ArticleInternational wound journal2023
A gene chip study suggests that miR-17-3p is associated with diabetic foot ulcers.
Article in International wound journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Computational analysis of miRNA mediated KDR gene regulation and natural VEGFR2 inhibitors from Persicaria hydropiper in hepatocellular carcinoma.Scientific reports · 2025Article
- Characterizing Circulating microRNA Signatures of Type 2 Diabetes Subtypes.International journal of molecular sciences · 2025Article
- The emerging modulators of non-coding RNAs in diabetic wound healing.Frontiers in endocrinology · 2024Review
- A gene chip study suggests that miR-17-3p is associated with diabetic foot ulcers.International wound journal · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background of the Study Diabetic foot ulcers (DFUs) are severe effect of diabetes. This research aimed to discover the role of micro-ribonucleic acid (miRNA) in treating DFUs involved in maggot debridement therapy (MDT) via a miRNA chip study. A miRNA chip approach was adopted. Patients with diabetes (type 1 or 2) who had at least one-foot ulcer (current or previous) were enrolled in the study. The alterations of miRNA expressions in the granulation tissue during treatment with MDT were measured. Following MDT, the increased expression of miR17-92 was verified in vivo. The miR-17-3p expression increased, and Flk-1 (vascular endothelial growth factor) expression was significantly reduced in patients with DFUs who received MDT (P < 0.01). Results from human umbilical vein endothelial cells that excrete or secrete showed consistency with in vitro findings (P < 0.001, P < 0.05). The overexpression of miR-17-3p demonstrated inhibitory activity on tube formation (P < 0.05). When DFUs were treated with MDT, it revealed that miR-17-3p had a negative regulatory effect on Flk-1.
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Registered trials
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