Mapping the Intellectual Architecture of Inflammation-Centered Macrophage Research in Hepatocellular Carcinoma: A Dual-Database Bibliometric and Scientometric Analysis, 2005-2025.
- 1Department of Pathology, South China Hospital, Medical School, Shenzhen University, Shenzhen, People's Republic of China.
- 2Department of Thyroid and Breast Surgery, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, People's Republic of China.
Abstract
Background
Chronic liver inflammation provides a major biological context for hepatocarcinogenesis, and macrophages link innate immune sensing, fibrogenesis, immune suppression and therapeutic resistance in hepatocellular carcinoma (HCC). Tumor-associated macrophages (TAMs), Kupffer cells and inflammation-associated myeloid populations have been extensively investigated in HCC; however, the intellectual structure and thematic connectivity of this inflammation-centered research field remain incompletely defined.Objective
This study aimed to map the intellectual architecture, evolutionary trajectory and inter-module connectivity of inflammation-centered macrophage research in HCC using bibliometric and scientometric methods.Methods
A total of 9218 English-language articles and reviews on macrophage-related HCC from 2005 to 2025 were retrieved from the Web of Science Core Collection and Scopus after systematic deduplication. CiteSpace, VOSviewer and bibliometrix were used to perform co-citation clustering, reference historiographic mapping, keyword co-occurrence analysis, publication-volume-adjusted keyword correlation analysis, citation burst detection, journal dual-map overlay and multi-level collaboration profiling.Results
Annual publication output increased from 84 articles in 2005 to 1129 in 2025. Co-citation analysis resolved 13 well-defined clusters (modularity Q = 0.744; mean silhouette S = 0.884), and historiographic mapping identified four sequential stages: foundational inflammation and hepatocarcinogenesis, mechanistic expansion of TAM function, immune-regulatory convergence and spatial immunology. Keyword dynamics showed a transition from viral hepatitis, innate immunity, Kupffer cells and fibroinflammatory terminology toward TAM-mediated immune suppression, immunotherapy, single-cell analysis, SPP1-positive macrophage-associated spatial immune barriers and computational precision oncology. After annual publication-volume adjustment, the foundational viral-innate module and the contemporary computational-precision oncology module showed a negative inter-module Pearson correlation (mean r = -0.383), lower than expected under label-permutation and temporal-succession null models (both p < 0.001). Three low-connectivity literature interfaces emerged: etiology-immunotherapy, TAM-organized spatial immune exclusion and TAM-MDSC shared myeloid biology.Conclusion
Macrophage-related HCC research has evolved from inflammation-centered hepatocarcinogenesis toward spatially resolved and computationally assisted immunology. The low-connectivity interfaces identified in this study should be interpreted as hypothesis-generating bibliometric signals rather than as evidence of biological or clinical disconnection or as stand-alone research priorities derived from network structure alone. Their potential translational relevance should be considered alongside published mechanistic and clinical evidence and requires future mechanistic, spatial and prospective clinical validation.
Related
- Mapping the intellectual landscape of lactylation research: a bibliometric analysis of global trends and emerging frontiers
- Convolutional, State-Space and Transformer Liver-Tumor Segmentation Models Trained on Hepatocellular Carcinoma Fail on the Same External Cases: Lesion Size Outweighs Architecture in Cross-Dataset Generalization
- A scientometric study on research trends and characteristics of lymph node metastasis in oral cancer.
- A scientometric study on research trends and characteristics of Kimura disease.
- Visualizing Emerging Trends and Global Hotspots in Ozempic, Weight Loss, and Pancreatitis Research: A Scientometric Analysis
BibTeX
@article{chai2026mapping,
title = {{Mapping the Intellectual Architecture of Inflammation-Centered Macrophage Research in Hepatocellular Carcinoma: A Dual-Database Bibliometric and Scientometric Analysis, 2005-2025.}},
author = {Ke Chai and Canbin Chen and Kang Wu and Xueyu Zhao},
journal = {Journal of inflammation research},
year = {2026},
month = oct,
doi = {10.2147/jir.s637035},
url = {https://europepmc.org/article/MED/42959746},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Mapping the Intellectual Architecture of Inflammation-Centered Macrophage Research in Hepatocellular Carcinoma: A Dual-Database Bibliometric and Scientometric Analysis, 2005-2025.
AU - Ke Chai
AU - Canbin Chen
AU - Kang Wu
AU - Xueyu Zhao
PY - 2026
DA - 2026/10/24
JO - Journal of inflammation research
DO - 10.2147/jir.s637035
UR - https://europepmc.org/article/MED/42959746
AB - Background Chronic liver inflammation provides a major biological context for hepatocarcinogenesis, and macrophages link innate immune sensing, fibrogenesis, immune suppression and therapeutic resistance in hepatocellular carcinoma (HCC). Tumor-associated macrophages (TAMs), Kupffer cells and inflammation-associated myeloid populations have been extensively investigated in HCC; however, the intellectual structure and thematic connectivity of this inflammation-centered research field remain incompletely defined.Objective This study aimed to map the intellectual architecture, evolutionary trajectory and inter-module connectivity of inflammation-centered macrophage research in HCC using bibliometric and scientometric methods.Methods A total of 9218 English-language articles and reviews on macrophage-related HCC from 2005 to 2025 were retrieved from the Web of Science Core Collection and Scopus after systematic deduplication. CiteSpace, VOSviewer and bibliometrix were used to perform co-citation clustering, reference historiographic mapping, keyword co-occurrence analysis, publication-volume-adjusted keyword correlation analysis, citation burst detection, journal dual-map overlay and multi-level collaboration profiling.Results Annual publication output increased from 84 articles in 2005 to 1129 in 2025. Co-citation analysis resolved 13 well-defined clusters (modularity Q = 0.744; mean silhouette S = 0.884), and historiographic mapping identified four sequential stages: foundational inflammation and hepatocarcinogenesis, mechanistic expansion of TAM function, immune-regulatory convergence and spatial immunology. Keyword dynamics showed a transition from viral hepatitis, innate immunity, Kupffer cells and fibroinflammatory terminology toward TAM-mediated immune suppression, immunotherapy, single-cell analysis, SPP1-positive macrophage-associated spatial immune barriers and computational precision oncology. After annual publication-volume adjustment, the foundational viral-innate module and the contemporary computational-precision oncology module showed a negative inter-module Pearson correlation (mean r = -0.383), lower than expected under label-permutation and temporal-succession null models (both p < 0.001). Three low-connectivity literature interfaces emerged: etiology-immunotherapy, TAM-organized spatial immune exclusion and TAM-MDSC shared myeloid biology.Conclusion Macrophage-related HCC research has evolved from inflammation-centered hepatocarcinogenesis toward spatially resolved and computationally assisted immunology. The low-connectivity interfaces identified in this study should be interpreted as hypothesis-generating bibliometric signals rather than as evidence of biological or clinical disconnection or as stand-alone research priorities derived from network structure alone. Their potential translational relevance should be considered alongside published mechanistic and clinical evidence and requires future mechanistic, spatial and prospective clinical validation.
SN - 1178-7031
ER -