摘要
目的 本研究通过分析肝硬化生物标志物领域的发文情况、共现、聚类、共被引及可视化分析，探索该领域2013年至2023年的发展状况、研究热点及动态前沿，为该范畴相关人员发展学术研讨提供参考。方法 在Web of Science （WOS）数据库中检索肝硬化生物标志物相关的英文文献（论著或综述）为对象，发表日期限定为2013 年—2023年。运用 CiteSpace 软件对检索到的文献进行可视化分析，并绘制相关可视化图谱。结果 共获得1469 篇文献，结果表明，肝硬化生物标志物范畴文献数量整体呈上升趋向。通过关键词聚类生成 4 个图谱，聚类结果显示研究集中于P53基因、growth factor（生长因子）、long noncoding RNA（长非编码RNA）及miRNA。结论 本研究使用citespace 软件对肝硬化生物标志物可视化分析，初步揭示该领域发展的动态前沿，特别是在长非编码RNA和miRNA这方面的生物标志物用于肝硬化的诊断将会在未来的研究中占有极其重要地位。
关键词： 肝硬化；生物标志物；Web of Science；CiteSpace；可视化分析
Abstract
Objective By analyzing the publication, co-occurrence, clustering, co-citation and visual analysis in the field of liver cirrhosis biomarkers, the study explored the development status, research hotspots and dynamic frontiers of this field from 2013 to 2023, and provided references for the development of academic research for relevant personnel in this field. Methods The English literature on liver cirrhosis biomarkers was searched in the Web of Science (WOS) database, and the publication dates were limited to2013-2023.CiteSpace software was used to visually analyze the retrieved literature and draw the relevant visual maps. Results A total of 1469 literatures were obtained, and the results showed that the number of literatures in the category of liver cirrhosis biomarkers showed an increasing trend. Four maps were generated by keyword clustering, and the clustering results showed that the research focused on P53 gene, growth factor, long noncoding RNA and miRNA. Conclusion In this study, CiteSpace software was used for visual analysis of liver cirrhosis biomarkers, which initially revealed the dynamic frontier of development in this field. In particular, biomarkers in long non-coding RNA and miRNA for the diagnosis of liver cirrhosis will play an extremely important role in future studies.
Key words： Cirrhosis; Biomarkers; Web of Science; CiteSpace; Visual analysis
参考文献 References
[1] Wong MCS, Huang JLW, George J, et al. The changing epidemiology of liver diseases in the Asia-Pacific region. Nat Rev Gastroenterol Hepatol. 2019;16(1):57-73.
[2] Asrani SK, Devarbhavi H, Eaton J, Kamath PS. Burden of liver diseases in the world. J Hepatol. 2019;70(1):151-171.
[3] HE K，WANG X，ZENG Y，et al．A scientometric review of emerging trends and new developments in agricultural eclogical compensation．Environ SciPollut Res Int.2018, 5(17)： 6522-16532．
[4] Chen J, Zhang R, Li F, Lin S, Wang J. Integrated analysis and validation of TRIM23/p53 signaling pathway in hepatic stellate cells ferroptosis and liver fibrosis. Dig Liver Dis. 2023 Jul 24:S1590-8658(23)00764-8.
[5] Vousden KH, Prives C. Blinded by the Light: The Growing Complexity of p53. Cell. 2009;137(3):413-431.
[6] Tian XF, Ji FJ, Zang HL, Cao H. Activation of the miR-34a/SIRT1/p53 Signaling Pathway Contributes to the Progress of Liver Fibrosis via Inducing Apoptosis in Hepatocytes but Not in HSCs. PLoS One. 2016 Jul 7;11(7):e0158657.
[7] Sola S, Ma X, Castro RE, Kren BT, Steer CJ, Rodrigues CM. Ursodeoxycholic acid modulates E2F-1 and p53 expression through a caspase-independent mechanism in transforming growth factor beta1-induced apoptosis of rat hepatocytes. J Biol Chem. 2003;278(49):48831-48838.
[8] Song L, Chen TY, Zhao XJ, Xu Q, Jiao RQ, Li JM, Kong LD. Pterostilbene prevents hepatocyte epithelial-mesenchymal transition in fructose-induced liver fibrosis through suppressing miR-34a/Sirt1/p53 and TGF-β1/Smads signalling. Br J Pharmacol. 2019 Jun;176(11): 1619-1634.
[9] Yao L, Hu X, Yuan M, et al. IGF2-NR4A2 Signaling Regulates Macrophage Subtypes to Attenuate Liver Cirrhosis. J Clin Transl Hepatol. 2023;11(4):787-799.
[10] Ren S, Chen J, Wang Q, et al. MicroRNA-744/transforming growth factor β1 relationship regulates liver cirrhosis. Hepatol Int. 2019;13(6):814-825.
[11] Ma L, Ma J, Ou HL. MicroRNA 219 overexpression serves a protective role during liver fibrosis by targeting tumor growth factor β receptor 2. Mol Med Rep. 2019;19(3): 1543-1550.
[12] Sak JJ, Prystupa A, Kiciński P, Luchowska-Kocot D, Kurys-Denis E, Bis-Wencel H. Leukocyte cell-derived chemotaxin-2 and fibroblast growth factor 21 in alcohol-induced liver cirrhosis. World J Hepatol. 2021;13(12): 2071-2080.
[13] Yu F, Dong P, Mao Y, et al. Loss of lncRNA-SNHG7 promotes the suppression of hepatic stellate cell activation via miR-378a-3p and DVL2[J]. Molecular Therapy-Nucleic Acids, 2019, 17: 235-244.
[14] Kong Y, Huang T, Zhang H, et al. The lncRNA NEAT1/miR-29b/Atg9a axis regulates IGFBPrP1-induced autophagy and activation of mouse hepatic stellate cells[J]. Life sciences, 2019, 237: 116902.
[15] Ye J, Lin Y, Yu Y, et al. LncRNA NEAT1/microRNA-129-5p/SOCS2 axis regulates liver fibrosis in alcoholic steatohepatitis[J]. Journal of Translational Medicine, 2020, 18(1): 1-12.
[16] Wang Q, Wei S, Li L, et al. miR-139-5p sponged by LncRNA NEAT1 regulates liver fibrosis via targeting β-catenin/SOX9/TGF-β1 pathway[J]. Cell Death Discovery, 2021, 7(1): 243.
[17] Su S B, Tao L, Liang X L, et al. Long noncoding RNA GAS5 inhibits LX-2 cells activation by suppressing NF-κB signalling through regulation of the miR-433–3p/TLR10 axis[J]. Digestive and Liver Disease, 2022, 54(8): 1066-1075.
[18] Han M H, Lee J H, Kim G, et al. Expression of the long noncoding RNA GAS5 correlates with liver fibrosis in patients with nonalcoholic fatty liver disease[J]. Genes, 2020, 11(5): 545.