Trisk95 Downregulation to Enhance Mitochondrial Function for Improved Diabetic Wound Healing

Abstract

Impaired wound healing in diabetic patients is a major clinical challenge, often associated with mitochondrial dysfunction, increased inflammation, and oxidative stress. Trisk95, a transmembrane protein, plays a critical role in calcium homeostasis, and its modulation may enhance wound repair processes. Benfotiamine, a thiamine derivative, improves diabetic complications by affecting oxidative stress, inflammation, metabolism, and signaling pathways. This study aimed to evaluate the efficacy of benfotiamine in diabetic wound healing by impacting Trisk95 expression and exerting anti-inflammatory and antioxidant effects. Benfotiamine was administered topically to the wounded area of diabetic mice and the wound closure rate was measured. The anti-inflammatory effects were quantified by measuring interleukin-6 (IL-6) and interleukin-10 (IL-10) levels. Antioxidant effects were assessed by measuring reactive oxygen species (ROS) level, and the activity of superoxide dismutase (SOD) and catalase (Cat). Benfotiamine significantly downregulated Trisk95, IL-6, and ROS levels, and upregulated IL-10. It increased the activity of SOD and Cat enzymes. In conclusion, benfotiamine promotes wound healing in diabetic mice by modulating Trisk95 and exerting anti-inflammatory and antioxidant effects, thereby improving mitochondrial function. Keywords: Trisk95, diabetic wound heali