ALKBH5-Mediated m6A Demethylation Fuels Cutaneous Wound Re-Epithelialization by Enhancing PELI2 mRNA Stability

Increasing m6A levels can improve skin cell growth and wound healing.

This review highlights that the RNA modification N⁶-methyladenosine (m⁶A) plays a crucial role in regulating wound healing and tissue remodeling, with dysregulation contributing to complications in chronic wounds, such as diabetic ulcers and burn injuries, through mechanisms like impaired angiogenesis and increased oxidative stress.

In this study using mice and human keratinocyte cells, researchers found that activating PKM2-mediated glycolysis and Wnt/β-catenin signaling, particularly via combined treatments, significantly accelerated wound healing and induced angiogenesis in wound beds.

The researchers reported that several m6A-related genes, particularly IGF2BP3, were differentially expressed in keloid tissue compared to normal skin, indicating potential targets for understanding keloid pathogenesis and treatment.

This study found that MK6a-deficient mice showed delayed reepithelialization after superficial wounding but not after full-thickness skin wounds, suggesting MK6a plays a role in activating follicular keratinocytes post-wounding.