Adipose-derived mesenchymal stem cells promote diabetic wound healing through ALDOA secretion.

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)

Introduction Diabetic wound healing is impaired by hyperglycemia-induced metabolic dysregulation and chronic inflammation. Adipose-derived mesenchymal stem cell (ADSC)-derived exosomes, noted for rich bioactive molecules and immunomodulation, are promising for wound healing, but their mechanisms in diabetic wounds remain unclear. This study investigated their impact and mechanism. Methods HaCaT cells were treated with high glucose to mimic in vitro diabetic conditions. C57BL/6 mice were treated with streptozotocin to construct the diabetic mouse model and induce skin wound. Exosomes were characterized by transmission electron microscopy and nanoparticle tracking analysis. Its role in vitro was evaluated by measuring cell viability, transwell and scratch wound assays. Hematoxylin-eosin and Masson staining were used to evaluate the pathological changes in mouse skin tissues. Microarray analysis, RNA sequencing and KEGG pathway enrichment analysis were performed to investigate the underlying mechanisms. Results Results showed that ADSC-derived exosomes enhanced migration and ECAR levels in HG-induced HaCaT cells, and promoted wound healing in diabetic mice. ALODA was enriched in glycolysis pathway, and its expression was reduced in HG-induced HaCaT cells, which was increased following exosomes treatment, even higher than that in the control group. ALDOA knockdown in exosomes inhib

Evidence level

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

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