Minireview: Latest Perspectives on Antiinflammatory Actions of Glucocorticoids

Taking into consideration that glucocorticoid ( GC) hormones have been used clinically for over half a century and that more than 20 yr have passed since the cloning of the GC receptor (GR), it is hard to imagine that novel aspects in the molecular mechanism by which GCs mediate their antiinflammatory actions are still being unveiled today. Partly, this is because almost on a daily basis, novel insights arise from parallel fields, e. g. nuclear receptor cofactor and chromatin regulation and their concomitant impact on gene transcription events, eventually leading to a revisitation or refinement of old hypotheses. On the other hand, it does remain striking and puzzling why GCs use different mechanisms in so many different cell types and on many different target genes to elicit an antiinflammatory effect. Meanwhile, the obvious question for the clinic remains: is the separation of GR functionalities through differential ligand design the strategy of choice to avoid most GC-mediated side effects? This minireview aims to highlight some of the latest findings on aspects of the antiinflammatory working mechanisms of GCs. ( Molecular Endocrinology 23: 281-291, 2009

Crosstalk in Inflammation: The Interplay of Glucocorticoid Receptor-Based Mechanisms and Kinases and Phosphatases

Glucocorticoids (GCs) are steroidal ligands for the GC receptor (GR), which can function as a ligand-activated transcription factor. These steroidal ligands and derivatives thereof are the first line of treatment in a vast array of inflammatory diseases. However, due to the general surge of side effects associated with long-term use of GCs and the potential problem of GC resistance in some patients, the scientific world continues to search for a better understanding of the GC-mediated antiinflammatory mechanisms