Most of us have had wounds at some point: some have healed with scars slightly similar in texture with the skin. Others have left heaped, ugly scars that we would wish to have disappeared. People who have had burns, from any cause, suffer debilitating wounds that heal with scars that not only disfigure them but also leave withering marks that culminate in disability and poor quality of life. The costs involved in treating scars are exorbitant. To prevent scarring is an ultimate goal that any human would wish to achieve. The good news is, in a new study, scientists were able to identify a gene that signals scarring during the wound healing process in mice. And when they knocked out the gene, the mice wounds healed without scarring.
For every wound, there’s a scar. Every scar tells a story. A story that reminds us how we survived. However, some scar tissues minify the story because they become ugly. Others form vast forms – keloids. The disfigurement and disability that may arise can lead to poor quality of life. Say, a poorly healed wound on the fingers that culminate in formation contractures. Contractures render the fingers less usable as they have stiffened. Imagine if all the wounds healed without a scar.
Wound healing is a process that involves the recruitment of cells – fibroblasts – that build up collagen and other extracellular matrix molecules as they interact with each other. The wound healing pathways involve a pivotal gene called engrailed-1 (En1). Mascharak et al. noted that when wounds are healing, the fibroblasts express this gene. As they interact with the tensile forces within the injured tissues, fibroblasts undergo conformational changes to form scar tissue around the wound.
Further still, Mascharak et al. identified the ability of verteporfin to block a crucial common pathway in wound healing. The FDA approved verteporfin to treat retinal neovascularization.
Once the drug blocks the pathway, the fibroblasts don’t express the En1 and therefore lose the ability to deposit collagen fibres that lead to scarring. They, however, noted that the process of healing in these knockout mice is slower than in the mice with the fully functional gene.
It’s an achievement that if clinicians can duplicate the findings into human beings, it will be revolutionary. The catch is, much as the drug – verteporfin – knocked out the En1 gene, it may not do so in human wounds. It’s noteworthy that verteporfin blocks the proliferation of cells within the liver. And can inhibit fibrosis in persistent cholestasis and within the lungs. Scarless wound healing may be the new phase in understanding skin regeneration.