{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T12:32:21Z","timestamp":1791894741020,"version":"4.3.4"},"reference-count":248,"publisher":"Bioscientifica","issue":"1","license":[{"start":{"date-parts":[[2018,7,1]],"date-time":"2018-07-01T00:00:00Z","timestamp":1530403200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["jme.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2018,7]]},"abstract":"<jats:p>Glucocorticoid hormones (GCs) have profound effects on bone metabolism. Via their nuclear hormone receptor \u2013 the GR \u2013 they act locally within bone cells and modulate their proliferation, differentiation, and cell death. Consequently, high glucocorticoid levels \u2013 as present during steroid therapy or stress \u2013 impair bone growth and integrity, leading to retarded growth and glucocorticoid-induced osteoporosis, respectively. Because of their profound impact on the immune system and bone cell differentiation, GCs also affect bone regeneration and fracture healing. The use of conditional-mutant mouse strains in recent research provided insights into the cell-type-specific actions of the GR. However, despite recent advances in system biology approaches addressing GR genomics in general, little is still known about the molecular mechanisms of GCs and GR in bone cells. Here, we review the most recent findings on the molecular mechanisms of the GR in general and the known cell-type-specific actions of the GR in mesenchymal cells and their derivatives as well as in osteoclasts during bone homeostasis, GC excess, bone regeneration and fracture healing.<\/jats:p>","DOI":"10.1530\/jme-18-0024","type":"journal-article","created":{"date-parts":[[2018,3,27]],"date-time":"2018-03-27T12:12:09Z","timestamp":1522152729000},"page":"R75-R90","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-6","source":"Crossref","is-referenced-by-count":84,"title":["Molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture"],"prefix":"10.1530","volume":"61","author":[{"given":"Yasmine","family":"Hachemi","sequence":"first","affiliation":[{"name":"1Institute of Comparative Molecular Endocrinology, Ulm University, Ulm, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna E","family":"Rapp","sequence":"additional","affiliation":[{"name":"2Institute of Orthopaedic Research and Biomechanics, Ulm University Medical Centre, Ulm, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ann-Kristin","family":"Picke","sequence":"additional","affiliation":[{"name":"1Institute of Comparative Molecular Endocrinology, Ulm University, Ulm, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gilbert","family":"Weidinger","sequence":"additional","affiliation":[{"name":"3Institute of Biochemistry and Molecular Biology, Ulm University, Ulm, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anita","family":"Ignatius","sequence":"additional","affiliation":[{"name":"2Institute of Orthopaedic Research and Biomechanics, Ulm University Medical Centre, Ulm, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan","family":"Tuckermann","sequence":"additional","affiliation":[{"name":"1Institute of 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