ArticleInternational wound journal2026
Negative-Pressure Induces Epithelial-Mesenchymal Transition via Thrombospondin-1 Upregulation in Intact Diabetic Skin.
Article in International wound journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
6 authors.
Funding
Abstract
Negative-pressure wound therapy (NPWT) is widely used in clinical practise to enhance wound healing; however, its biological effects on intact skin remain poorly understood. Given the expanding applications of NPWT, understanding its impact beyond open wounds is increasingly important. This study aimed to evaluate the biological responses of intact skin to negative-pressure, specifically focusing on epithelial-mesenchymal transition (EMT). The effects of negative-pressure loading were assessed using an in vitro model of non-diabetic human keratinocytes and an in vivo model of intact diabetic mouse skin. Human keratinocytes exposed to negative-pressure exhibited increased expression of thrombospondin-1 (THBS1), transforming growth factor-beta 1 (TGF-β1), plasminogen activator inhibitor-1 (PAI-1), and hypoxia-inducible factor 1-alpha (HIF-1α), alongside decreased epithelial markers and increased mesenchymal markers. These EMT-related changes were mitigated by inhibiting the THBS1-TGF-β1 interaction. Similarly, in diabetic mice, intermittent negative-pressure loading applied to intact dorsal skin significantly increased THBS1 and TGF-β1 levels, resulting in epidermal and dermal thickening, and promoted hypoxic, prothrombotic and angiogenic responses, as evidenced by increased HIF-1α, PAI-1, fibrinogen and vascular endothelial growth factor expression. These findings suggest that negative-pressure loading can induce EMT-like responses and tissue remodelling in intact skin primarily via mechanisms involving the THBS1-TGF-β1 signalling axis. This study expands the understanding of the biological influence of NPWT beyond traditional wound treatment applications, potentially informing future therapeutic considerations and safety guidelines.
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