Fig. 8: Schematic diagram of circCDK13OE-sEVs promoting wound healing. | Nature Communications

Fig. 8: Schematic diagram of circCDK13OE-sEVs promoting wound healing.

From: circCDK13-loaded small extracellular vesicles accelerate healing in preclinical diabetic wound models

Fig. 8

AGEs accumulation and high glucose microenvironment are significant contributors to the poor healing of diabetic wounds, which could inhibit the expression of circCDK13 in skin wound repair cells. Mechanistically, circCDK13 interacts with IGF2BP3 in an m6A-dependent manner, synergistically enhancing the stability of CD44 and c-MYC mRNA, thereby boosting the expression of CD44 and c-MYC, which in turn promotes the proliferation and migration of HDFs and HEKs. Furthermore, circCDK13OE-sEVs promote the proliferation and migration of HDFs and HEKs to accelerate wound healing partly through the circCD13-IGF2BP3-CD44/c-MYC ternary complex.

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