CD73 + mesenchymal stem cell (MSC) transplantation improves pressure ulcer healing by promoting angiogenesis through the HIF-1α/VEGF pathway in diabetic mice.

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

Abstract (original English)

Diabetic wound healing remains a major clinical challenge. Although therapies based on mesenchymal stem cells (MSCs) have emerged as promising strategies to address this impairment, the specific contribution of CD73 expression to the therapeutic potential of MSCs has not been previously explored. In this study, we explored the role of CD73 expression in the therapeutic potential of human adipose tissue-derived mesenchymal stem cells (hADMSCs) for treating diabetic pressure ulcers in a mouse model. Our findings demonstrated that CD73-positive hADMSCs (CD73 + hADMSCs) could promote enhanced wound healing in diabetic mice and mitigate the endothelial dysfunction caused by high glucose levels. Conversely, inhibition of CD73 impairs these therapeutic effects. CD73 could modulate vascular endothelial growth factor A (VEGFA) expression under hypoxic conditions via a hypoxia-inducible factor-1α (HIF-1α)-dependent pathway. Furthermore, CD73 expression was shown to regulate the activation of the PI3K/Akt signaling pathway, contributing to accelerated wound closure in diabetic pressure ulcer mice. These findings provide new insights into the potential of MSC-based therapies for treating conditions marked by immune dysregulation and impaired vascularization, including metabolic and ischemic diseases.

Evidence level

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

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.