Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Hypoxia-induced adipose derived stem cells-derived exosomes promote diabetic wound healing through circ-0001747/miR-199a-5p/HIF-1α axis.

Wang Z., Feng C., Liu H., Xia Y., Shan M., Hao Y.

Animal Study on Diabetic Foot, Chronic Wound, published in Arch Dermatol Res (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
Arch Dermatol Res (2025)
Country
Germany
Reported sample size
—
Source database
PubMed
PMID
39987303
DOI
10.1007/s00403-025-03921-9
Citations
8

Abstract (original English)

Diabetic foot ulcers (DFU) are a serious complication of diabetes that lead to significant morbidity and mortality. The studies reported that promoting angiogenesis is a key step in wound healing. Hypoxia-induced adipose-derived mesenchymal stem cell-derived exosomes (ADSC-Exo) were observed to promote skin wound healing and alleviate DFU development. Howere, the detailed molecular mechanism of hypoxia-induced ADSC-Exo in wound healing of DFU remain undetermined. In this study, we identified aberrantly expressed circRNAs in normoxic-induced ADSC-Exo (Exo) versus hypoxia-induced ADSC-Exo (HExo) by high-throughput sequencing. The expression of circ-0001747 in Exo and HExo were detected by qRT-PCR. Subsequently, the overexpression of circ_0001747-HExo was constructed to observe the wound healing and therapeutic effect of DFU mice. Bioinformatics analysis, luciferase reporter gene assays, qRT-PCR, flow cytometry and angiogenesis assay, were used to study the regulatory mechanism of circ-0001747. The results showed that circ-0001747 was higher in HExo. Compared with the Exo group, overexpression of circ-0001747-HExo significantly restored wound healing, promoted vascular differentiation, and inhibited cell apoptosis and ROS production. Additionally, miR-199a-5p and HIF1α were identified as downstream targets of circ-0001747 and further verified by luciferase reporter gene analysis.

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.

How we grade evidence
AnimalsExosomesMicroRNAsHypoxia-Inducible Factor 1, alpha SubunitWound HealingMiceRNA, CircularDiabetic FootHumansMesenchymal Stem Cells

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