Skin and glucocorticoids: Effects of local skin glucocorticoid impairment on skin homeostasis

Abstract

The role of skin as a de novo source of glucocorticoids and the importance of cutaneous glucocorticoidogenesis as a homeostatic mechanism in human skin is highlighted by Slominski et al. in a recently published issue. Impairment of glucocorticoidogenesis through noxious stimuli, such as UVB, can explain pathophysiology of skin diseases (e.g. rosacea). In addition to keratinocytes, melanocytes and fibroblasts, cutaneous adnexes also play a significant role as targets and sources of glucocorticoids, because they express most of the enzymes required for steroidogenesis. Glucocorticoids are also involved in the pathogenesis of acne lesions, affecting sebum production in vivo and in vitro. Certain steroidogenic enzymes, such as 11β-hydroxysteroid dehydrogenase, are upregulated in acne lesions. On this background, the paper by Slominski et al. provides further insights into dermatoendocrinology, with emphasis on the importance of an impairment of the skin's own hypothalamic-pituitary-adrenal-like axis in the pathophysiology of several skin diseases.