SUN-217 Skin Glucocorticoid Metabolism in Burn Injury: Towards Novel Treatments That Reduce Scarring

摘要

The most common and severe complication of burn injury is the development of excessive scarring/tissue fibrosis. No current treatments reduce scarring after burns. Prolonged exposure to high levels of glucocorticoids (Cushing’s syndrome) detrimentally impacts skin, leading to reduced collagen production and impaired wound healing. Skin can generate active glucocorticoids locally through expression and activity of the 11β-hydroxysteroid dehydrogenase type 1 enzyme (11β-HSD1). We hypothesised that local glucocorticoid activation by 11β-HSD1 is an important regulator of wound healing, fibrosis and scarring after burn injury. We additionally proposed that pharmacological manipulation of this system would improve outcomes of burn wound healing.