期刊
JOURNAL OF MOLECULAR ENDOCRINOLOGY
卷 61, 期 1, 页码 R75-R90出版社
BIOSCIENTIFICA LTD
DOI: 10.1530/JME-18-0024
关键词
glucocorticoid receptor; osteoblast; osteoclast; bone regeneration; fracture healing
资金
- German Research Foundation within the Collaborative Research Centre 'Danger Response, Disturbance Factors, and Regenerative Potential after Acute Trauma' [CRC 1149]
Glucocorticoid hormones (GCs) have profound effects on bone metabolism. Via their nuclear hormone receptor - the GR - they act locally within bone cells and modulate their proliferation, differentiation, and cell death. Consequently, high glucocorticoid levels - as present during steroid therapy or stress - 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.
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