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中国医药导刊 ›› 2024, Vol. 26 ›› Issue (10): 1053-1059.

• 管理实践 • 上一篇    下一篇

基于CiteSpace对国内外近十年关于高尿酸血症发病机制研究的可视化分析

童俐娜, 李花, 陆遥, 陶晓阳*   

  1. 上海交通大学医学院附属第九人民医院黄浦分院肾内科,上海 200011
  • 收稿日期:2024-08-26 修回日期:2024-10-30 出版日期:2024-10-28 发布日期:2024-10-28

Visualized Analysis of Researches on Pathogenesis of Hyperuricemia in Recent Ten Years at Home and Abroad Based on CiteSpace

  1. Department of Nephrology Huangpu Branch of Shanghai Ninth People's Hospital Shanghai Jiao Tong University School of
    Medicine Shanghai 200011, China
  • Received:2024-08-26 Revised:2024-10-30 Online:2024-10-28 Published:2024-10-28

摘要:

目的:基于CiteSpace软件对国内外近十年高尿酸血症发病机制研究进行可视化分析。方法:检索Web of ScienceWOS)及PubMed数据库中20141月至202312月发表的关于高尿酸血症发病机制的相关文献,应用CiteSpace软件对文献作者、国家及关键词进行可视化分析,使用对数似然率(LLR)聚类对中、英文关键词进行聚类分析。结果:共纳入2788篇文献,其中国内806篇,国外1982篇。20142023年,关于高尿酸血症发病机制研究的年度发文量总体呈缓步上升趋势,于2022年发文量最高,达388篇,2023年稍有回落,为363篇。通过作者及国家分析发现该研究领域作者间合作尚可,国家间合作相对紧密。关键词经LLR聚类分析共得到9个聚类,依次为uric acid(尿酸)、serum uric acid(血清尿酸)、oxidative stress(氧化应激)、chronic kidney disease(慢性肾脏疾病)、metabolic syndrome(代谢综合征)、hyperuricemic nephropathy(高尿酸血症肾病)、xanthine oxidase(黄嘌呤氧化酶)、xanthine oxidase inhibitor(黄嘌呤氧化酶抑制剂)及body mass index(体质量)。突现词分析显示,2019年以前高尿酸血症发病机制相关研究着眼于免疫细胞失调、炎症反应及氧化应激方面,2020年及以后,基于代谢组学技术日趋成熟,有充足证据表明肠道菌群紊乱及胆汁酸异常为高尿酸血症发病机制。结论:既往关于高尿酸血症发病机制的研究局限于细胞及组织层面,治疗方案相对匮乏,且缺乏个体化治疗,随着代谢技术日臻成熟,从分子层面角度出发,发现肠道菌群紊乱及胆汁酸异常为高尿酸血症发病机制,在高尿酸血症预防及个体化治疗中具有指导意义。

关键词: 高尿酸血症, 发病机制, CiteSpace, 可视化

Abstract:

Objective: To conduct a visualized analysis of researches on the pathogenesis of hyperuricemia in recent ten years in China and abroad based on CiteSpace software.Methods: Literature on the pathogenesis of hyperuricemia in the Web of Science WOS and PubMed databases from January 2014 to December 2023 were searched. CiteSpace software was used to conduct visualized analysis of the authors countries and keywords of the literature and logarithmic likelihood ratio LLR clustering was used to cluster Chinese and English keywords.Results: A total of 2788 articles were included including 806 domestic articles and 1982 foreign articles. From 2014 to 2023 the annual number of papers on the pathogenesis of hyperuricemia showed a gradual upward trend with the highest number of papers in 2022 reaching 388 and a slight decline in 2023 reaching 363. Through the analysis of authors and countries it was found that the cooperation between authors in this research field is reasonable and the cooperation between countries is relatively close. A total of 9 clusters were obtained by LLR cluster analysis which were uric acid serum uric acid oxidative stress chronic kidney disease metabolic syndrome hyperuricemic nephropathy xanthine oxidase xanthine oxidase inhibitor and body mass index. Burst word analysis showed that in 2019 and previous studies on the pathogenesis of hyperuricemia focused on immune cell dysfunction inflammatory response and oxidative stress. In 2020 and later based on the increasingly mature metabolomics technology there is sufficient evidence that intestinal flora disturbance and bile acid abnormalities are the pathogenesis of hyperuricemia.Conclusion: Previous studies on the pathogenesis of hyperuricemia were limited to the cellular and tissue levels and treatment plans were relatively scarce and individualized treatment was lacking. As metabolic technology became more and more mature it was found that intestinal flora disturbance and bile acid abnormality were the pathogenesis of hyperuricemia from the perspective of molecular level which had guiding significance in the prevention and individualized treatment of hyperuricemia.

 

Key words: Hyperuricemia , Pathogenesis , CiteSpace , Visualization

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