A Multi-Database Bibliometric and Translational Mapping of Microglial Mechanisms in Spinal Cord Pain Signaling

Lingji Zhou^1,2Weiyu Pu^1,2Shuxian Wang^1,2Shihong Li^1,2Song Cao^1,3*

• ¹Zunyi Medical University, Zunyi, China
• ²Affiliated Hospital of Zunyi Medical University, Zunyi, China
• ³The Tenth Affiliated Hospital of Southern Medical University, Dongguan, China

Objective: This multi-source bibliometric and translational mapping study provides a panoramic synthesis of how research on microglia-mediated spinal pain signaling has evolved from foundational mechanistic exploration to clinically oriented innovation. The aim is to identify developmental trajectories, mechanistic hotspots, and translational opportunities, thereby offering strategic insight into the reconfiguration of neuropathic pain research. Methods: A total of 1,313 original research articles indexed in the Web of Science Core Collection (2005–2024) were analyzed using CiteSpace and VOSviewer to construct co-authorship networks, journal landscapes, and keyword-based mechanistic clusters. To complement this, a PubMed-based targeted search strategy ("microglia AND spinal cord AND (translational OR therapeutic OR drug targets)") yielded 692 additional records, enabling a translational overlay across mechanistic domains and clinical intent. Results: Scientometric analysis revealed a distinct thematic evolution from early descriptive models of spinal cord pain pathology to the emergence of precise regulatory mechanisms. Core mechanistic themes include glial activation, oxidative stress, mitochondrial dysfunction, and microglial polarization, with expanding interest in heat shock protein pathways and sex-specific microglial responses. High-frequency keywords such as "activated protein kinase" and "neuroinflammation" demonstrate conceptual continuity, while the recent surge in terms like "BDNF" and "spinal cord stimulation" (2020–2021; burst intensity = 2.56) signals a shift toward circuit-level modulation and neuromodulatory interventions. The PubMed subset indicates that 33.6% of studies explicitly address therapeutic development, with growing emphasis on gene therapy, intrathecal delivery, and microenvironmental repair. Conclusion: These findings outline a research ecosystem undergoing epistemological expansion— from inflammation-centric narratives to systems-level intervention strategies. The rising prominence of homeostatic and anti-inflammatory microglial phenotypes, together with the incorporation of sex-based and metabolic variables, reflects a broader shift toward immunoreparative and personalized therapeutic frameworks. As microglial profiling integrates with circuit modulation and bioengineered delivery platforms, the field is well-positioned to generate next-generation, disease-modifying solutions for chronic pain.