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Updated: Jan 7, 2026

Systems Analysis of the Neuroinflammatory and Hemodynamic Response to Traumatic Brain Injury
Published on: May 27, 2022
Bibliometric analysis and core target identification of network pharmacology on neuroinflammation in central nervous
Yifeng Zhang1, Shuai Hou2, Jian Li1
1Department of Neurology II Affiliated Hospital of Shandong Second Medical University, School of Clinical Medicine, Shandong Second Medical University Weifang Shandong China.
Abstract:
Neuroinflammation is increasingly recognized as a critical driver of central nervous system (CNS) disorders, and network pharmacology has emerged as a promising approach to elucidate its complex mechanisms and therapeutic strategies. This study provides a comprehensive bibliometric and scientometric analysis of publications over the past 13 years to characterize research trends, identify key contributors, and uncover core therapeutic targets in this field. Articles published between January 2012 and May 2024 were retrieved from the Web of Science Core Collection. Visualization and quantitative analyses were performed using CiteSpace (version 6.3.R1, Drexel University, PA, United States) and VOSviewer (version 1.6.20, Leiden University - CWTS, Netherlands) followed by network interaction analysis to identify central targets implicated in neuroinflammation. A total of 156 publications were analyzed, with the United States, China, and Germany leading global output. Beijing University of Chinese Medicine, Case Western Reserve University, and University System of Ohio were identified as the most influential institutions. Nucleic Acids Research was the most frequently cited journal, whereas Journal of Ethnopharmacology contributed the largest number of publications. Co-occurrence clustering revealed 13 thematic research areas, highlighting apoptosis, Panax notoginseng, dihydrochalcones, and quercetin as representative hotspots. Target interaction analysis identified signal transducer and activator of transcription 3 (STAT3), jun proto-oncogene (JUN), AKT serine/threonine kinase 1 (AKT1), tumor protein 53 (TP53), and interleukin-6 (IL6) as core molecular targets. The findings delineate a dynamic and evolving research landscape in this domain and clarify its organization around several pivotal molecular targets. The field is shifting away from the conventional "one drug, one target" paradigm toward multi-target therapeutic strategies, reflecting the multifactorial nature of neuroinflammation in CNS disorders. These insights highlight key molecular nodes and research directions, providing a foundation for precision medicine approaches and innovative drug development to improve treatment outcomes in neuroinflammatory CNS diseases.
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