Projects per year
Abstract / Description of output
Since the discovery of cortisone in the 1940s and its early success in treatment of rheumatoid arthritis, glucocorticoids have remained the mainstay of anti-inflammatory therapies. However, cortisone itself is intrinsically inert. To be effective, it requires conversion to cortisol, the active glucocorticoid, by the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Despite the identification of 11β-HSD in liver in 1953 (which we now know to be 11β-HSD1), its physiological role has been little explored until recently. Over the past decade, however, it has become apparent that 11β-HSD1 plays an important role in shaping endogenous glucocorticoid action. Acute inflammation is more severe with 11β-HSD1-deficiency or inhibition, yet in some inflammatory settings such as obesity or diabetes, 11β-HSD1-deficiency/inhibition is beneficial, reducing inflammation. Current evidence suggests both beneficial and detrimental effects may result from 11β-HSD1 inhibition in chronic inflammatory disease. Here we review recent evidence pertaining to the role of 11β-HSD1 in inflammation.
Original language | English |
---|---|
Pages (from-to) | 82-92 |
Number of pages | 11 |
Journal | Journal of Steroid Biochemistry and Molecular Biology |
Volume | 137 |
Early online date | 19 Feb 2013 |
DOIs | |
Publication status | Published - Sept 2013 |
Keywords / Materials (for Non-textual outputs)
- Glucocorticoid
- mineralocorticoid
- 11β-hydroxysteroid dehydrogenase
- macrophage
- inflammation
- arthritis
Fingerprint
Dive into the research topics of 'Changing glucocorticoid action: 11β-hydroxysteroid dehydrogenase type 1 in acute and chronic inflammation'. Together they form a unique fingerprint.Projects
- 2 Finished
-
How does 11B-hydroxysteriod dehydrogenase type 1 limit inflammation.
Chapman, K., Gray, M., Savill, J. & Seckl, J.
1/10/08 → 30/04/12
Project: Research
-
Edinburgh centre for inflammation research
Savill, J. & Haslett, C.
30/09/04 → 30/09/10
Project: Research