A team of Stanford Medicine researchers looking to figure out why we scar recently identified a drug that can prevent scarring altogether. They published the research April 23 in Science.
Scars form because they seal an opening in the skin more quickly than normal skin can grow. “A scar is a spot weld — it covers the wound quickly,” said Michael Longaker, MD, a senior author of the study and the Deane P. and Louise Mitchell Professor in the School of Medicine.
But the result can be problematic: Scars lack hair follicles and oil glands and are weaker, thicker and less flexible than other skin.
The study started with exploring the role our skin’s tightness plays in scarring — a clue borne from the scientists’ observations that children and adults scar, but fetal tissue doesn’t, and that the loose skin of older people has minimal scarring.
Their research found that a gene called engrailed signals fibroblasts — a skin cell type that drives scarring — to form scar tissue, but only when skin is stressed. The study’s lead author, graduate student Shamik Mascharak, identified an eye-disease drug called verteporfin that, when applied to surgical wounds in mice, blocked engrailed from signaling scar formation.
“It’s estimated that 45% of Americans die from a disease that involves scarring in some form,” Longaker said. “So there are potentially many more applications.”
Geoffrey Gurtner, MD, the Johnson & Johnson Distinguished Professor in Surgery II, shared senior authorship with Longaker.