Endothelial-to-mesenchymal transition and vasculogenic mimicry in tumor vascular plasticity: a comparative bibliometric analysis and mechanistic framework.

Background: Endothelial-to-mesenchymal transition (EndMT) and vasculogenic mimicry (VM) are distinct forms of cellular and vascular plasticity that may contribute to tumor vascular adaptation. Although they have largely evolved as separate research fields, emerging experimental observations suggest potential convergence in their regulation by the tumor microenvironment. Methods: We performed a comparative bibliometric analysis of EndMT and VM using the Web of Science Core Collection and Scopus for publications from 2005 to 2025. After cross-database deduplication and retraction screening using a custom open-source data-fusion pipeline, 4,746 records were retained (2,056 EndMT; 2,695 VM).Publication trends, collaboration networks, keyword co-occurrence, thematic structures, and citation bursts were analyzed using bibliometrix/Biblioshiny, VOSviewer, and CiteSpace. Results: Only five publications explicitly addressed both EndMT and VM in an oncological context, indicating limited formal overlap between the two literatures. Nevertheless, keyword co-occurrence, citation-burst, and thematic analyses revealed convergent research interests involving the tumor microenvironment, cellular plasticity, extracellular-matrix remodeling, and therapeutic resistance. These patterns motivated a mechanistic synthesis centered on three potential points of convergence: shared upstream signaling involving TGF-β, hypoxia/HIF-1α, and context-dependent Notch activity; EndMT-associated stromal and extracellular-matrix remodeling that may facilitate VM; and partial or hybrid cellular states. Conclusions: EndMT and VM should be considered distinct but potentially interconnected components of tumor vascular plasticity rather than simple alternatives to conventional angiogenesis. The bibliometric convergence provides a rationale for investigating their potential interactions, but does not establish a causal or bidirectional relationship. We therefore propose a testable conceptual framework in which shared microenvironmental pressures may influence both processes, while EndMT-associated stromal remodeling may provide one potential route toward a VM-permissive niche. Spatial transcriptomics, lineage tracing, co-culture models, and organoid systems may help determine whether these interactions occur