{"title":"主动脉夹层中分子驱动因素的影响","authors":"Cuihong Tian, Yequn Chen, Xuerui Tan","doi":"10.1002/ctd2.323","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Background</h3>\n \n <p>Aortic dissection (AD) is a lethal cardiovascular emergency involving high mortality and disability. However, its specific pathogenesis remains to be elucidated.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>A bibliometric analysis based on the Web of Science database, VOSviewer software and Citex platforms was conducted to have a knowledge of the development trends, frontiers and hot spots of AD. Subsequently, the top five AD-related genes from the titles and abstracts of published literature were searched. Lastly, the roles of the top five genes and their encoded proteins in the onset of AD were reviewed.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>The bibliometrics showed that most studies are exploring the molecular drivers related to AD, especially gene mutations. The top five AD-related genes were transforming growth factor-β (<i>TGFB</i>)-related genes, elastin (<i>ELN</i>), fibrillin-1 (<i>FBN1</i>), angiotensinogen (<i>AGT</i>) and matrix metalloproteinase 9 (<i>MMP9</i>). In particular, regulation of the structure of elastic fiber by <i>TGFB-</i>related genes<i>, ELN</i> and <i>FBN1</i>, appears to be the principal mechanism contributing to AD onset. Activation of the renin-angiotensin system is the principal mechanism by which <i>AGT</i> triggers AD. <i>MMP9</i> promotes the formation and development of AD by degrading extracellular matrix components.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p><i>TGFB, ELN, FBN1, AGT</i> and <i>MMP9</i> are the five top molecular drivers of AD, providing a comprehensive mechanistic insight into AD.</p>\n </section>\n </div>","PeriodicalId":72605,"journal":{"name":"Clinical and translational discovery","volume":"4 4","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ctd2.323","citationCount":"0","resultStr":"{\"title\":\"Impacts of molecular drivers in aortic dissection\",\"authors\":\"Cuihong Tian, Yequn Chen, Xuerui Tan\",\"doi\":\"10.1002/ctd2.323\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Background</h3>\\n \\n <p>Aortic dissection (AD) is a lethal cardiovascular emergency involving high mortality and disability. 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引用次数: 0
摘要
背景 主动脉夹层（AD）是一种致命的心血管急症，死亡率和致残率都很高。然而，其具体发病机制仍有待阐明。 方法 基于 Web of Science 数据库、VOSviewer 软件和 Citex 平台进行文献计量分析，以了解 AD 的发展趋势、前沿和热点。随后，从已发表文献的标题和摘要中搜索与 AD 相关的前五位基因。最后，对这五大基因及其编码的蛋白质在 AD 发病中的作用进行了综述。 结果 文献计量学显示，大多数研究都在探索与AD相关的分子驱动因素，尤其是基因突变。与AD相关的前五位基因是转化生长因子-β（TGFB）相关基因、弹性蛋白（ELN）、纤连蛋白-1（FBN1）、血管紧张素原（AGT）和基质金属蛋白酶9（MMP9）。其中，TGFB 相关基因 ELN 和 FBN1 对弹性纤维结构的调节似乎是导致注意力缺失症发病的主要机制。肾素-血管紧张素系统的激活是 AGT 引发注意力缺失症的主要机制。MMP9 通过降解细胞外基质成分促进 AD 的形成和发展。 结论 TGFB、ELN、FBN1、AGT和MMP9是导致AD的五大分子驱动因素，它们从机理上全面揭示了AD。
Aortic dissection (AD) is a lethal cardiovascular emergency involving high mortality and disability. However, its specific pathogenesis remains to be elucidated.
Methods
A bibliometric analysis based on the Web of Science database, VOSviewer software and Citex platforms was conducted to have a knowledge of the development trends, frontiers and hot spots of AD. Subsequently, the top five AD-related genes from the titles and abstracts of published literature were searched. Lastly, the roles of the top five genes and their encoded proteins in the onset of AD were reviewed.
Results
The bibliometrics showed that most studies are exploring the molecular drivers related to AD, especially gene mutations. The top five AD-related genes were transforming growth factor-β (TGFB)-related genes, elastin (ELN), fibrillin-1 (FBN1), angiotensinogen (AGT) and matrix metalloproteinase 9 (MMP9). In particular, regulation of the structure of elastic fiber by TGFB-related genes, ELN and FBN1, appears to be the principal mechanism contributing to AD onset. Activation of the renin-angiotensin system is the principal mechanism by which AGT triggers AD. MMP9 promotes the formation and development of AD by degrading extracellular matrix components.
Conclusion
TGFB, ELN, FBN1, AGT and MMP9 are the five top molecular drivers of AD, providing a comprehensive mechanistic insight into AD.
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