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. 2014 Jul 17;5:169. doi: 10.3389/fphar.2014.00169

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Copyright © 2014 Cheng, Morand and Yang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Strategies to improve glucocorticoid therapy. (A) Cellular effects of glucocorticoids (GC). GCs bind to glucocorticoid receptor (GR) and activate intracellular signaling pathways. Previously, it was believed that transactivation predominantly accounts for the adverse metabolic effects, whereas transrepression/cis-repression mainly mediates anti-inflammatory functions of GCs. (B) The strategy to develop “selective glucocorticoid receptor modulators (SGRM)” based on the paradigm that metabolic effects but not immune-suppressive effects depended on transactivation. (C) The anti-inflammatory effects of GILZ are independent of GR function and may conceivably avoid metabolic effects entirely.