Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

Engineered sEVs encapsulated in GelMA facilitated diabetic wound healing by promoting angiogenesis via targeting thrombospondin-1

Cong Y., Meng S., Xie X., Chen Y., Li Y., Zhou Y.

Animal Study on Diabetic Foot, Chronic Wound, published in Burns Trauma (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Burns Trauma (2025)
Reported sample size
—
Source database
Europe PMC
PMID
41141921
PMCID
PMC12548737
DOI
10.1093/burnst/tkaf036
Citations
1

Abstract (original English)

Background Chronic nonhealing wounds are major complications in diabetic patients, with impaired angiogenesis playing a critical role in the delayed healing process. Current treatments for diabetic wounds are inadequate. The dysregulation of endothelial cell genes, particularly thrombospondin-1 (TSP-1), impairs neovascularization and delays wound repair. In recent years, hydrogel-based wound dressings have gained widespread application in biomedicine. The study introduced a new therapeutic approach, embedding miR-221-3p-loaded small extracellular vesicles (miR-221 OE -sEVs) within gelatin methacryloyl (GelMA) hydrogels to reduce TSP-1 levels and improve healing in diabetic wounds. Methods First, we observed upregulated TSP-1 expression in human umbilical vein endothelial cells (HUVECs) when cultured in a high-glucose (HG) environment. We employed small interfering RNA (siRNA) and miR-221-3p to suppress TSP-1 expression and then evaluate the functional effects on HUVECs. Subsequently, miR-221-3p was encapsulated in sEVs via lentiviral transfection. The effects of miR-221 OE -sEVs on HUVECs under HG conditions were evaluated. Finally, miR-221 OE -sEVs were incorporated into a GelMA hydrogel (G-miR-221 OE -sEVs) and applied to a diabetic murine wound model to evaluate their effects on wound closure and angiogenesis. Results Under HG conditions, the use of siTSP-1 to silence TSP-1

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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