This study aims to investigate the function of positive feedback loops involving noncoding RNA in diabetic wound healing. We developed a mouse diabetic wound model to confirm that hyperglycemia can impair wound healing. We also used an keratinocyte model in high-glucose conditions to investigate the mechanism of delayed wound healing. was decreased in diabetic mouse wound tissue and can promote keratinocyte biological functions. could bind to miR-106a-5p to modulate the expression of , a target gene of miR-106a-5p. Surprisingly, ZNF148 bound to a region in the promoter to stimulate gene expression. ZNF148-activated increases expression by competitively binding miR-106a-3p, generating a positive feedback loop that enhances keratinocyte function.
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