To integrate bibliometric analysis with GEO-based transcriptomic profiling to systematically characterize the research landscape, core immune mechanisms, and potential modules warranting further investigation in dermatomyositis (DM).

Publications related to DM from 1992 to 2025 were retrieved from the Web of Science Core Collection (WOSCC) using a targeted search strategy. Bibliometric and visual analyses were performed using CiteSpace (v6.4.R1), VOSviewer (v1.6.20), and Microsoft Excel 2019 to identify publication trends, influential countries, authors, institutions, co-cited references, and emerging research hotspots. In parallel, GEO transcriptomic datasets of DM and control muscle samples were analyzed to validate disease-associated immune pathways. Module-based analyses were conducted focusing on type I interferon (IFN-I), chemokine, T-cell, humoral immune, complement, and neutrophil/NET-related signatures. Correlation, regression, and residual analyses were further used to assess the extent to which these modules were dependent on IFN-I signaling.

A total of 855 publications were included, and annual output increased markedly after 2017, reaching a peak during the COVID-19 pandemic era. The United States ranked first in publication output, citation frequency, and international collaboration, followed by China. Influential authors included Lundberg, Ingrid E. and Miller, Frederick W., whereas major contributing institutions included Johns Hopkins University and Karolinska Institute. Keyword co-occurrence analysis revealed five major thematic clusters, including autoimmune mechanisms, malignancy associations, therapeutic strategies, myositis-specific autoantibodies (MSAs), and T-cell-mediated immunity. Burst keyword analysis identified “risk,” “diagnosis,” “risk factors,” “classification,” “efficacy,” and “adult” as recent frontiers. Co-citation analysis generated 17 major clusters, among which “clinical trials” and “anti-melanoma differentiation-associated gene 5 (MDA5) antibody” were particularly prominent.

GEO-based transcriptomic analysis confirmed that IFN-I signaling remained the dominant molecular feature in DM. In addition to the IFN-I signature, chemokine, humoral immune, complement, T-cell, and neutrophil/NET modules were all elevated to varying degrees. Correlation and regression analyses showed that the chemokine and complement modules were most strongly coupled to IFN-I activit. By contrast, the T-cell and neutrophil/NET modules showed relatively lower IFN-I dependence than the others, suggesting that these two modules may contain additional regulatory components beyond the canonical IFN-I-driven inflammatory program. Although residual analysis indicated that none of the tested modules retained a robust between-group difference after removal of IFN-related effects, the comparatively weaker IFN-I coupling of the T-cell and neutrophil/NET modules suggests that they may represent promising directions for further mechanistic stratification.

This study provides an integrated knowledge map of DM by combining bibliometric analysis with transcriptomic validation. The results confirm the central role of IFN-I signaling and MSA-associated immune mechanisms in DM, while also showing that multiple inflammatory modules remain broadly constrained by the IFN-I axis. Importantly, compared with chemokine, complement, and humoral immune programs, the T-cell and neutrophil/NET modules exhibited relatively weaker IFN-I dependence, indicating that they may serve as key candidate modules for future in-depth mechanistic investigation. This combined bibliometric-transcriptomic framework may help refine the understanding of DM pathogenesis and identify potential directions for subsequent translational research.