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Discussion In the present study, we revealed that impaired healing of diabetic wounds was tightly associated with the downregulation of circCDK13, and then confirmed a potential wound healing-promoting mechanism that circCDK13 directly interacted with IGF2BP3 to form a circRNA-protein-mRNA ternary complex, which synergistically enhanced the stability of CD44 and c-MYC mRNA to promote the proliferation and migration of HDFs and HEKs
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