Qi WY, Zheng SH, Li SZ, Wang W, Wang QY, Liu QY, Li XK, Zhang JX, Gan DN, Ye YA, Zao XB. Immune cells in metabolic associated fatty liver disease: Global trends and hotspots (2004-2024). World J Hepatol 2025; 17(3): 103327 [PMID: 40177204 DOI: 10.4254/wjh.v17.i3.103327]
Corresponding Author of This Article
Xiao-Bin Zao, Department of Spleen and Stomach Diseases, Dong-zhimen Hospital of Beijing University of Chinese Medicine, No. 5 Haiyuncang Road, Dongcheng District, Beijing 100700, China. a3417@bucm.edu.cn
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Scientometrics
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Wen-Ying Qi, Shi-Hao Zheng, Si-Ze Li, Wei Wang, Qiu-Yue Wang, Qi-Yao Liu, Xiao-Ke Li, Jia-Xin Zhang, Da-Nan Gan, Yong-An Ye, Xiao-Bin Zao, Department of Spleen and Stomach Diseases, Dongzhimen Hospital of Beijing University of Chinese Medicine, Beijing 100700, China
Qi-Yao Liu, Xiao-Ke Li, Jia-Xin Zhang, Da-Nan Gan, Yong-An Ye, Xiao-Bin Zao, Institute of Hepatology, Dongzhimen Hospital of Beijing University of Chinese Medicine, Beijing 100700, China
Qi-Yao Liu, Xiao-Bin Zao, Key Laboratory of Chinese Internal Medicine of Ministry of Education, Dongzhimen Hospital of Beijing University of Chinese Medicine, Beijing 100700, China
Co-first authors: Wen-Ying Qi and Shi-Hao Zheng.
Co-corresponding authors: Yong-An Ye and Xiao-Bin Zao.
Author contributions: Qi WY and Zheng SH participated in data processing and statistical analysis, they contributed equally to this article, they are the co-first authors of this manuscript; Qi WY, Zheng SH, Li SZ, and Wang W drafted the manuscript; Wang QY, Liu QY, Li XK, Zhang JX, and Gan DN contributed to data analysis and interpretation; Qi WY, Zheng SH, Zao XB, and Ye YA supervised the review of the study; Zao XB and Ye YA conceived and designed the study, they contributed equally to this article, they are the co-corresponding authors of this manuscript; and all authors seriously revised and approved the final manuscript.
Supported by Horizontal Project of Dongzhimen Hospital, No. HX-DZM-202343.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
PRISMA 2009 Checklist statement: The authors have read the PRISMA 2009 Checklist, and the manuscript was prepared and revised according to the PRISMA 2009 Checklist.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Xiao-Bin Zao, Department of Spleen and Stomach Diseases, Dong-zhimen Hospital of Beijing University of Chinese Medicine, No. 5 Haiyuncang Road, Dongcheng District, Beijing 100700, China. a3417@bucm.edu.cn
Received: November 18, 2024 Revised: February 7, 2025 Accepted: March 5, 2025 Published online: March 27, 2025 Processing time: 131 Days and 3 Hours
Abstract
BACKGROUND
The interplay between immune cells and metabolic associated fatty liver disease (MAFLD) is a critical research frontier, bridging immunology and hepatology. The bibliometric findings can guide future research and funding priorities in the field by highlighting key areas of focus and potential therapeutic targets.
AIM
To analyze the literature on immune cells and MAFLD, identifying research trends and future hotspots.
METHODS
A systematic search in the Web of Science Core Collection from January 1, 2004 to May 20, 2024, yielded 1936 articles on immune cells and MAFLD. Excluding non-research documents, the data were analyzed using R packages Cluster profiler, enrichplot, ggplot2, VOSviewer and CiteSpace. Visualizations were created for countries, institutions, authors, journals, fields, co-cited references, keywords, genes, and diseases, with gene a disease data from Citexs.
RESULTS
The field gained momentum in 2006, with the United States of America and China as leading contributors. Key research themes included oxidative stress, metabolic syndrome, liver fibrosis, and the role of Kupffer cells. Bioinformatics identified interleukin-6, tumor necrosis factor and signal transducer and activator of transcription 3 as central proteins in immune responses and inflammation, suggesting potential therapeutic targets for MAFLD. Clinically, these hub genes play pivotal roles in the pathogenesis of MAFLD. For instance, targeting the tumor necrosis factor signaling pathway could reduce inflammation, while modulating interleukin-6 and signal transducer and activator of transcription 3 expression may improve metabolic function, offering new strategies for MAFLD therapy.
CONCLUSION
This bibliometric analysis reports on the research hotspots and emerging trends in the field of immune cells and MAFLD, highlighting key proteins and potential therapeutic strategies through bioinformatics.
Core Tip: This study provides a comprehensive bibliometric analysis of global trends and hotspots in research on immune cells and metabolic associated fatty liver disease from 2004 to 2024. It highlights key proteins (e.g., interleukin-6, tumor necrosis factor, signal transducer and activator of transcription 3) and potential therapeutic targets identified through bioinformatics, emphasizing the critical roles of oxidative stress, metabolic syndrome, and Kupffer cells in metabolic associated fatty liver disease pathogenesis. The findings offer a roadmap for future research and clinical strategies to address this growing health challenge.
