Activated phosphatidylinositol 3 kinase/Protein kinase B (PI3K/AKT) signalling with increased or reduced mTOR and GSK3β activity influences the wound repair process. Diabetic wounds, usually ulcerated, are characterised by reduced growth factors and cellular performance. The occurrence of diabetic ulcers is linked to peripheral arterial disease, neuropathy, and wound contamination. Lasers or light emitting diodes (LEDs) provide photon energy with therapeutic benefits (Photobiomodulation-PBM), and has been broadly commended to quicken diabetic wound healing. PBM is efficient in the visible red and near-infrared electromagnetic spectrum, and fluencies ranging from 2 to 6 J/cm². However, cellular and molecular mechanisms induced by PBM are not fully understood. In this review we discuss PBM and the PI3K/AKT pathway with specific focus on the mTOR and GSK3β downstream activity in diabetic wound healing.

活化的磷脂酰肌醇3-激酶/蛋白激酶B（PI3K / AKT）与增加或减少mTOR和GSK3信令β活性的影响伤口修复过程。通常为溃疡的糖尿病伤口的特征在于生长因子和细胞性能的降低。糖尿病性溃疡的发生与周围动脉疾病，神经病和伤口污染有关。激光或发光二极管（LED）为光子能量提供治疗益处（Photobiomodulation-PBM），并被广泛推荐用于加快糖尿病伤口的愈合。PBM在可见的红色和近红外电磁光谱中非常有效，并且通量范围为2至6 J / cm ²。但是，尚未完全了解PBM诱导的细胞和分子机制。在这次审查中，我们讨论了具体的重点mTOR和GSK3 PBM和PI3K / AKT通路β糖尿病伤口愈合的下游活动。