basic, translational, and clinical studies. The Journal emphasizes novel approaches to help both to understand clinical phenomenon through basic science tools, and to translate basic science discoveries into the development of new strategies for the prevention, assessment, treatment, and enhancement of central nervous system repair after stroke and other forms of neurotrauma. Translational Stroke Research focuses on translational research and is relevant to both basic scientists and physicians, including but not restricted to neuroscientists, vascular biologists, neurologists, neuroimagers, and neurosurgeons.
×
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