Update on the impact of lipid and glucose control on diabetic wound healing
2025
Rui Sun | Yang Xu | Zhenjun Ji | Xingxing Li | Zaixiao Tao | Weichen Luo | Yuyu Yao | Lijuan Chen | Genshan Ma
This review summarizes current insights into the molecular mechanisms by which hyperglycemia and dyslipidemia contribute to chronic diabetic wounds. It discusses the roles of key metabolic pathways, including the hexosamine biosynthetic and polyol pathways, along with the significance of inflammatory mediators and oxidative stress in this process. In addition, emerging therapeutic strategies are evaluated, such as the use of metformin to activate AMPK, PPAR agonists, SGLT2 inhibitors, and GLP-1 receptor agonists, which hold promise for modulating the inflammatory microenvironment and restoring cellular function. Combination therapies, advanced wound dressings, negative pressure wound therapy (NPWT), hyperbaric oxygen therapy (HBOT), and regenerative approaches such as stem cell therapies and bioengineered skin substitutes are also reviewed as integrated strategies that target both systemic metabolic dysregulation and local wound-specific challenges. These findings underscore the critical role of improved glucose and lipid control in optimizing diabetic wound healing and suggest that personalized, multimodal therapeutic approaches may offer enhanced clinical outcomes for patients with diabetic ulcers and other chronic wounds.
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