Wound healing is a highly coordinated physiological process, which is essential for restoring the structural and functional integrity of damaged tissues. The present review explores the multifaceted roles of epigenetic modifications in wound healing and their potential as therapeutic targets. Epigenetic mechanisms, including DNA methylation, histone modifications, regulation by non‑coding RNAs (ncRNAs) and RNA methylation, influence the speed and quality of wound repair by regulating gene expression, cell function and intercellular signaling. During the hemostasis phase, DNA methylation of genes such as platelet endothelial aggregation receptor 1 can impact platelet function, while histone methylation and acetylation serve critical roles in modulating inflammation and fibroblast activation. ncRNAs, such as microRNAs and long ncRNAs, regulate cell proliferation, collagen deposition and scar formation. N6‑methyladenosine modifications, a type of RNA methylation, impact autophagy and fibrosis through their interaction with YTH domain family proteins. Key epigenetic regulators influence wound healing outcomes, providing valuable insights for the development of novel therapeutic strategies. However, challenges remain in translating these findings into clinical applications due to the complexity of epigenetic networks and the need for precise regulatory tools. Future research should focus on elucidating the cell‑specific and spatiotemporal regulatory mechanisms of epigenetic modifications in wound healing, and exploring their potential as therapeutic targets for reducing scar formation and preventing chronic wounds.
Cheng et al. (Sat,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: