Blocking a crucial enzyme that produces the stress hormone cortisol could lead to improved wound healing in individuals with diabetes-related ulcers, elderly patients who have undergone surgery, or patients treated for burns, according to new research from the University of Birmingham, England. Poor healing of ulcers is a major complication of diabetes, and can lead to infection and possible amputation of the affected area.
Researchers found that wound healing improved when an enzyme called 11β-hydroxysteroid dehydrogenase type 1 gene (11β-HSD1) was deleted or blocked-inhibitors of this enzyme were used to speed up wound healing. The findings, published in the Journal of Clinical Investigation, demonstrate that aged human skin, as well as that exposed to sunlight is associated with higher levels of 11β-HSD1 activity compared to younger skin. Skin 11β-HSD1 generates the steroid hormone cortisol, which is known to affect skin integrity. Cortisol has a negative effect on collagen, which is important for skin elasticity and the ability to heal wounds.
By deleting the 11βHSD1 gene from a group of mice, the researchers found that age-induced thinning of the skin with a loose collagen network was prevented; aged mice had skin quality similar to young counterparts. Wound healing in these mice was significantly accelerated, by up to 50 percent, compared to mice that still had the gene. The researchers said a similar result was noted for mice treated with an 11β-HSD1 inhibitor, which has considerable translational potential.This leads to the possibility of using a topical 11βHSD1 inhibitor to combat age-related skin impairments, or even assist the wound healing process in patients with diabetes-related ulcers.
Editor’s note: This story was adapted from materials provided by the University of Birmingham.