Key molecule in wound healing identified

The study focuses on the molecular processes in wound healing that regulate the transition from inflammation -- a critical defence mechanism -- to a proliferative phase, where new cells form to repair damaged tissue. Researchers have now mapped lncRNA (long non-coding RNA molecules) in human skin wounds in tissue samples from Karolinska University Hospital, identifying a key regulator in wound healing.

"Our study reveals that the lncRNA molecule SNHG26 plays a pivotal role in guiding skin cells through the stages of wound healing, from an inflammatory stage to a healing phase," explains Ning Xu Landén, docent at the Department of Medicine, Solna, Karolinska Institutet.

The researchers also used mouse models to uncover how this molecule interacts with genes involved in inflammation and tissue regeneration. In mice lacking SNHG26, wound healing was delayed, emphasising the molecule's importance in the balance between inflammation and tissue repair. The discovery paves the way for new therapeutic approaches for acute and chronic wounds.

"By targeting SNHG26, we may be able to accelerate healing and reduce complications, particularly in chronic wounds where prolonged inflammation is a major problem," says Ning Xu Landén.

Her research group at Karolinska Institutet is studying how healing processes in the skin are controlled by so-called regulatory RNA molecules, i.e. RNA molecules that regulate gene activity and include both lncRNAs and the now Nobel Prize-awarded microRNA molecules. The researchers will now continue to study how other regulatory RNA molecules are involved in tissue repair, with the aim of developing innovative treatments for hard-to-heal wounds.

The study was done in close collaboration with Dongqing Li at the Chinese Academy of Medical Sciences. It was supported by the Swedish Research Council, the Ragnar Söderberg Foundation, the LEO Foundation, Ming Wai Lau Centre for Reparative Medicine, Welander and Finsens Foundation, Karolinska Institutet, and National Natural Science Foundation of China. The authors declare no competing interests.