ArticleInflammation2025
SIRT6 Overexpression Enhances Diabetic Foot Ulcer Healing via Nrf2 Pathway Activation.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Article
- Orchestrating diabetic wound repair via mitochondria-targeted delivery of dihydromyricetin with tailored ADSC-derived biohybrid nanovesicles.Materials today. Bio · 2026Article
- Single-cell RNA sequencing in diabetic foot ulcers: pathogenesis, biomarkers, and translational potential.Frontiers in clinical diabetes and healthcare · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sirtuin-6 (SIRT6) has a pivotal role in a wide array of cellular biological functions and is linked to the progression of various diseases. Previous findings have identified SIRT6 as a protective modulator against numerous diabetic complications. However, whether SIRT6 exerts a protective role in diabetic foot ulcer (DFU) remains unstudied. This work established a rat model of DFU and evaluated the possible role of SIRT6 in mediating the wound healing in DFU. Marked reductions in SIRT6 levels were observed in wound samples from DFU patients and rats. Increasing SIRT6 expression in wound tissues remarkably decreased wound area, accelerated epithelialisation, increased collagen deposition and improved angiogenesis. Moreover, up-modulation of SIRT6 relieved the oxidative stress and inflammation in DFU rats. The increase of SIRT6 in cultured vascular endothelial cells restrained cell apoptosis, oxidative stress and inflammation elicited by high glucose (HG). HG-impaired migration capacity and angiogenesis of vascular endothelial cells was also recovered by increasing SIRT6 expression. Mechanism research revealed that SIRT6 overexpression reinforced the activation of the Nrf2 pathway in wound tissues of DFU rats and HG-exposed vascular endothelial cells. Pharmacological suppression of Nrf2 reversed the protective effect of SIRT6 overexpression on HG-triggered endothelial dysfunction. The findings of this work indicate that the positive role of SIRT6 in DFU wound healing is related to Nrf2 activation which contributes to the suppression of oxidative stress and inflammation and the improvement of angiogenesis in vascular endothelial cells. This study highlights the previously unaddressed role of SIRT6 in DFU wound healing, providing novel insights into its protective functions. The findings hold significant clinical value by identifying SIRT6 as a promising therapeutic target for improving DFU wound healing.
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