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Molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture
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...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Bioscientifica Ltd
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5976078/ https://www.ncbi.nlm.nih.gov/pubmed/29588427 http://dx.doi.org/10.1530/JME-18-0024 |
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author | Hachemi, Yasmine Rapp, Anna E Picke, Ann-Kristin Weidinger, Gilbert Ignatius, Anita Tuckermann, Jan |
author_facet | Hachemi, Yasmine Rapp, Anna E Picke, Ann-Kristin Weidinger, Gilbert Ignatius, Anita Tuckermann, Jan |
author_sort | Hachemi, Yasmine |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-5976078 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Bioscientifica Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-59760782018-06-04 Molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture Hachemi, Yasmine Rapp, Anna E Picke, Ann-Kristin Weidinger, Gilbert Ignatius, Anita Tuckermann, Jan J Mol Endocrinol Review 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. Bioscientifica Ltd 2018-03-27 /pmc/articles/PMC5976078/ /pubmed/29588427 http://dx.doi.org/10.1530/JME-18-0024 Text en © 2018 The authors http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 Unported License (http://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Review Hachemi, Yasmine Rapp, Anna E Picke, Ann-Kristin Weidinger, Gilbert Ignatius, Anita Tuckermann, Jan Molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture |
title | Molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture |
title_full | Molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture |
title_fullStr | Molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture |
title_full_unstemmed | Molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture |
title_short | Molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture |
title_sort | molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5976078/ https://www.ncbi.nlm.nih.gov/pubmed/29588427 http://dx.doi.org/10.1530/JME-18-0024 |
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