Dendritic Cell Repression by TNF-α-Primed Exosomes Accelerate T2DM Wound Healing Through miR-146a-5p/TXNIP/NLRP3 Axis.

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 Type 2 diabetes mellitus (T2DM) impairs wound healing due to hyperglycemia-induced immune dysfunction. Dendritic cells (DCs) in the skin are crucial for wound healing but are adversely affected by hyperglycemic microenvironment. Exosomes derived from mesenchymal stem cells (MSC-exos), especially adipose-derived MSCs (ADSCs) with higher accessibility, have shown potential for immune regulation. However, their yield and efficacy can be limited. This study aims to explore the effects of TNF-α-preconditioned ADSCs-exos (T-exos) on restoring DC function and accelerating wound healing in T2DM. Methods T-exos were isolated from ADSCs pretreated with TNF-α. The regulatory effects of T-exos on DC immune responses under high glucose conditions were assessed. Subsequently, the roles of DCs treated with T-exos in diabetic wound healing were evaluated. Finally, the mechanism underlying T-exos-mediated regulation of DCs was investigated in detail. Results Under high glucose conditions, T-exos suppressed DC activation, as evidenced by reduced CD80/CD86 expression and NLRP3 inflammasome activity. In vivo studies showed that T-exos promoted wound closure in T2DM mice, enhancing collagen deposition, angiogenesis, and fibroblast proliferation. Mechanistically, TNF-α enriched miR-146a-5p in exosomes, which targeted TXNIP to inhibit NLRP3 inflammasome activation in DCs. Knockdown of mi

Evidence level

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

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