Unraveling the Diabetes-Inflammation Axis with Single-Cell Analysis and Two-Decade Bibliometric Mapping.

Abstract

BACKGROUND: Diabetes is a multifactorial chronic metabolic disorder in which chronic low-grade inflammation contributes to the initiation and progression of type 2 diabetes mellitus (T2DM). Investigations of the diabetes-inflammation axis have remained persistently compartmentalized, compelling a systematic synthesis of macroscale bibliometric trajectories with microscale microenvironmental circuitry. PURPOSE: This study integrates a 20-year bibliometric analysis with single-cell transcriptomic analysis to characterize the research landscape and examine inflammatory activity at cellular resolution. METHODS: A corpus of 55,147 English‑language publications spanning 2006-2026 was curated from the Web of Science Core Collection (WoSCC). CiteSpace, Bibliometrix, and Tableau were harnessed to perform collaboration network mapping, co‑citation dissection, and thematic evolution tracing. In parallel, single-cell RNA sequencing data from two T2DM and two control peripheral blood mononuclear cell samples (GSE280401) were analyzed; after quality control, 2,611 T2DM cells and 4,138 control cells were retained, AUCell was used to quantify inflammatory pathway activity, and CellChat was used to infer intercellular immune communication. RESULTS: Macroscopically, the field has witnessed exponential publication acceleration, with China and the United States constituting the dominant research poles and U.S. institutions commanding disproportionate network centrality. The thematic epicenter has undergone a decisive migration from classical inflammatory cytokine postulates toward immunometabolic network orchestration and multi‑target therapeutic frameworks, while cardiovascular protection, oxidative stress, and molecular docking have crystallized as the defining frontier. At the single-cell level, T cells were the most abundant population, overall inflammatory-response scores were higher in T2DM cells, and CellChat suggested reduced global communication with relative enrichment of several pro-inflammatory pathways. CONCLUSION: By erecting a macro-micro dual‑scale knowledge architecture, this study renders visible the foundational intellectual scaffolding and evolutionary trajectory of the diabetes-inflammation axis. The findings identify testable priorities in immunometabolic regulation and ligand-receptor signaling that require confirmation in larger cohorts and functional studies. Diabetes often occurs with long-lasting, low-level inflammation. We examined publications from 2006 to May 2026 to show how research priorities changed over time. We also reanalyzed a public single-cell dataset from blood samples of two people with T2DM and two controls. The literature increasingly focused on immune metabolism, oxidative stress, cardiovascular disease, and multi-omics. The single-cell analysis found higher overall inflammatory scores in T2DM cells and changes in predicted communication among immune cells. These results identify questions for future research but need confirmation in larger patient groups.

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