Published online Mar 27, 2025. doi: 10.4254/wjh.v17.i3.103327
Revised: February 7, 2025
Accepted: March 5, 2025
Published online: March 27, 2025
Processing time: 131 Days and 3 Hours
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.
To analyze the literature on immune cells and MAFLD, identifying research trends and future hotspots.
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.
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 tran
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.