Cell migration in diabetic wound healing: Molecular mechanisms and therapeutic strategies (Review).

Abstract

Diabetic wounds are among the most prevalent forms of chronic wound and are a prominent clinical challenge in contemporary healthcare. Impaired cell migration represents one of the key mechanisms underlying the difficulty in diabetic wound healing, involving multiple cell types including neutrophils, macrophages, keratinocytes, endothelial cells and fibroblasts. Under the influence of pathological factors, including hyperglycemia, chronic inflammation, oxidative stress and an abnormal microenvironment, the cell migration becomes impaired, leading to delayed wound healing. Key signaling pathways including Rho GTPase, PI3K/Akt, TGF‑β/Smad and Wnt/β‑catenin are involved in the regulation of cell migration. Non‑coding RNAs exert a pivotal influence on diabetic wound healing by modulating these signaling pathways or their downstream targets. Notably, stem cells and their exosomes, growth factor therapy, drug‑loaded dressings and traditional Chinese medicine can modulate cell migration via non‑coding RNAs and associated signaling pathways, thereby establishing a therapeutic regulatory axis. This review systematically consolidates advances in this field, providing novel insight into the mechanisms of cell migration in diabetic wounds and facilitating the development of innovative therapeutic strategies.