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.
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
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.
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