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Diabetic Foot Ulcer

Diabetic Foot Ulcer

Definition A diabetic foot ulcer (DFU) is a chronic, non-healing wound that develops in individuals with diabetes. It typically occurs on pressure-bearing areas such as the heel, metatarsal heads, or hallux, and carries a high risk of infection and amputation.Pathophysiology • The development of DFUs can be explained by four interconnected mechanisms: neuropathy, ischemia, infection, and impaired wound healing. • Neuropathy is the most common factor. Sensory...

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Updated: Apr 30, 2026

Creation and Transplantation of an Adipose-derived Stem Cell ASC Sheet in a Diabetic Wound-healing Model

Creation and Transplantation of an Adipose-derived Stem Cell ASC Sheet in a Diabetic Wound-healing Model

Published on: August 4, 2017

Optimizing adipose-derived stem cell therapy for diabetic foot ulcers.

Jing Cao¹, Zi-Chao Liu¹, Wen-Qiang An¹

¹Department of Research and Development, Beijing AegleStem Therapeutics Co., Ltd, Beijing 102600, China.

World Journal of Diabetes

|November 24, 2025

Summary

Adipose-derived mesenchymal stem cells (ADSCs) significantly improve diabetic foot ulcer (DFU) healing by promoting blood vessel growth and reducing inflammation. Subcutaneous injection into the foot is the most effective delivery method for these stem cells in DFU treatment.

Keywords:

Adipose-derived stem cell Diabetic foot ulcer Dose-response relationship Notch signaling pathway Phosphatidylinositol 3-kinase

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Prospective, Randomized, and Controlled Study of a Human Umbilical Cord Mesenchymal Stem Cell Injection for Treating Diabetic Foot Ulcers

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Area of Science:

Regenerative Medicine
Stem Cell Therapy
Diabetic Complications Research

Background:

Diabetic foot ulcers (DFUs) are a major cause of lower limb amputation due to impaired wound healing.
Adipose-derived mesenchymal stem cells (ADSCs) show promise for DFU treatment due to their regenerative properties.
Limited understanding exists regarding the molecular mechanisms of ADSCs in DFU healing.

Purpose of the Study:

To determine the dose-response relationship of ADSCs for DFU healing.
To identify the optimal administration route and assess the persistence of ADSCs in DFU models.
To elucidate the molecular mechanisms by which ADSCs promote DFU healing.

Main Methods:

Human ADSCs were isolated, cultured, and characterized.
A DFU mouse model was used to evaluate dose-dependent effects and persistence of subcutaneously or intramuscularly administered ADSCs.
Wound healing, angiogenesis, inflammation, and collagen deposition were assessed; in vitro studies explored molecular mechanisms.

Main Results:

ADSC treatment significantly improved wound closure, angiogenesis, and tissue regeneration while modulating inflammation in DFU models.
Subcutaneous injection of 5 × 10^5 ADSCs into the foot demonstrated optimal therapeutic efficacy and prolonged retention.
ADSCs promote healing via PI3K/VEGF signaling for angiogenesis and Notch signaling for anti-inflammation and regeneration.

Conclusions:

ADSCs are effective in promoting diabetic foot ulcer healing.
ADSC-based therapy holds significant clinical potential for chronic non-healing diabetic wounds.
This study provides a basis for optimizing ADSC therapies for DFUs.