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. 2023 Sep 18;19(15):4989–5003. doi: 10.7150/ijbs.88461

Figure 4.

Figure 4

Autophagy in various skin cells in diabetic wound healing. (A) Autophagy in fibroblasts: High expression of miR-106b-5p in EVs from AGEs-treated HUVEC, reduces the ERK1/2 expression to activate autophagy in fibroblasts, leading to delayed diabetic wound healing. TOP-N53 can promote fibroblast p62/SQSTM1 expression to activate autophagy and improve diabetic wound healing. (B) Autophagy in KCs: High glucose can affect the P38/MAPK pathway and YTHDC1 to inhibit KCs autophagy, causing delayed diabetic wound healing, while BNIP3, TGF-β1, and rapamycin can activate autophagy to accelerate diabetic wound healing. (C) Autophagy in ECs: Several factors have been found to promote the healing of diabetic wounds by activating autophagy in ECs. Including triazole derivatives, hydrogen sulfide, circ-Klhl8, and mmu_circ_0000250. SIRT1 and melatonin can activate the autophagy of ECs and inhibit their apoptosis, thus inducing the healing of diabetic wounds. (D) Autophagy in macrophages: Stem cell exosomes, far-infrared, and negative pressure wound therapy, can all activate autophagy in macrophages to promote the healing of diabetic wounds. EVs, Extracellular Vehicles; AGEs, Advanced Glycation End products; HUVECs, Human Umbilical Vein Endothelial Cells; KCs, Keratinocytes; ECs, Endothelial Cells.