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<p>In the wound of diabetic patients, Fibroblasts are extensively senescent and dysfunctional, resulting in prolonged skin wound healing time. The aim of this study was to investigate the impact of aFGF on diabetic wound healing and the senescence of fibroblasts induced by high glucose, and to explore the underlying mechanisms. We injected aFGF locally into the back wound of (Streptozocin) STZ-induced diabetic rats, and subsequently assessed its therapeutic impact on wound healing in vivo by measuring the wound healing rate and the expression of aging markers. Next, we conducted a series of in vitro experiments utilizing HG-induced L929 fibroblasts to evaluate the effects of aFGF on their aging and modulation of oxidative stress. Finally, we evaluated the changes of SIRT1 expression levels and phosphorylation STAT3 (Y705) levels, and observed whether the therapeutic effect of aFGF on diabetic wounds is related to the regulation of this pathway. Local injection of aFGF into diabetic wounds accelerates wound closure and decreases senescence associated secretory phenotype (SASP) expression. In vitro, aFGF enhanced the anti-senescence and antioxidant capacity of HG-induced senescent fibroblasts. It was found that aFGF effectively rescued SIRT1 expression and inhibited STAT3 phosphorylation in senescent tissue of diabetic wound. Our findings suggested that aFGF ameliorates the dysfunction of senescent fibroblasts by modulating the SIRT1/STAT3 signaling axis, thereby accelerating diabetic wound healing. aFGF is a promising therapeutic candidate for the treatment of diabetic wounds.</p>

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aFGF rescues high glucose-induced senescent fibroblasts and improves diabetic wound healing by regulating SIRT1/STAT3 pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月9日

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  • Xiaoyang Wang,
  • Meiqi Lu,
  • Shanshan Jia,
  • Jingjuan Zhang,
  • Xiao Wang,
  • Yongjun Qi,
  • Nian Shi,
  • Ya Jiao,
  • Jie Zhao,
  • Xiaochuan Wang,
  • Jixun Zhang,
  • Duyin Jiang

摘要

In the wound of diabetic patients, Fibroblasts are extensively senescent and dysfunctional, resulting in prolonged skin wound healing time. The aim of this study was to investigate the impact of aFGF on diabetic wound healing and the senescence of fibroblasts induced by high glucose, and to explore the underlying mechanisms. We injected aFGF locally into the back wound of (Streptozocin) STZ-induced diabetic rats, and subsequently assessed its therapeutic impact on wound healing in vivo by measuring the wound healing rate and the expression of aging markers. Next, we conducted a series of in vitro experiments utilizing HG-induced L929 fibroblasts to evaluate the effects of aFGF on their aging and modulation of oxidative stress. Finally, we evaluated the changes of SIRT1 expression levels and phosphorylation STAT3 (Y705) levels, and observed whether the therapeutic effect of aFGF on diabetic wounds is related to the regulation of this pathway. Local injection of aFGF into diabetic wounds accelerates wound closure and decreases senescence associated secretory phenotype (SASP) expression. In vitro, aFGF enhanced the anti-senescence and antioxidant capacity of HG-induced senescent fibroblasts. It was found that aFGF effectively rescued SIRT1 expression and inhibited STAT3 phosphorylation in senescent tissue of diabetic wound. Our findings suggested that aFGF ameliorates the dysfunction of senescent fibroblasts by modulating the SIRT1/STAT3 signaling axis, thereby accelerating diabetic wound healing. aFGF is a promising therapeutic candidate for the treatment of diabetic wounds.