Global perspectives and hotspots of VEGF signaling pathway in liver disease from 2008 to 2023: A bibliometric analysis and visualization

2008年至2023年全球VEGF信号通路在肝病中的应用现状及热点:文献计量分析与可视化

阅读:2

Abstract

BACKGROUND: The vascular endothelial growth factor (VEGF) signaling pathway is closely related to pathological angiogenesis in liver disease. Anti-angiogenesis is an effective intervention in the clinical treatment of liver disease. Some antiangiogenic drugs are resistant and have limitations in clinical use. METHODS: This research uses bibliometric methods to assess the literature on the VEGF signaling pathway in liver disease from 2008 to 2023. RESULTS: The number of publications has generally increased over the past 16 years, meaning that enormous researchers are interested in this field. China and the USA have published the most articles and cooperate closely with each other. Plos one has published the largest number of articles in this area, and Hepatology and Journal of Hepatology is the most authoritative journal. Llovet JM is an outstanding researcher in the field with the highest citations. Keywords and research hotspots analysis indicated that researchers are very concerned about the application and clinical research status of anti-angiogenic drugs in hepatocellular carcinoma (HCC). Continuing to deepen the research on the use of anti-angiogenic drugs alone and in combination is necessary. In addition, the resistance of anti-angiogenic therapeutic drugs leads to a complex mechanism of angiogenesis response caused by hypoxia, which requires further research. CONCLUSIONS: This study analyzed the research situation related to the VEGF signaling pathway in liver disease from a bibliometric and visual perspective. Our analysis helps researchers better understand the research directions and hotspots in this area, enabling them to better carry out research in the future.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。