This study investigates the therapeutic potential of circCDK13-loaded small extracellular vesicles (sEVs) in diabetic wound healing. CircCDK13, a circular RNA, was identified as a downregulated molecule in diabetic wounds and shown to stimulate the proliferation and migration of human dermal fibroblasts (HDFs) and human epidermal keratinocytes (HEKs) by interacting with insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) in an N6-methyladenosine (m6A)-dependent manner. Engineered sEVs overexpressing circCDK13 (circCDK13^OE-sEVs) were constructed and shown to accelerate wound healing in both type II diabetic mice (db/db) and type I diabetic rats. The results indicate that circCDK13^OE-sEVs restore the functions of age-related end products (AGEs)-induced HDFs and HEKs in vitro and promote wound healing in diabetic animals. The mechanism involves the formation of a circCDK13-IGF2BP3-CD44/c-MYC ternary complex, which enhances the stability of CD44 and c-MYC mRNAs. This study suggests that circCDK13^OE-sEVs may represent a promising therapeutic strategy for diabetic wound healing.This study investigates the therapeutic potential of circCDK13-loaded small extracellular vesicles (sEVs) in diabetic wound healing. CircCDK13, a circular RNA, was identified as a downregulated molecule in diabetic wounds and shown to stimulate the proliferation and migration of human dermal fibroblasts (HDFs) and human epidermal keratinocytes (HEKs) by interacting with insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) in an N6-methyladenosine (m6A)-dependent manner. Engineered sEVs overexpressing circCDK13 (circCDK13^OE-sEVs) were constructed and shown to accelerate wound healing in both type II diabetic mice (db/db) and type I diabetic rats. The results indicate that circCDK13^OE-sEVs restore the functions of age-related end products (AGEs)-induced HDFs and HEKs in vitro and promote wound healing in diabetic animals. The mechanism involves the formation of a circCDK13-IGF2BP3-CD44/c-MYC ternary complex, which enhances the stability of CD44 and c-MYC mRNAs. This study suggests that circCDK13^OE-sEVs may represent a promising therapeutic strategy for diabetic wound healing.