ArticleMolecular biology reports2025
Upregulation of miR-155-5p impaired ginsenoside Rg1-mediated wound healing in diabetic foot ulcers by targeting E2F2/CDCA7L signaling : Rg1 improves DFU wound healing via inhibiting miR-155-5p.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
What it found
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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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Who cites it
1 citing paper in PubMed.
- Advanced Natural Therapeutics and Delivery Strategies for Diabetic Foot Ulcers: A Mini Review.Drug design, development and therapy · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
Abstract
backgroundNumerous studies have confirmed that ginsenoside Rg1 can promote wound healing in diabetic foot ulcers (DFU), yet the underlying mechanisms remain unclear. This study aimed to investigate the function of miR-155 in Rg1-mediated DFU wound healing and its regulatory mechanism.
methodsA DFU mouse model was established, and wound healing was assessed using macroscopic observation and HE staining. The oxidative stress level was evaluated by ELISA and immunohistochemistry assays. In vitro, ELISA, RT-qPCR, CCK-8, transwell migration, and tube formation assays were used to evaluate oxidative stress, wound closure, and angiogenesis in high glucose (HG)-induced HUVECs, respectively. Dual luciferase-reporter assay determined the interaction between miR-155-5p and E2F2.
resultsHere, we observed that Rg1 dramatically promoted angiogenesis and alleviated oxidative stress in the DFU mouse model and HG-induced HUVECs, thus accelerating wound healing. Importantly, miR-155-5p was proved to be upregulated in DFU wound tissues and HG-induced HUVECs, and overexpression of miR-155-5p remarkably impaired angiogenesis and stimulated oxidative stress in Rg1-administrated DFU mice and HG-induced HUVECs. Moreover, E2F2, a transcriptional activator of CDCA7L, was a direct downstream target of miR-155-5p. Rescue experiments showed that the reverse roles of miR-155-5p upregulation on Rg1-mediated oxidative stress repression and angiogenesis were obviously diminished by E2F2 downregulation.
conclusionOverall, our data revealed for the first time that Rg1 promoted wound healing in DFU via regulating miR-155-5p/E2F2/CDCA7L axis, which demonstrated a novel underlying mechanism of Rg1 in the treatment of DFU and provided some novel target for DFU therapy.
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Registered trials
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