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Updated: Jan 15, 2026
Prospective, Randomized, and Controlled Study of a Human Umbilical Cord Mesenchymal Stem Cell Injection for Treating Diabetic Foot Ulcers
Published on: March 3, 2023
Human Mesenchymal Stem Cell Derived Exosomes Endowed with miR-13474 as a Therapeutic Delivery Vehicle for Diabetic
Hui Shi1,2,3, Xinye Han2,4, Yuting Lu1,5
1Department of Otorhinolaryngology, the Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212013, China.
Abstract:
A delayed healing process in diabetic wounds is intractable. In this study, a high-glucose condition was found to be responsible for skin structure destruction, inflammatory infiltration, and vital cell dysfunction. Extracellular vesicles, particularly exosomes secreted by hucMSCs, contribute to improved diabetic wound healing, largely by promoting tissue repair and re-establishing normal function in affected cells. Small RNA-sequencing revealed that hucMSC-derived exosomes (hucMSC-Ex) were highly enriched in NC_000019.10_13474 (miR-13474), which was predicted to be an miRNA with an undiscovered function. miR-13474 showed a reduced expression level in high-glucose-treated skin cells as well as diabetic foot ulcer (DFU) rats. Moreover, there is also a significant expression difference between the wound area and the wound edge in DFU patients, indicating the potential clinical value of miR-13474. Blocking miR-13474 in hucMSC-Ex obviously diminished the therapeutic effects. Furthermore, exosomal miR-13474 was found to target the CPEB2/TWIST1 axis to improve the impaired function of skin cells. On this basis, hucMSC-Ex were used as a vehicle for the delivery of therapeutic miR-13474 to optimize the repairing effect. The study has revealed the role of hucMSC-derived exosomes and the underlying molecular mechanism in diabetic wound healing and proposes a cell-free-based modification strategy for refractory wound management.
Insights
Human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) promote diabetic wound healing. These exosomes deliver miR-13474, which targets the CPEB2/TWIST1 axis to restore skin cell function and improve healing in diabetic foot ulcers.
Area of Science:
- Regenerative Medicine
- Molecular Biology
- Wound Healing Research
Background:
- Diabetic wounds exhibit delayed healing due to high glucose, causing tissue damage and cellular dysfunction.
- Extracellular vesicles, specifically exosomes from human umbilical cord mesenchymal stem cells (hucMSCs), show therapeutic potential for diabetic wound repair.
- The precise molecular mechanisms underlying exosome-mediated diabetic wound healing require further elucidation.
Purpose of the Study:
- To investigate the role of hucMSC-derived exosomes (hucMSC-Ex) in promoting diabetic wound healing.
- To identify novel therapeutic molecules within hucMSC-Ex and elucidate their mechanism of action.
- To explore a cell-free therapeutic strategy for managing refractory diabetic wounds.
Main Methods:
- Small RNA sequencing to identify key microRNAs in hucMSC-Ex.
- In vitro studies on high-glucose-treated skin cells and in vivo studies using diabetic foot ulcer (DFU) rat models.
- Investigating the regulatory axis targeted by the identified microRNA, including CPEB2/TWIST1.
Main Results:
- hucMSC-Ex were enriched in miR-13474, a microRNA with reduced expression in high-glucose conditions and DFU models.
- miR-13474 levels differed significantly between wound areas and edges in DFU patients, suggesting clinical relevance.
- Blocking miR-13474 in hucMSC-Ex attenuated their therapeutic effects; exosomal miR-13474 targeted CPEB2/TWIST1 to restore skin cell function.
Conclusions:
- hucMSC-derived exosomes are crucial for diabetic wound healing, primarily through the delivery of miR-13474.
- miR-13474 functions by targeting the CPEB2/TWIST1 axis, thereby improving impaired skin cell function.
- Exosomal miR-13474 represents a promising cell-free therapeutic agent for enhancing diabetic wound management.
Related Concept Videos
01:19Clinical Applications of Epidermal Stem Cells
01:19Mesenchymal Stem Cells