The enzyme, 11β-HSD1, helps to produce cortisol….
Weakened wound healing can lead to the infection of limbs which can become so severe that amputation of the affected area is necessary.
The newly discovered enzyme, 11β-hydroxysteroid dehydrogenase type 1 gene (11β-HSD1), helps to produce the stress hormone, cortisol, which affects skin composition. Cortisol has damaging effects on collagen, an important component of skin elasticity and its ability to heal wounds.
But 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%) compared to mice which still had the gene. Importantly, and of considerable translational potential, a similar result was noted for mice treated with an 11β-HSD1 inhibitor.
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 associated ulcers.
Dr. Gareth Lavery and Professor Paul Stewart, from the University of Birmingham, UK, said, "Poor wound healing is a huge burden for patients with diabetes, with some people having ulcers that heal poorly. Our findings linking poor skin quality — similar to that of aged skin — to 11β-HSD1, raises the exciting possibility that these patients may benefit from 11β-HSD1 inhibitors. ”
11β-hydroxysteroid dehydrogenase type 1 blockade prevents age-induced skin structure and function defects, Journal of Clinical Investigation, 2013.